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  • Articles  (716)
  • Mice  (716)
  • 2000-2004  (406)
  • 1995-1999  (159)
  • 1980-1984  (92)
  • 1975-1979  (59)
  • 2002  (225)
  • 2000  (181)
  • 1998  (159)
  • 1982  (92)
  • 1978  (57)
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  • Articles  (716)
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  • 2000-2004  (406)
  • 1995-1999  (159)
  • 1980-1984  (92)
  • 1975-1979  (59)
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  • 1
    Electronic Resource
    Electronic Resource
    Neutralizing antibody provided protection against enterovirus type 71 lethal challenge in neonatal mice (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 523-528 
    Details
    ISSN: 1423-0127
    Keywords: Enterovirus type 71 ; Experimental infection ; Mice ; Neutralizing antibody ; Vaccine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Experimental infection with enterovirus type 71 (EV71) induced death in neonatal mice in an age- and dose-dependent manner. The mortality rate was 100% following intraperitoneal inoculation 1-day-old ICR mice and this gradually decreased as the age at the time of inoculation increased (60% in 3-day-old mice and no deaths occurred in mice older than 6 days of age). A lethal dose greater than 108 PFU was necessary. Lethargy, failure to gain weight, rear limb tremors and paralysis were observed in the infected mice before death. EV71 was isolated from various tissues of the dead mice. Using a reverse transcription polymerase chain reaction technique with a specific primer pair, a 332-bp product was detected in the tissues that produced a culture positive for EV71. Protection against EV71 challenge in neonatal mice was demonstrated following passive transfer of serum from actively immunized adult mice 1 day after inoculation with the virus. Pups from hyperimmune dams were resistant to EV71 challenge. Additionally, maternal immunization with a formalin-inactivated whole-virus vaccine prolonged the survival of pups after EV71 lethal challenge.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253368
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  • 2
    Electronic Resource
    Electronic Resource
    Direct and maternal genetic effects on body weight maturing patterns in mice (1978)
    Springer
    Theoretical and applied genetics 51 (1978), S. 249-260 
    Details
    ISSN: 1432-2242
    Keywords: Mice ; Maternal Effects ; Body Weight ; Maturity ; Sex-linkage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Direct and maternal genetic effects were evaluated for maturing patterns of body weight in mice using a crossfostering design. Crossfostering was performed in one group using dams from populations selected for rapid growth rate (M16 and H6) and their reciprocal F1. crosses. A second crossfostering group consisted of dams from the respective control populations (ICR and C2) and their reciprocal F1. 's. Population differences were partitioned into direct and maternal effects due to genetic origin, correlated selection responses, heterosis and cytoplasmic or sex-linked effects. Degree of maturity was calculated at birth, 12, 21, 31 and 42 days of age by dividing body weight at each age by 63-day weight. Absolute and relative maturing rates were calculated in adjacent age intervals between birth and 63 days. Genetic origin effects (ICR vs. C2; M16 vs. H6) were significant for many maturity traits, with average direct being more important than average maternal genetic effects. In general, correlated responses to selection for maturity traits were larger in the M16 population (M16 vs. ICR) than in the H6 population (H6 vs. C2) and correlated responses in average direct effects were larger than average maternal effects. Positive correlated responses in average direct effects were found for relative maturing rates at all ages and for absolute maturing rates from 31 to 63 days. Apparent correlated responses in degree of maturity were negative for M16 and H6. However, further analysis suggested that the correlated response for degree of maturity in H6 may be positive at later ages and negative at earlier ages. Direct and maternal heterosis for degree of maturity was positive in the selected and control crosses. Absolute and relative maturing rates showed positive heterosis initially, followed by negative heterosis. Reciprocal differences due to the cytoplasm or sex-linkage were not important for patterns of maturity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00273772
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  • 3
    Electronic Resource
    Electronic Resource
    Feed efficiency and body composition of selected and unselected mice (1977)
    Springer
    Theoretical and applied genetics 50 (1977), S. 179-184 
    Details
    ISSN: 1432-2242
    Keywords: Mice ; Feed Efficiency ; Body Composition ; Protein Content ; Selection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary An examination was carried out of the feed intake, feed efficiency and body composition of selected and unselected mice. It was demonstrated that selected mice utilised food more economically, and, in total, produced more protein than the control animals. However, selection had a negative influence on the percentage content of protein and ash. Also, selection caused greater adiposity of selected females and a greater water content in the bodies of selected males (in %).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277739
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  • 4
    Electronic Resource
    Electronic Resource
    The relative importance of prenatal and postnatal maternal influences on growth in mice (1977)
    Springer
    Theoretical and applied genetics 51 (1977), S. 119-125 
    Details
    ISSN: 1432-2242
    Keywords: Mice ; Cross-nursing Technique ; Body Weight ; Prenatal and Postnatal Maternal Influences
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The cross-nursing technique was used to assess the relative importance of prenatal and postnatal maternal influences on growth in mice from an unselected population originated from a cross of four highly inbred strains. Body weights were studied at birth, 7-, 14-, 21- and 42-days, in addition to the weight gains between these ages and tail length at 21 and 42 days of age. At littering, each dam in each nursing set retained two of her own offspring and two were transfereed to each of the other dams in the set, so that each nursed litter contained six young representing three mothers. Prenatal influences accounted for 37, 15, 10, 11 and 13 % of the total variation in the respective body weights, while postnatal influences accounted for 0, 64, 65, 49 and 14% at the respective ages. In the case of weight gains, prenatal influences were responsible for 16, 4, 6 and 30%, while postnatal influences were responsible for 66, 66, 31 and 7% of the total variation in gain during the respective four periods examined. Apparently the individual weight gain from 7 to 14 days was a better measure of the lactational performance of the dam than individual 14-day weight. For tail length, prenatal influences accounted for 6 % and 4 % of the total variation in tail length at 21 and 42 days, respectively, while postnatal influences accounted for 60 % and 24 % at the respective ages. Generally, there was no indication of an important interaction between the nurse and the nursed young at any stage studied.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00273823
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  • 5
    Electronic Resource
    Electronic Resource
    Correlated responses of growth traits to selection for high and low plasma alkaline phosphatase in mice (1982)
    Springer
    Theoretical and applied genetics 62 (1982), S. 281-287 
    Details
    ISSN: 1432-2242
    Keywords: Growth ; Alkaline phosphatase ; Selection ; Correlated responses ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The effectiveness of two way selection for plasma alkaline phosphatase (ALP) was investigated in order to determine its influences on growth traits through thirteen generations. The responses of the two lines selected for high (HP) and low (LP) ALP at 45 days of age were compared to that of the mice selected for large (L) and small (SM) body size. The selection responses of plasma ALP were very effective for both HP and LP lines, with average responses per generation calculated from linear regressions of 0.227±0.037 and −0.088±0.022 respectively. The final levels of ALP in HP and LP were 5.54±0.71 and 1.27±0.20 in the thirtheenth generation, while the SM, L and base population had levels of 3.49±0.08, 0.86±0.55 and 2.77±0.56 respectively. The body weight at 45 days of age in LP (31.4±1.4 g) as a correlated response was significantly higher than HP (23.4±1.8 g) at generation 10. The correlated response of milk yield, measured by weight gain up to 12 days of age, was significantly greater in the LP line than in HP, but the correlated response of gains after weaning was not so different as the response of milk yield. The response of litter size and weight in LP showed significant higher levels than that of HP, but pups' birth weight did not differ between LP and HP. It is suggested that the correlated response of milk yield contributed more to the divergence of body size between HP and LP than the gain after weaning. Realized heritabilities of ALP were 0.335±0.059 (HP) and 0.279±0.051 (LP). Realized genetic correlations between ALP and 45 days' body weight were −0.27±0.13 (HP with SM) and −0.52±0.19 (LP with L). Realized genetic correlations between ALP and milk yield were −0.95±0.03 (HP) and −0.37±0.29 (LP). Correlations between ALP and postweaning gains were fairly low.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00276252
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  • 6
    Electronic Resource
    Electronic Resource
    Direct and correlated responses to selection for post-weaning weight gain on ad libitum or restricted feeding in mice (1982)
    Springer
    Theoretical and applied genetics 63 (1982), S. 145-150 
    Details
    ISSN: 1432-2242
    Keywords: Mice ; Selection ; Growth rate ; ad libitum feeding ; Restricted feeding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Selection for post-weaning weight gain in mice from 21 to 42 days, on either a full or restricted feeding level during this period was carried out for seven generations. Control lines were maintained for each feeding level. The rate of selection response was higher on full feeding due to a higher heritability and a larger phenotypic variance. Realised heritabilities of 0.29±0.05 and 0.19±0.04 for selection on full and restricted feeding respectively, were in close agreement with base population estimates. Selection on full feeding led to positive correlated responses in 21 day weight, 42 day weight, food intake and efficiency between 21 and 42 days, and 42 day tail length, but with little change in reproductive performance. Correlated responses to selection on restricted feeding were reduced 21 day weight, but an increase in 42 day weight and increased efficiency from 21 to 42 days. However, overall reproductive performance fell.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00303697
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  • 7
    Electronic Resource
    Electronic Resource
    Co-housing in a stable hierarchical group is not aversive for dominant and subordinate individuals (2000)
    Springer
    Neuroscience and behavioral physiology 30 (2000), S. 195-200 
    Details
    ISSN: 1573-899X
    Keywords: Mice ; dominance ; subordinacy ; stress ; aggression ; locomotor activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The behavior of individaals and their responses to external stimuli are controlled by the microsocial environment, which for most mammals is associated with dominant-subordinate relationships. Physiological and behavioral differences between dominant and subordinate individuals may be ‘primary’ (genetically determined) or ‘secondary’ (due to position in the group's hierarchical structure). A series of experiments was conducted to investigate the physiological (pain response threshold), immunological (thymus, spleen weights, primary immune response), and behavioral (motor activity, behavior in a shuttle box test) characteristics of dominant and subordinate individuals in groups of three laboratory mice formed on the basis of linear hierarchy. Assessment of the effects of group conditions was made using a conditioned reflex location preference test. The results showed: 1) there are no statistically significant differences in physiological and behavioral (except for motor activity) parameters between dominant and subordinate mice; 2) co-housing of dominant and subordinate individuals in groups with stable hierarchical relationships was not aversive for them.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02463158
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  • 8
    Electronic Resource
    Electronic Resource
    Genetic and Developmental Influences on Infant Mouse Ultrasonic Calling. II. Developmental Patterns in the Calls of Mice 2–12 Days of Age (1998)
    Springer
    Behavior genetics 28 (1998), S. 315-325 
    Details
    ISSN: 1573-3297
    Keywords: Mice ; ultrasonic calls ; infants ; individual differences ; signatures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Psychology
    Notes: Abstract Infant house mice, Mus musculus, produce ultrasonic calls that reliably lead to retrieval by adult mice. While individual differences in calls have been demonstrated both among and within species, the influences of age and sex on call characteristics have not been systematically investigated in mice. This study examined the influences of age, sex, and genotype (inbred versus hybrid) on the rate, length, and frequency characteristics of the calls of 486 male and female mice from 2 to 12 days of age. Rate of calling followed a shallow inverted U-shaped function across days. Call lengths decreased and call frequency characteristics increased, in a linear manner, with age. Females emitted fewer calls, with a smaller bandwidth, at some ages than males. Hybrid pups produced more calls of greater length and a lower frequency than inbred pups. These results indicate the presence of cues that could allow adult mice to behave differentially toward pups as a function of their age and sex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1021679615792
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  • 9
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    Cancer. BRCA2 enters the fray (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, John H -- Elledge, Stephen J -- New York, N.Y. -- Science. 2002 Sep 13;297(5588):1822-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12228708" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; BRCA2 Protein/*chemistry/*metabolism ; Binding Sites ; Breast Neoplasms/genetics ; Crystallography, X-Ray ; DNA/*metabolism ; DNA Damage ; *DNA Repair ; DNA, Single-Stranded/metabolism ; DNA-Binding Proteins/metabolism ; Female ; Genes, BRCA1 ; Genes, BRCA2 ; Genetic Predisposition to Disease ; Humans ; Mice ; Ovarian Neoplasms/genetics ; Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rad51 Recombinase ; Rats ; Recombination, Genetic ; Replication Protein A
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Direct recognition of cytomegalovirus by activating and inhibitory NK cell receptors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-16
    Description: Natural killer (NK) cells express inhibitory receptors for major histocompatibility complex (MHC) class I antigens, preventing attack against healthy cells. Mouse cytomegalovirus (MCMV) encodes an MHC-like protein (m157) that binds to an inhibitory NK cell receptor in certain MCMV-susceptible mice. In MCMV-resistant mice, this viral protein engages a related activating receptor (Ly49H) and confers host protection. These activating and inhibitory receptors are highly homologous, suggesting the possibility that one evolved from the other in response to selective pressure imposed by the pathogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arase, Hisashi -- Mocarski, Edward S -- Campbell, Ann E -- Hill, Ann B -- Lanier, Lewis L -- AI30363/AI/NIAID NIH HHS/ -- CA89294/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 May 17;296(5571):1323-6. Epub 2002 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and the Cancer Research Institute, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11950999" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antigens, Ly/chemistry/genetics/*immunology/metabolism ; Cell Line ; Coculture Techniques ; Disease Susceptibility ; Evolution, Molecular ; Herpesviridae Infections/*immunology ; Histocompatibility Antigens Class I/immunology ; Hybridomas ; Immunity, Innate ; Interferon-gamma/biosynthesis ; Killer Cells, Natural/*immunology ; Lectins, C-Type ; Ligands ; Lymphocyte Activation ; Membrane Glycoproteins/chemistry/genetics/*immunology/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Muromegalovirus/genetics/*immunology/metabolism ; NK Cell Lectin-Like Receptor Subfamily A ; Protein Binding ; Receptors, Immunologic/chemistry/genetics/*immunology/metabolism ; Receptors, NK Cell Lectin-Like ; Recombinant Fusion Proteins/metabolism ; Transfection ; Viral Proteins/chemistry/genetics/*immunology/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Genomic instability in mice lacking histone H2AX (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-06
    Description: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Celeste, Arkady -- Petersen, Simone -- Romanienko, Peter J -- Fernandez-Capetillo, Oscar -- Chen, Hua Tang -- Sedelnikova, Olga A -- Reina-San-Martin, Bernardo -- Coppola, Vincenzo -- Meffre, Eric -- Difilippantonio, Michael J -- Redon, Christophe -- Pilch, Duane R -- Olaru, Alexandru -- Eckhaus, Michael -- Camerini-Otero, R Daniel -- Tessarollo, Lino -- Livak, Ferenc -- Manova, Katia -- Bonner, William M -- Nussenzweig, Michel C -- Nussenzweig, Andre -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):922-7. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934988" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology/physiology ; Base Sequence ; Cell Aging ; Cell Cycle ; Cells, Cultured ; *Chromosome Aberrations ; DNA Damage ; *DNA Repair ; Female ; Gene Targeting ; Histones/chemistry/*genetics/*physiology ; Immunoglobulin Class Switching ; Infertility, Male/genetics/physiopathology ; Lymphocyte Count ; Male ; Meiosis ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Phosphorylation ; *Recombination, Genetic ; Spermatocytes/physiology ; T-Lymphocytes/immunology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Chemical synthesis of poliovirus cDNA: generation of infectious virus in the absence of natural template (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-13
    Description: Full-length poliovirus complementary DNA (cDNA) was synthesized by assembling oligonucleotides of plus and minus strand polarity. The synthetic poliovirus cDNA was transcribed by RNA polymerase into viral RNA, which translated and replicated in a cell-free extract, resulting in the de novo synthesis of infectious poliovirus. Experiments in tissue culture using neutralizing antibodies and CD155 receptor-specific antibodies and neurovirulence tests in CD155 transgenic mice confirmed that the synthetic virus had biochemical and pathogenic characteristics of poliovirus. Our results show that it is possible to synthesize an infectious agent by in vitro chemical-biochemical means solely by following instructions from a written sequence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cello, Jeronimo -- Paul, Aniko V -- Wimmer, Eckard -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):1016-8. Epub 2002 Jul 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-5222, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12114528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Capsid/metabolism ; Cell-Free System ; DNA, Complementary/*chemical synthesis/genetics ; DNA-Directed RNA Polymerases/genetics ; Female ; *Genome, Viral ; HeLa Cells ; Humans ; Male ; *Membrane Proteins ; Mice ; Mice, Transgenic ; Neutralization Tests ; Poliomyelitis/virology ; *Poliovirus/genetics/immunology/pathogenicity/physiology ; Promoter Regions, Genetic ; Protein Biosynthesis ; RNA, Viral/*chemical synthesis/genetics/physiology ; Receptors, Virus/genetics/immunology/metabolism ; Transcription, Genetic ; Viral Plaque Assay ; Viral Proteins ; Virulence ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: There is a relation between stress and alcohol drinking. We show that the corticotropin-releasing hormone (CRH) system that mediates endocrine and behavioral responses to stress plays a role in the control of long-term alcohol drinking. In mice lacking a functional CRH1 receptor, stress leads to enhanced and progressively increasing alcohol intake. The effect of repeated stress on alcohol drinking behavior appeared with a delay and persisted throughout life. It was associated with an up-regulation of the N-methyl-d-aspartate receptor subunit NR2B. Alterations in the CRH1 receptor gene and adaptional changes in NR2B subunits may constitute a genetic risk factor for stress-induced alcohol drinking and alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sillaber, Inge -- Rammes, Gerhard -- Zimmermann, Stephan -- Mahal, Beatrice -- Zieglgansberger, Walter -- Wurst, Wolfgang -- Holsboer, Florian -- Spanagel, Rainer -- New York, N.Y. -- Science. 2002 May 3;296(5569):931-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany. sillaber@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988580" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; *Alcohol Drinking ; Alcoholism/*etiology/genetics ; Animals ; Brain/metabolism ; Corticotropin-Releasing Hormone/physiology ; Ethanol/blood ; Female ; Hippocampus/physiology ; In Vitro Techniques ; Male ; Mice ; Mice, Knockout ; Models, Animal ; Mutation ; Receptors, AMPA/metabolism ; Receptors, Corticotropin-Releasing Hormone/*genetics/*physiology ; Receptors, Kainic Acid/metabolism ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Signal Transduction ; Stress, Physiological/physiopathology ; Stress, Psychological/*physiopathology ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Intellectual property. DuPont ups ante on use of Harvard's OncoMouse (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, Eliot -- New York, N.Y. -- Science. 2002 May 17;296(5571):1212.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016275" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Models, Animal ; Drug Industry/legislation & jurisprudence ; Drug Screening Assays, Antitumor ; Mice ; *Mice, Transgenic ; National Institutes of Health (U.S.)/legislation & jurisprudence ; *Neoplasms, Experimental ; *Patents as Topic ; United States ; Universities/legislation & jurisprudence
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Pheromone reception. When in doubt, mice mate rather than hate (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckman, Mary -- New York, N.Y. -- Science. 2002 Feb 1;295(5556):782.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11823614" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Animals ; *Behavior, Animal ; Cues ; Female ; Male ; Membrane Proteins/*genetics/*physiology ; Mice ; Mice, Knockout ; Neurons/physiology ; Pheromones/*physiology ; Sex Characteristics ; *Sexual Behavior, Animal ; TRPC Cation Channels ; Vomeronasal Organ/*innervation/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Inflammatory arthritis. How immune system gangs up on joints (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckman, Mary -- New York, N.Y. -- Science. 2002 Sep 6;297(5587):1626-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12215618" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*immunology ; Arthritis, Rheumatoid/immunology ; Autoantibodies/immunology ; Humans ; Joints/*immunology ; Mast Cells/immunology ; Mice
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Generation of an LFA-1 antagonist by the transfer of the ICAM-1 immunoregulatory epitope to a small molecule (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-09
    Description: The protein-protein interaction between leukocyte functional antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) is critical to lymphocyte and immune system function. Here, we report on the transfer of the contiguous, nonlinear epitope of ICAM-1, responsible for its association with LFA-1, to a small-molecule framework. These LFA-1 antagonists bound LFA-1, blocked binding of ICAM-1, and inhibited a mixed lymphocyte reaction (MLR) with potency significantly greater than that of cyclosporine A. Furthermore, in comparison to an antibody to LFA-1, they exhibited significant anti-inflammatory effects in vivo. These results demonstrate the utility of small-molecule mimics of nonlinear protein epitopes and the protein epitopes themselves as leads in the identification of novel pharmaceutical agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gadek, T R -- Burdick, D J -- McDowell, R S -- Stanley, M S -- Marsters, J C Jr -- Paris, K J -- Oare, D A -- Reynolds, M E -- Ladner, C -- Zioncheck, K A -- Lee, W P -- Gribling, P -- Dennis, M S -- Skelton, N J -- Tumas, D B -- Clark, K R -- Keating, S M -- Beresini, M H -- Tilley, J W -- Presta, L G -- Bodary, S C -- New York, N.Y. -- Science. 2002 Feb 8;295(5557):1086-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioorganic Chemistry, Genentech, One DNA Way, South San Francisco, CA 94080, USA. trg@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11834839" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemical ; synthesis/chemistry/metabolism/pharmacology ; Cyclosporine/pharmacology ; Dermatitis, Irritant/drug therapy ; Dinitrofluorobenzene ; Drug Design ; Enzyme-Linked Immunosorbent Assay ; Epitopes ; Female ; Humans ; Immunoglobulin Fab Fragments/immunology/pharmacology ; Immunosuppressive Agents/chemical synthesis/chemistry/metabolism/*pharmacology ; Intercellular Adhesion Molecule-1/chemistry/*immunology/*metabolism ; Lymphocyte Culture Test, Mixed ; Lymphocyte Function-Associated Antigen-1/immunology/*metabolism ; Mice ; Mice, Inbred BALB C ; Molecular Mimicry ; Mutagenesis ; Protein Structure, Secondary ; Structure-Activity Relationship ; Thiophenes/*chemical synthesis/chemistry/metabolism/*pharmacology ; beta-Alanine/analogs & derivatives/*chemical ; synthesis/chemistry/metabolism/*pharmacology
    Print ISSN: 0036-8075
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  • 18
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    Critical roles of activation-induced cytidine deaminase in the homeostasis of gut flora (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-16
    Description: Activation-induced cytidine deaminase (AID) plays an essential role in class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes. We report here that deficiency in AID results in the development of hyperplasia of isolated lymphoid follicles (ILFs) associated with a 100-fold expansion of anaerobic flora in the small intestine. Reduction of bacterial flora by antibiotic treatment of AID-/- mice abolished ILF hyperplasia as well as the germinal center enlargement seen in secondary lymphoid tissues. Because an inability to switch to immunoglobulin A on its own does not lead to a similar phenotype, these results suggest that SHM of ILF B cells plays a critical role in regulating intestinal microflora.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fagarasan, Sidonia -- Muramatsu, Masamichi -- Suzuki, Keiichiro -- Nagaoka, Hitoshi -- Hiai, Hiroshi -- Honjo, Tasuku -- New York, N.Y. -- Science. 2002 Nov 15;298(5597):1424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12434060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents ; B-Lymphocytes/immunology ; Bacteria, Aerobic/*growth & development ; Bacteria, Anaerobic/*growth & development ; Cell Division ; Colony Count, Microbial ; Cytidine Deaminase/genetics/*metabolism ; Dendritic Cells, Follicular/immunology ; Drug Therapy, Combination/pharmacology ; Genes, Immunoglobulin ; Germinal Center/immunology ; Homeostasis ; Hyperplasia ; Immunization ; Immunoglobulin Class Switching ; Immunoglobulin Variable Region/genetics ; Intestine, Small/immunology/*microbiology ; Lymphocyte Activation ; Lymphoid Tissue/immunology/*pathology ; Metronidazole/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Peyer's Patches/pathology ; Somatic Hypermutation, Immunoglobulin ; T-Lymphocytes/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Inhibition of excess nodal signaling during mouse gastrulation by the transcriptional corepressor DRAP1 (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-10
    Description: The formation and patterning of mesoderm during mammalian gastrulation require the activity of Nodal, a secreted mesoderm-inducing factor of the transforming growth factor-beta (TGF-beta) family. Here we show that the transcriptional corepressor DRAP1 has a very specific role in regulation of Nodal activity during mouse embryogenesis. We find that loss of Drap1 leads to severe gastrulation defects that are consistent with increased expression of Nodal and can be partially suppressed by Nodal heterozygosity. Biochemical studies indicate that DRAP1 interacts with and inhibits DNA binding by the winged-helix transcription factor FoxH1 (FAST), a critical component of a positive feedback loop for Nodal activity. We propose that DRAP1 limits the spread of a morphogenetic signal by down-modulating the response to the Nodal autoregulatory loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iratni, Rabah -- Yan, Yu-Ting -- Chen, Canhe -- Ding, Jixiang -- Zhang, Yi -- Price, Sandy M -- Reinberg, Danny -- Shen, Michael M -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1996-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, Division of Nucleic Acids Enzymology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471260" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Line ; Crosses, Genetic ; DNA/metabolism ; DNA-Binding Proteins/metabolism ; *Embryonic and Fetal Development ; Female ; Forkhead Transcription Factors ; Gastrula/*physiology ; Gene Expression Regulation, Developmental ; Gene Targeting ; Heterozygote ; In Situ Hybridization ; Left-Right Determination Factors ; Male ; Mesoderm/cytology/physiology ; Mice ; Morphogenesis ; Mutation ; Nodal Protein ; Phenotype ; Protein Binding ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; *Signal Transduction ; Transcription Factors/metabolism ; Transforming Growth Factor beta/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Genomics. Mmu 16--comparative genomic highlights (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, Neal G -- Jenkins, Nancy A -- O'Brien, Stephen J -- New York, N.Y. -- Science. 2002 May 31;296(5573):1617-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, 21702, USA. copeland@ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12040165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Biological Evolution ; Chromosome Aberrations ; Chromosomes/*genetics ; Chromosomes, Human/genetics ; Computational Biology ; Conserved Sequence ; Evolution, Molecular ; Gene Duplication ; Gene Rearrangement ; Genes ; Genome ; *Genome, Human ; Genomics ; Humans ; Mice ; Mice, Inbred Strains/*genetics ; Multigene Family ; *Sequence Analysis, DNA ; Species Specificity ; Synteny
    Print ISSN: 0036-8075
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  • 21
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    Structural basis of plasticity in T cell receptor recognition of a self peptide-MHC antigen (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: The T cell receptor (TCR) inherently has dual specificity. T cells must recognize self-antigens in the thymus during maturation and then discriminate between foreign pathogens in the periphery. A molecular basis for this cross-reactivity is elucidated by the crystal structure of the alloreactive 2C TCR bound to self peptide-major histocompatibility complex (pMHC) antigen H-2Kb-dEV8 refined against anisotropic 3.0 angstrom resolution x-ray data. The interface between peptide and TCR exhibits extremely poor shape complementarity, and the TCR beta chain complementarity-determining region 3 (CDR3) has minimal interaction with the dEV8 peptide. Large conformational changes in three of the TCR CDR loops are induced upon binding, providing a mechanism of structural plasticity to accommodate a variety of different peptide antigens. Extensive TCR interaction with the pMHC alpha helices suggests a generalized orientation that is mediated by the Valpha domain of the TCR and rationalizes how TCRs can effectively "scan" different peptides bound within a large, low-affinity MHC structural framework for those that provide the slight additional kinetic stabilization required for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia, K C -- Degano, M -- Pease, L R -- Huang, M -- Peterson, P A -- Teyton, L -- Wilson, I A -- AI42266/AI/NIAID NIH HHS/ -- AI42267/AI/NIAID NIH HHS/ -- R01 CA58896/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1166-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute of Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9469799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallization ; Crystallography, X-Ray ; H-2 Antigens/*chemistry/*immunology/metabolism ; Ligands ; Mice ; Mice, Transgenic ; Models, Molecular ; Mutation ; Oligopeptides/*chemistry/immunology/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/*immunology/metabolism ; Recombinant Proteins
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  • 22
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    Identification of alpha-dystroglycan as a receptor for lymphocytic choriomeningitis virus and Lassa fever virus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: A peripheral membrane protein that is interactive with lymphocytic choriomeningitis virus (LCMV) was purified from cells permissive to infection. Tryptic peptides from this protein were determined to be alpha-dystroglycan (alpha-DG). Several strains of LCMV and other arenaviruses, including Lassa fever virus (LFV), Oliveros, and Mobala, bound to purified alpha-DG protein. Soluble alpha-DG blocked both LCMV and LFV infection. Cells bearing a null mutation of the gene encoding DG were resistant to LCMV infection, and reconstitution of DG expression in null mutant cells restored susceptibility to LCMV infection. Thus, alpha-DG is a cellular receptor for both LCMV and LFV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, W -- Henry, M D -- Borrow, P -- Yamada, H -- Elder, J H -- Ravkov, E V -- Nichol, S T -- Compans, R W -- Campbell, K P -- Oldstone, M B -- AG 00080/AG/NIA NIH HHS/ -- AI 09484/AI/NIAID NIH HHS/ -- DK09712/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2079-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851928" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arenavirus/metabolism ; Cell Line ; Cytoskeletal Proteins/chemistry/genetics/*metabolism ; Dystroglycans ; Lassa virus/*metabolism/physiology ; Lymphocytic choriomeningitis virus/*metabolism/physiology ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Receptors, Virus/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Role of IQGAP1, a target of the small GTPases Cdc42 and Rac1, in regulation of E-cadherin- mediated cell-cell adhesion (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: The small guanosine triphosphatases (GTPases) Cdc42 and Rac1 regulate E-cadherin-mediated cell-cell adhesion. IQGAP1, a target of Cdc42 and Rac1, was localized with E-cadherin and beta-catenin at sites of cell-cell contact in mouse L fibroblasts expressing E-cadherin (EL cells), and interacted with E-cadherin and beta-catenin both in vivo and in vitro. IQGAP1 induced the dissociation of alpha-catenin from a cadherin-catenin complex in vitro and in vivo. Overexpression of IQGAP1 in EL cells, but not in L cells expressing an E-cadherin-alpha-catenin chimeric protein, resulted in a decrease in E-cadherin-mediated cell-cell adhesive activity. Thus, IQGAP1, acting downstream of Cdc42 and Rac1, appears to regulate cell-cell adhesion through the cadherin-catenin pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuroda, S -- Fukata, M -- Nakagawa, M -- Fujii, K -- Nakamura, T -- Ookubo, T -- Izawa, I -- Nagase, T -- Nomura, N -- Tani, H -- Shoji, I -- Matsuura, Y -- Yonehara, S -- Kaibuchi, K -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):832-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694656" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadherins/*metabolism ; *Cell Adhesion ; Cell Cycle Proteins/*metabolism ; Cell Membrane/metabolism ; Cytoskeletal Proteins/metabolism ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; GTPase-Activating Proteins ; L Cells (Cell Line) ; Mice ; Mutation ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; *Trans-Activators ; alpha Catenin ; beta Catenin ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    A receptor/cytoskeletal movement triggered by costimulation during T cell activation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: During T cell activation, the engagement of costimulatory molecules is often crucial to the development of an effective immune response, but the mechanism by which this is achieved is not known. Here, it is shown that beads attached to the surface of a T cell translocate toward the interface shortly after the start of T cell activation. This movement appears to depend on myosin motor proteins and requires the engagement of the major costimulatory receptor pairs, B7-CD28 and ICAM-1-LFA-1. This suggests that the engagement of costimulatory receptors triggers an active accumulation of molecules at the interface of the T cell and the antigen-presenting cell, which then increases the overall amplitude and duration of T cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wulfing, C -- Davis, M M -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2266-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Antigens, CD/*metabolism ; Antigens, CD28/metabolism ; Antigens, CD86 ; Biotinylation ; CHO Cells ; Calcium/metabolism ; Cricetinae ; Cytoskeleton/*physiology ; Intercellular Adhesion Molecule-1/metabolism ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Microspheres ; Molecular Motor Proteins/physiology ; Myosins/physiology ; Phosphatidylinositol 3-Kinases/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism/ultrastructure ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 25
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    Automating a mouse (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 May 15;280(5366):1101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Library ; Gene Targeting ; *Genetic Techniques ; Genetic Vectors ; Mice ; Mice, Knockout/*genetics ; Mutagenesis, Insertional ; Sequence Analysis, DNA ; *Stem Cells
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 26
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    Mismatch repair co-opted by hypermutation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Mice homozygous for a disrupted allele of the mismatch repair gene Pms2 have a mutator phenotype. When this allele is crossed into quasi-monoclonal (QM) mice, which have a very limited B cell repertoire, homozygotes have fewer somatic mutations at the immunoglobulin heavy chain and lambda chain loci than do heterozygotes or wild-type QM mice. That is, mismatch repair seems to contribute to somatic hypermutation rather than stifling it. It is suggested that at immunoglobulin loci in hypermutable B cells, mismatched base pairs are "corrected" according to the newly synthesized DNA strand, thereby fixing incipient mutations instead of eliminating them.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cascalho, M -- Wong, J -- Steinberg, C -- Wabl, M -- 1R01 GM37699/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1207-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco, CA 94143-0670, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9469811" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenosine Triphosphatases ; Alleles ; Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; Base Composition ; Base Sequence ; Cloning, Molecular ; Crosses, Genetic ; *DNA Repair ; *DNA Repair Enzymes ; *DNA-Binding Proteins ; Female ; Gene Rearrangement ; *Genes, Immunoglobulin ; Heterozygote ; Immunoglobulin Heavy Chains/chemistry/genetics ; Immunoglobulin Variable Region/chemistry/*genetics ; Immunoglobulin lambda-Chains/chemistry/genetics ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; *Mutation ; Proteins/*genetics/physiology
    Print ISSN: 0036-8075
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  • 27
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    New potential for human embryonic stem cells (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gearhart, J -- New York, N.Y. -- Science. 1998 Nov 6;282(5391):1061-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Gynecology and Obstetrics, Johns Hopkins Medicine, Baltimore, MD 21287, USA. gearhart@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*cytology ; *Cell Culture Techniques ; Cell Differentiation ; *Cell Line ; Cell Lineage ; *Embryo Research ; Embryo, Mammalian/*cytology ; Federal Government ; Germ Cells/*cytology ; Government Regulation ; Guidelines as Topic ; Humans ; Major Histocompatibility Complex ; Mice ; Research Support as Topic ; Risk Assessment ; Stem Cell Transplantation ; Stem Cells/*cytology ; Transplantation Immunology ; United States
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  • 28
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    Expansion of the allelic exclusion principle? (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chess, A -- New York, N.Y. -- Science. 1998 Mar 27;279(5359):2067-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. chess@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9537917" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; CD4-Positive T-Lymphocytes/*immunology ; DNA Replication ; *Gene Expression Regulation ; Genes, Immunoglobulin ; Interleukin-2/*genetics ; Lymphocyte Activation ; Mice ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; Transcription, Genetic
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  • 29
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    Impaired locomotion and dopamine signaling in retinoid receptor mutant mice (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-28
    Description: In the adult mouse, single and compound null mutations in the genes for retinoic acid receptor beta and retinoid X receptors beta and gamma resulted in locomotor defects related to dysfunction of the mesolimbic dopamine signaling pathway. Expression of the D1 and D2 receptors for dopamine was reduced in the ventral striatum of mutant mice, and the response of double null mutant mice to cocaine, which affects dopamine signaling in the mesolimbic system, was blunted. Thus, retinoid receptors are involved in the regulation of brain functions, and retinoic acid signaling defects may contribute to pathologies such as Parkinson's disease and schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krezel, W -- Ghyselinck, N -- Samad, T A -- Dupe, V -- Kastner, P -- Borrelli, E -- Chambon, P -- New York, N.Y. -- Science. 1998 Feb 6;279(5352):863-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS, INSERM, Universite Louis Pasteur, College de France, Boite Postale 163, 67404 Illkirch Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9452386" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/pharmacology ; Corpus Striatum/*metabolism ; Dimerization ; Dopamine/*metabolism ; Locomotion ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; *Motor Activity/drug effects ; Muscle, Skeletal/physiology ; Parkinson Disease/etiology ; Peripheral Nervous System/physiology ; Receptors, Dopamine D1/genetics/metabolism ; Receptors, Dopamine D2/genetics/metabolism ; Receptors, Retinoic Acid/genetics/*physiology ; Retinoid X Receptors ; Schizophrenia/etiology ; *Signal Transduction ; Transcription Factors/genetics/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Molecular basis of T cell inactivation by CTLA-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: CTLA-4, a negative regulator of T cell function, was found to associate with the T cell receptor (TCR) complex zeta chain in primary T cells. The association of TCRzeta with CTLA-4, reconstituted in 293 transfectants, was enhanced by p56(lck)-induced tyrosine phosphorylation. Coexpression of the CTLA-4-associated tyrosine phosphatase, SHP-2, resulted in dephosphorylation of TCRzeta bound to CTLA-4 and abolished the p56(lck)-inducible TCRzeta-CTLA-4 interaction. Thus, CTLA-4 inhibits TCR signal transduction by binding to TCRzeta and inhibiting tyrosine phosphorylation after T cell activation. These findings have broad implications for the negative regulation of T cell function and T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K M -- Chuang, E -- Griffin, M -- Khattri, R -- Hong, D K -- Zhang, W -- Straus, D -- Samelson, L E -- Thompson, C B -- Bluestone, J A -- P01 AI35294-6/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute for Cancer Research, and Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856951" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, Differentiation/*metabolism ; CTLA-4 Antigen ; Cell Line ; Cells, Cultured ; Humans ; *Immunoconjugates ; Intracellular Signaling Peptides and Proteins ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Models, Immunological ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; SH2 Domain-Containing Protein Tyrosine Phosphatases ; *Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; src Homology Domains
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, W C -- de la Pompa, J L -- McCurrach, M E -- Shu, H B -- Elia, A J -- Shahinian, A -- Ng, M -- Wakeham, A -- Khoo, W -- Mitchell, K -- El-Deiry, W S -- Lowe, S W -- Goeddel, D V -- Mak, T W -- CA13106/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, University of Toronto, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506948" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/physiology ; *Apoptosis ; Carrier Proteins/genetics/*physiology ; Cell Transformation, Neoplastic ; Cells, Cultured ; Doxorubicin/pharmacology ; *Embryonic and Fetal Development ; Endothelium, Vascular/embryology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression ; Gene Targeting ; Heart/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncogenes ; Receptors, Tumor Necrosis Factor/genetics/physiology ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Progress in progressive hearing loss (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steel, K P -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1870-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Institute of Hearing Research, Nottingham NG7 2RD, UK. karen@ihr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9537904" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Carrier Proteins/genetics/physiology ; Cell Differentiation ; Chromosome Mapping ; Chromosomes, Human, Pair 5/genetics ; Deafness/*genetics ; Dyneins ; Female ; Gene Targeting ; Genes, Dominant ; Hair Cells, Auditory/physiology ; Hearing Loss, Sensorineural/*genetics ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Male ; Mice ; Myosins/genetics/physiology ; Pedigree ; Sequence Deletion ; Transcription Factor Brn-3C ; Transcription Factors/*genetics/metabolism/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of the proinflammatory effects of Fas ligand (CD95L) (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: Fas ligand (CD95L) inhibits T cell function in immune-privileged organs such as the eye and testis, yet in most tissues CD95L expression induces potent inflammatory responses. With a stably transfected colon carcinoma cell line, CT26-CD95L, the molecular basis for these divergent responses was defined. When injected subcutaneously, rejection of CT26-CD95L was caused by neutrophils activated by CD95L. CT26-CD95L survived in the intraocular space because of the presence of transforming growth factor-beta (TGF-beta), which inhibited neutrophil activation. Providing TGF-beta to subcutaneous sites protected against tumor rejection. Thus, these cytokines together generate a microenvironment that promotes immunologic tolerance, which may aid in the amelioration of allograft rejection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J J -- Sun, Y -- Nabel, G J -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1714-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan Medical Center, Departments of Internal Medicine and Biological Chemistry, 1150 West Medical Center Drive, 4520 Medical Science Research Building I, Ann Arbor, MI 48109-0650, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Chamber ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cytotoxicity, Immunologic ; Fas Ligand Protein ; Female ; Graft Rejection ; Humans ; Immune Tolerance ; Inflammation/*immunology ; Jurkat Cells ; Membrane Glycoproteins/*physiology ; Mice ; Mice, Inbred BALB C ; *Mitogen-Activated Protein Kinases ; Neoplasm Transplantation ; Neoplasms, Experimental/*immunology/pathology ; *Neutrophil Activation ; Neutrophils/immunology ; Transfection ; Transforming Growth Factor beta/pharmacology ; Tumor Cells, Cultured ; p38 Mitogen-Activated Protein Kinases
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    BSE and prions: uncertainties about the agent (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chesebro, B -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):42-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Persistent Virus Diseases, Rocky Mountain Laboratories, Hamilton, MT 59840, USA. bchesebro@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9441410" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/chemistry ; Amyloidosis/metabolism ; Animals ; Cattle ; Creutzfeldt-Jakob Syndrome/epidemiology/*etiology/transmission ; Disease Susceptibility ; Encephalopathy, Bovine Spongiform/epidemiology/*etiology/transmission ; Gene Expression ; Great Britain/epidemiology ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Prion Diseases/*etiology/transmission ; Prions/chemistry/genetics/metabolism/*pathogenicity ; Virus Physiological Phenomena ; Viruses/pathogenicity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    BRCA1 required for transcription-coupled repair of oxidative DNA damage (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: The breast and ovarian cancer susceptibility gene BRCA1 encodes a zinc finger protein of unknown function. Association of the BRCA1 protein with the DNA repair protein Rad51 and changes in the phosphorylation and cellular localization of the protein after exposure to DNA-damaging agents are consistent with a role for BRCA1 in DNA repair. Here, it is shown that mouse embryonic stem cells deficient in BRCA1 are defective in the ability to carry out transcription-coupled repair of oxidative DNA damage, and are hypersensitive to ionizing radiation and hydrogen peroxide. These results suggest that BRCA1 participates, directly or indirectly, in transcription-coupled repair of oxidative DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gowen, L C -- Avrutskaya, A V -- Latour, A M -- Koller, B H -- Leadon, S A -- CA40453/CA/NCI NIH HHS/ -- CA70490/CA/NCI NIH HHS/ -- IP50CA58223/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):1009-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Curriculum in Genetics and Molecular Biology and Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703501" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; BRCA1 Protein/genetics/*physiology ; Cell Line ; DNA Damage ; *DNA Repair ; Hydrogen Peroxide ; Mice ; Oxidation-Reduction ; Stem Cells ; Thymine/analogs & derivatives/immunology/metabolism ; Transcription, Genetic ; Ultraviolet Rays
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Molecular mimicry by herpes simplex virus-type 1: autoimmune disease after viral infection (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Viral infection is sometimes associated with the initiation or exacerbation of autoimmune disease, although the underlying mechanisms remain unclear. One proposed mechanism is that viral determinants that mimic host antigens trigger self-reactive T cell clones to destroy host tissue. An epitope expressed by a coat protein of herpes simplex virus-type 1 (HSV-1) KOS strain has now been shown to be recognized by autoreactive T cells that target corneal antigens in a murine model of autoimmune herpes stromal keratitis. Mutant HSV-1 viruses that lacked this epitope did not induce autoimmune disease. Thus, expression of molecular mimics can influence the development of autoimmune disease after viral infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Z S -- Granucci, F -- Yeh, L -- Schaffer, P A -- Cantor, H -- AI 37562/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1344-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, and Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478893" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Amino Acid Sequence ; Animals ; Autoantigens/immunology ; Autoimmune Diseases/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Capsid/chemistry/genetics/*immunology ; *Capsid Proteins ; Cornea/*immunology ; Epitopes ; Eye Proteins/immunology ; Herpesvirus 1, Human/*immunology ; Keratitis, Herpetic/*immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mice, SCID ; *Molecular Mimicry ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oligopeptides/immunology ; Viral Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    More deafness genes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steel, K P -- Brown, S D -- New York, N.Y. -- Science. 1998 May 29;280(5368):1403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Institute of Hearing Research, University Park, Nottingham NG7 2RD, UK. karen@ihr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9634418" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Animals ; Cilia/physiology ; Deafness/*genetics ; Dyneins ; Extracellular Matrix Proteins/*genetics/physiology ; GPI-Linked Proteins ; Hair Cells, Auditory/physiology/ultrastructure ; Hearing ; Humans ; Membrane Glycoproteins/*genetics/physiology ; Mice ; Mice, Mutant Strains ; Mutation ; Myosin Heavy Chains/genetics/physiology ; Myosins/*genetics/physiology ; Tectorial Membrane/physiology
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    Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: Hormones and neurotransmitters may mediate common responses through receptors that couple to the same class of heterotrimeric guanine nucleotide-binding (G) protein. For example, several receptors that couple to Gq class proteins can induce cardiomyocyte hypertrophy. Class-specific inhibition of Gq-mediated signaling was produced in the hearts of transgenic mice by targeted expression of a carboxyl-terminal peptide of the alpha subunit Galphaq. When pressure overload was surgically induced, the transgenic mice developed significantly less ventricular hypertrophy than control animals. The data demonstrate the role of myocardial Gq in the initiation of myocardial hypertrophy and indicate a possible strategy for preventing pathophysiological signaling by simultaneously blocking multiple receptors coupled to Gq.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akhter, S A -- Luttrell, L M -- Rockman, H A -- Iaccarino, G -- Lefkowitz, R J -- Koch, W J -- HL-03041/HL/NHLBI NIH HHS/ -- HL-09436/HL/NHLBI NIH HHS/ -- HL-16037/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554846" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/pharmacology ; Animals ; Atrial Natriuretic Factor/genetics ; COS Cells ; Diglycerides/metabolism ; Enzyme Activation ; GTP-Binding Proteins/antagonists & inhibitors/genetics/*metabolism ; Gene Expression Regulation ; Gene Targeting ; Hypertrophy, Left Ventricular/*metabolism/prevention & control ; Inositol Phosphates/metabolism ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 1/metabolism ; Myocardium/*metabolism ; Peptide Fragments/genetics/metabolism ; Phenylephrine/pharmacology ; Receptors, Adrenergic, alpha/*metabolism ; Signal Transduction ; Transfection ; Transgenes ; Ventricular Pressure
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  • 39
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    Control of neonatal tolerance to tissue antigens by peripheral T cell trafficking (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: Self tolerance is acquired by the developing immune system. As reported here, particular properties of the neonatal tissue contribute to this process. Neonatal skin, but not adult skin, was accessible for naive CD8 T cells. In mouse bone marrow chimeras generated at different ages, recent thymic emigrants were tolerized to a skin-expressed major histocompatibility complex class I antigen only during a neonatal period but not during adulthood. Blockade of T cell migration neonatally prevented tolerance induction. Thus, T cell trafficking through nonlymphoid tissues in the neonate is crucial for the establishment of self tolerance to sessile, skin-expressed antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alferink, J -- Tafuri, A -- Vestweber, D -- Hallmann, R -- Hammerling, G J -- Arnold, B -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1338-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumor Immunology Program, German Cancer Research Center, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antigen Presentation ; Bone Marrow Transplantation ; CD8-Positive T-Lymphocytes/*immunology ; Cell Movement ; Graft Rejection ; H-2 Antigens/*immunology ; Keratinocytes/immunology ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Neoplasms, Experimental/immunology ; Self Tolerance/*immunology ; Skin/*immunology ; Skin Transplantation ; T-Lymphocytes/*immunology ; Thymus Gland/immunology ; Transplantation Chimera
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Reovirus therapy of tumors with activated Ras pathway (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: Human reovirus requires an activated Ras signaling pathway for infection of cultured cells. To investigate whether this property can be exploited for cancer therapy, severe combined immune deficient mice bearing tumors established from v-erbB-transformed murine NIH 3T3 cells or human U87 glioblastoma cells were treated with the virus. A single intratumoral injection of virus resulted in regression of tumors in 65 to 80 percent of the mice. Treatment of immune-competent C3H mice bearing tumors established from ras-transformed C3H-10T1/2 cells also resulted in tumor regression, although a series of injections were required. These results suggest that, with further work, reovirus may have applicability in the treatment of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coffey, M C -- Strong, J E -- Forsyth, P A -- Lee, P W -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1332-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology Research Group and Department of Microbiology and Infectious Diseases, University of Calgary Health Science Centre, Calgary, Alberta, T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812900" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies, Viral/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line, Transformed ; Genes, erbB ; *Genes, ras ; Humans ; Male ; Mammalian orthoreovirus 3/immunology/*physiology ; Mice ; Mice, Inbred C3H ; Mice, SCID ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism/pathology/*therapy/virology ; Signal Transduction ; Tumor Cells, Cultured ; Virus Replication ; ras Proteins/*metabolism
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    Bone marrow cells may provide muscle power (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1998 Mar 6;279(5356):1456.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9508720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/cytology/*physiology ; Bone Marrow Transplantation ; Cell Differentiation ; Humans ; Mice ; Mice, Transgenic ; Muscle, Skeletal/cytology/pathology/*physiology ; Muscular Dystrophies/pathology/*therapy ; Muscular Dystrophy, Animal/pathology/therapy ; *Regeneration ; Stem Cells/*physiology ; Stromal Cells/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cancer treatment by targeted drug delivery to tumor vasculature in a mouse model (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: In vivo selection of phage display libraries was used to isolate peptides that home specifically to tumor blood vessels. When coupled to the anticancer drug doxorubicin, two of these peptides-one containing an alphav integrin-binding Arg-Gly-Asp motif and the other an Asn-Gly-Arg motif-enhanced the efficacy of the drug against human breast cancer xenografts in nude mice and also reduced its toxicity. These results indicate that it may be possible to develop targeted chemotherapy strategies that are based on selective expression of receptors in tumor vasculature.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arap, W -- Pasqualini, R -- Ruoslahti, E -- CA30199/CA/NCI NIH HHS/ -- CA62042/CA/NCI NIH HHS/ -- CA74238-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):377-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9430587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antineoplastic Agents/*administration & dosage/therapeutic use/toxicity ; Bacteriophages ; Coronary Vessels/drug effects ; Doxorubicin/*administration & dosage/*analogs & ; derivatives/metabolism/therapeutic use/toxicity ; *Drug Carriers ; Heart/drug effects ; Humans ; Integrin alphaV ; Integrins/metabolism ; Liver/blood supply/drug effects ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental/*blood supply/*drug therapy/pathology ; Oligopeptides/*administration & dosage/metabolism/therapeutic use/toxicity ; Peptide Library ; Random Allocation ; Transplantation, Heterologous ; Tumor Cells, Cultured
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    An essential role for ectodomain shedding in mammalian development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: The ectodomains of numerous proteins are released from cells by proteolysis to yield soluble intercellular regulators. The responsible protease, tumor necrosis factor-alpha converting enzyme (TACE), has been identified only in the case when tumor necrosis factor-alpha (TNFalpha) is released. Analyses of cells lacking this metalloproteinase-disintegrin revealed an expanded role for TACE in the processing of other cell surface proteins, including a TNF receptor, the L-selectin adhesion molecule, and transforming growth factor-alpha (TGFalpha). The phenotype of mice lacking TACE suggests an essential role for soluble TGFalpha in normal development and emphasizes the importance of protein ectodomain shedding in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peschon, J J -- Slack, J L -- Reddy, P -- Stocking, K L -- Sunnarborg, S W -- Lee, D C -- Russell, W E -- Castner, B J -- Johnson, R S -- Fitzner, J N -- Boyce, R W -- Nelson, N -- Kozlosky, C J -- Wolfson, M F -- Rauch, C T -- Cerretti, D P -- Paxton, R J -- March, C J -- Black, R A -- CA43793/CA/NCI NIH HHS/ -- DK53804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101, USA. peschon@immunex.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812885" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Amino Acid Sequence ; Animals ; Catalytic Domain ; Cell Membrane/*metabolism ; Cells, Cultured ; Crosses, Genetic ; *Embryonic and Fetal Development ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Protein Processing, Post-Translational ; Receptors, Tumor Necrosis Factor/metabolism ; Transforming Growth Factor alpha/metabolism ; Tumor Necrosis Factor-alpha/*metabolism
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    Increased vascularization in mice overexpressing angiopoietin-1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: The angiopoietins and members of the vascular endothelial growth factor (VEGF) family are the only growth factors thought to be largely specific for vascular endothelial cells. Targeted gene inactivation studies in mice have shown that VEGF is necessary for the early stages of vascular development and that angiopoietin-1 is required for the later stages of vascular remodeling. Here it is shown that transgenic overexpression of angiopoietin-1 in the skin of mice produces larger, more numerous, and more highly branched vessels. These results raise the possibility that angiopoietins can be used, alone or in combination with VEGF, to promote therapeutic angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suri, C -- McClain, J -- Thurston, G -- McDonald, D M -- Zhou, H -- Oldmixon, E H -- Sato, T N -- Yancopoulos, G D -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9774272" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Animals ; Capillaries/anatomy & histology/ultrastructure ; Endothelial Growth Factors/genetics/physiology ; Endothelium, Vascular/ultrastructure ; Gene Expression ; Keratinocytes/metabolism ; Lymphokines/genetics/physiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; *Neovascularization, Physiologic ; Skin/*blood supply/metabolism ; Transgenes ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Venules/anatomy & histology/ultrastructure
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  • 45
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    Perspectives: neurobiology. The CRYs fo flies and mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardin, P E -- Glossop, N R -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2460-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Houston, Houston, TX 77204, USA. phardin@uh.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10636810" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/*physiology ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cryptochromes ; Darkness ; Drosophila ; *Drosophila Proteins ; *Eye Proteins ; Feedback ; Flavoproteins/genetics/*physiology ; Gene Expression Regulation ; Light ; Mice ; Mice, Knockout ; Nuclear Proteins/*genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Promoter Regions, Genetic ; Receptors, G-Protein-Coupled ; Repressor Proteins/genetics/physiology ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/physiology ; Transcription Factors/physiology ; *Transcription, Genetic
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  • 46
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    Photic induction of mPer1 and mPer2 in cry-deficient mice lacking a biological clock (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: Mice lacking mCry1 and mCry2 are behaviorally arrhythmic. As shown here, cyclic expression of the clock genes mPer1 and mPer2 (mammalian Period genes 1 and 2) in the suprachiasmatic nucleus and peripheral tissues is abolished and mPer1 and mPer2 mRNA levels are constitutively high. These findings indicate that the biological clock is eliminated in the absence of both mCRY1 and mCRY2 (mammalian cryptochromes 1 and 2) and support the idea that mammalian CRY proteins act in the negative limb of the circadian feedback loop. The mCry double-mutant mice retain the ability to have mPer1 and mPer2 expression induced by a brief light stimulus known to phase-shift the biological clock in wild-type animals. Thus, mCRY1 and mCRY2 are dispensable for light-induced phase shifting of the biological clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okamura, H -- Miyake, S -- Sumi, Y -- Yamaguchi, S -- Yasui, A -- Muijtjens, M -- Hoeijmakers, J H -- van der Horst, G T -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Brain Science, Kobe University School of Medicine, Kobe 650-0017, Japan. okamurah@kobe-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617474" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*physiology ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cryptochromes ; *Drosophila Proteins ; *Eye Proteins ; Feedback ; Flavoproteins/genetics/*physiology ; Gene Expression Regulation ; In Situ Hybridization ; *Light ; Liver/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mutation ; Nuclear Proteins/*genetics ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Polymerase Chain Reaction ; RNA, Messenger/genetics/metabolism ; Receptors, G-Protein-Coupled ; Retina/metabolism ; Suprachiasmatic Nucleus/metabolism ; Transcription Factors
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  • 47
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    Leakage-resistant blood vessels in mice transgenically overexpressing angiopoietin-1 (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-01-05
    Description: Angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors. Direct comparison of transgenic mice overexpressing these factors in the skin revealed that the VEGF-induced blood vessels were leaky, whereas those induced by Ang1 were nonleaky. Moreover, vessels in Ang1-overexpressing mice were resistant to leaks caused by inflammatory agents. Coexpression of Ang1 and VEGF had an additive effect on angiogenesis but resulted in leakage-resistant vessels typical of Ang1. Ang1 therefore may be useful for reducing microvascular leakage in diseases in which the leakage results from chronic inflammation or elevated VEGF and, in combination with VEGF, for promoting growth of nonleaky vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thurston, G -- Suri, C -- Smith, K -- McClain, J -- Sato, T N -- Yancopoulos, G D -- McDonald, D M -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2511-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco, CA 94143-0452, USA. gavint@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617467" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Animals ; Arterioles/anatomy & histology/physiology ; Binding Sites ; Capillaries/anatomy & histology/physiology ; *Capillary Permeability ; Ear ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/metabolism ; Inflammation/chemically induced ; Inflammation Mediators/pharmacology ; Lymphokines/genetics/*physiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; Microcirculation/anatomy & histology/*physiology ; Mustard Plant ; *Neovascularization, Physiologic ; Plant Extracts/pharmacology ; Plant Lectins ; Plant Oils ; Plants, Medicinal ; Platelet Activating Factor/pharmacology ; Ricin/metabolism ; Serotonin/pharmacology ; Skin/blood supply/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Venules/anatomy & histology/physiology
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    Role of the mouse ank gene in control of tissue calcification and arthritis (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-07-15
    Description: Mutation at the mouse progressive ankylosis (ank) locus causes a generalized, progressive form of arthritis accompanied by mineral deposition, formation of bony outgrowths, and joint destruction. Here, we show that the ank locus encodes a multipass transmembrane protein (ANK) that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. A highly conserved gene is present in humans and other vertebrates. These results identify ANK-mediated control of pyrophosphate levels as a possible mechanism regulating tissue calcification and susceptibility to arthritis in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, A M -- Johnson, M D -- Kingsley, D M -- 5T32GM07365/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):265-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Howard Hughes Medical Institute, Beckman Center B300, Stanford University School of Medicine, Stanford, CA 94305-5327, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*genetics/metabolism/pathology ; Base Sequence ; Biological Transport ; COS Cells ; Calcinosis/*genetics ; Chromosome Mapping ; Cloning, Molecular ; Dna ; Diphosphates/*metabolism ; Durapatite/metabolism ; Gene Expression ; Genetic Complementation Test ; Humans ; Membrane Proteins/*genetics/metabolism/*physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Phenotype ; Phosphate Transport Proteins ; Physical Chromosome Mapping ; Sequence Homology, Nucleic Acid ; Tissue Distribution
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    Regulation of area identity in the mammalian neocortex by Emx2 and Pax6 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: The contribution of extrinsic and genetic mechanisms in determining areas of the mammalian neocortex has been a contested issue. This study analyzes the roles of the regulatory genes Emx2 and Pax6, which are expressed in opposing gradients in the neocortical ventricular zone, in specifying areas. Changes in the patterning of molecular markers and area-specific connections between the cortex and thalamus suggest that arealization of the neocortex is disproportionately altered in Emx2 and Pax6 mutant mice in opposing manners predicted from their countergradients of expression: rostral areas expand and caudal areas contract in Emx2 mutants, whereas the opposite effect is seen in Pax6 mutants. These findings suggest that Emx2 and Pax6 cooperate to regulate arealization of the neocortex and to confer area identity to cortical cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, K M -- Goudreau, G -- O'Leary, D D -- NS31558/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):344-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10764649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cadherins/biosynthesis/genetics ; DNA-Binding Proteins/*genetics/physiology ; Eye Proteins ; *Gene Expression ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; *Genes, Regulator ; Homeodomain Proteins/*genetics/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Mutant Strains ; Morphogenesis ; Neocortex/*embryology/metabolism ; Neural Pathways ; Occipital Lobe/embryology/metabolism ; Paired Box Transcription Factors ; Repressor Proteins ; Somatosensory Cortex/embryology/metabolism ; Thalamus/embryology ; Transcription Factors ; Visual Cortex/embryology/metabolism
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    Effects of environment on compensatory mutations to ameliorate costs of antibiotic resistance (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjorkman, J -- Nagaev, I -- Berg, O G -- Hughes, D -- Andersson, D I -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688795" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Anti-Bacterial Agents/*pharmacology ; *Antiporters ; Carrier Proteins/genetics ; Culture Media ; Drug Resistance, Microbial/*genetics ; Escherichia coli Proteins ; Evolution, Molecular ; Female ; Fusidic Acid/pharmacology ; Membrane Proteins/genetics ; Mice ; Mice, Inbred BALB C ; *Mutation ; Peptide Elongation Factor G/genetics ; Ribosomal Proteins/genetics ; Salmonella typhimurium/*drug effects/*genetics/growth & development/metabolism ; Selection, Genetic ; Serial Passage ; Streptomycin/pharmacology ; Suppression, Genetic
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    Prostaglandin D2 as a mediator of allergic asthma (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-17
    Description: Allergic asthma is caused by the aberrant expansion in the lung of T helper cells that produce type 2 (TH2) cytokines and is characterized by infiltration of eosinophils and bronchial hyperreactivity. This disease is often triggered by mast cells activated by immunoglobulin E (IgE)-mediated allergic challenge. Activated mast cells release various chemical mediators, including prostaglandin D2 (PGD2), whose role in allergic asthma has now been investigated by the generation of mice deficient in the PGD receptor (DP). Sensitization and aerosol challenge of the homozygous mutant (DP-/-) mice with ovalbumin (OVA) induced increases in the serum concentration of IgE similar to those in wild-type mice subjected to this model of asthma. However, the concentrations of TH2 cytokines and the extent of lymphocyte accumulation in the lung of OVA-challenged DP-/- mice were greatly reduced compared with those in wild-type animals. Moreover, DP-/- mice showed only marginal infiltration of eosinophils and failed to develop airway hyperreactivity. Thus, PGD2 functions as a mast cell-derived mediator to trigger asthmatic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, T -- Hirata, M -- Tanaka, H -- Takahashi, Y -- Murata, T -- Kabashima, K -- Sugimoto, Y -- Kobayashi, T -- Ushikubi, F -- Aze, Y -- Eguchi, N -- Urade, Y -- Yoshida, N -- Kimura, K -- Mizoguchi, A -- Honda, Y -- Nagai, H -- Narumiya, S -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2013-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720327" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Asthma/immunology/metabolism/pathology/*physiopathology ; Bronchial Hyperreactivity ; Bronchoalveolar Lavage Fluid/cytology/immunology ; Crosses, Genetic ; Female ; Gene Targeting ; Humans ; Immunoglobulin E/blood ; Interferon-gamma/metabolism ; Interleukins/metabolism ; Lung/immunology/metabolism/pathology ; Lymphocytes/immunology ; Male ; Mast Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Mucus/secretion ; Ovalbumin/immunology ; Prostaglandin D2/metabolism/*physiology ; *Receptors, Immunologic ; Receptors, Prostaglandin/genetics/metabolism/*physiology ; Respiratory Mucosa/secretion
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    Localized Rac activation dynamics visualized in living cells (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-10-13
    Description: Signaling proteins are thought to be tightly regulated spatially and temporally in order to generate specific and localized effects. For Rac and other small guanosine triphosphatases, binding to guanosine triphosphate leads to interaction with downstream targets and regulates subcellular localization. A method called FLAIR (fluorescence activation indicator for Rho proteins) was developed to quantify the spatio-temporal dynamics of the Rac1 nucleotide state in living cells. FLAIR revealed precise spatial control of growth factor-induced Rac activation, in membrane ruffles and in a gradient of activation at the leading edge of motile cells. FLAIR exemplifies a generally applicable approach for examining spatio-temporal control of protein activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kraynov, V S -- Chamberlain, C -- Bokoch, G M -- Schwartz, M A -- Slabaugh, S -- Hahn, K M -- AG15430/AG/NIA NIH HHS/ -- GM39434/GM/NIGMS NIH HHS/ -- R01 GM-57464/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):333-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030651" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/metabolism ; Animals ; Biosensing Techniques ; Blood ; Cell Membrane/*enzymology/physiology/ultrastructure ; *Cell Movement ; Cell Nucleus/*enzymology ; Cell Polarity ; Enzyme Activation ; Fluorescence ; Guanosine Triphosphate/*metabolism ; Mice ; Nuclear Envelope/enzymology ; Platelet-Derived Growth Factor/pharmacology ; Recombinant Fusion Proteins/metabolism ; Spectrometry, Fluorescence ; rac1 GTP-Binding Protein/*metabolism
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  • 53
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    Selective inhibition of NF-kappaB activation by a peptide that blocks the interaction of NEMO with the IkappaB kinase complex (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-09-01
    Description: Activation of the transcription factor nuclear factor (NF)-kappaB by proinflammatory stimuli leads to increased expression of genes involved in inflammation. Activation of NF-kappaB requires the activity of an inhibitor of kappaB (IkappaB)-kinase (IKK) complex containing two kinases (IKKalpha and IKKbeta) and the regulatory protein NEMO (NF-kappaB essential modifier). An amino-terminal alpha-helical region of NEMO associated with a carboxyl-terminal segment of IKKalpha and IKKbeta that we term the NEMO-binding domain (NBD). A cell-permeable NBD peptide blocked association of NEMO with the IKK complex and inhibited cytokine-induced NF-kappaB activation and NF-kappaB-dependent gene expression. The peptide also ameliorated inflammatory responses in two experimental mouse models of acute inflammation. The NBD provides a target for the development of drugs that would block proinflammatory activation of the IKK complex without inhibiting basal NF-kappaB activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉May, M J -- D'Acquisto, F -- Madge, L A -- Glockner, J -- Pober, J S -- Ghosh, S -- AI 33443/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1550-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968790" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemistry/pharmacology ; COS Cells ; Cells, Cultured ; E-Selectin/biosynthesis/genetics ; Endothelium, Vascular/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; I-kappa B Kinase ; Inflammation/drug therapy ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; NF-kappa B/*metabolism ; Peptides/chemistry/*pharmacology ; Point Mutation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism
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    A role for histone acetylation in the developmental regulation of VDJ recombination (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: VDJ recombination is developmentally regulated in vivo by enhancer-dependent changes in the accessibility of chromosomal recombination signal sequences to the recombinase, but the molecular nature of these changes is unknown. Here histone H3 acetylation was measured along versions of a transgenic VDJ recombination reporter and the endogenous T cell receptor alpha/delta locus. Enhancer activity was shown to impart long-range, developmentally regulated changes in H3 acetylation, and H3 acetylation status was tightly linked to VDJ recombination. H3 hyperacetylation is proposed as a molecular mechanism coupling enhancer activity to accessibility for VDJ recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMurry, M T -- Krangel, M S -- GM 41052/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):495-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Post Office Box 3010, Duke University Medical Center, Durham NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642553" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Chromatin/metabolism ; DNA Nucleotidyltransferases/metabolism ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; *Gene Rearrangement, T-Lymphocyte ; *Genes, T-Cell Receptor alpha ; Genes, T-Cell Receptor beta ; *Genes, T-Cell Receptor delta ; Histones/*metabolism ; Homeodomain Proteins/metabolism ; Humans ; Mice ; Mice, Transgenic ; Nuclear Proteins ; Protein Sorting Signals ; *Recombination, Genetic ; T-Lymphocytes/*metabolism ; Transgenes ; VDJ Recombinases
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    Functional requirement for class I MHC in CNS development and plasticity (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, G S -- Boulanger, L M -- Du, H -- Riquelme, P A -- Brotz, T M -- Shatz, C J -- 1F32EY07016/EY/NEI NIH HHS/ -- EY06912/EY/NEI NIH HHS/ -- F32 EY007016/EY/NEI NIH HHS/ -- F32 EY007016-02/EY/NEI NIH HHS/ -- F32 EY007016-03/EY/NEI NIH HHS/ -- MH48108/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2155-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. gshuh@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/genetics/*physiology ; Brain/growth & development/*physiology ; Excitatory Postsynaptic Potentials ; Gene Expression Profiling ; Genes, MHC Class I ; Geniculate Bodies/physiology ; Hippocampus/growth & development/physiology ; Histocompatibility Antigens Class I/genetics/*physiology ; In Situ Hybridization ; Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Neural Pathways ; *Neuronal Plasticity ; Neurons/*physiology ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Retina/growth & development/physiology ; Retinal Ganglion Cells/physiology ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission ; Visual Pathways
    Print ISSN: 0036-8075
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    Property claims. A deluge of patents creates legal hassles for research (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):255-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10777404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; Drug Industry ; Europe ; Genome ; Mice ; *Mice, Knockout/genetics ; *Mice, Transgenic/genetics ; National Institutes of Health (U.S.) ; *Patents as Topic ; *Research/legislation & jurisprudence ; Sequence Analysis, DNA ; Technology Transfer ; United States ; Universities
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    Epitopes involved in antibody-mediated protection from Ebola virus (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-04
    Description: To determine the ability of antibodies to provide protection from Ebola viruses, monoclonal antibodies (mAbs) to the Ebola glycoprotein were generated and evaluated for efficacy. We identified several protective mAbs directed toward five unique epitopes on Ebola glycoprotein. One of the epitopes is conserved among all Ebola viruses that are known to be pathogenic for humans. Some protective mAbs were also effective therapeutically when administered to mice 2 days after exposure to lethal Ebola virus. The identification of protective mAbs has important implications for developing vaccines and therapies for Ebola virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, J A -- Hevey, M -- Bakken, R -- Guest, S -- Bray, M -- Schmaljohn, A L -- Hart, M K -- New York, N.Y. -- Science. 2000 Mar 3;287(5458):1664-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virology Division, U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, Frederick, MD 21702-5011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10698744" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Antibodies, Viral/*immunology ; Antibody Affinity ; Antigens, Viral/immunology ; Binding, Competitive ; Complement System Proteins/immunology ; Ebolavirus/*immunology/physiology ; Epitopes/immunology ; Female ; Hemorrhagic Fever, Ebola/*prevention & control/therapy ; Humans ; Immunoglobulin G/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutralization Tests ; Specific Pathogen-Free Organisms ; Viral Envelope Proteins/*immunology ; Viral Plaque Assay
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    Crystal structure of a gammadelta T cell receptor ligand T22: a truncated MHC-like fold (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: Murine T10 and T22 are highly related nonclassical major histocompatibility complex (MHC) class Ib proteins that bind to certain gammadelta T cell receptors (TCRs) in the absence of other components. The crystal structure of T22b at 3.1 angstroms reveals similarities to MHC class I molecules, but one side of the normal peptide-binding groove is severely truncated, which allows direct access to the beta-sheet floor. Potential gammadelta TCR-binding sites can be inferred from functional mapping of T10 and T22 point mutants and allelic variants. Thus, T22 represents an unusual variant of the MHC-like fold and indicates that gammadelta and alphabeta TCRs interact differently with their respective MHC ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wingren, C -- Crowley, M P -- Degano, M -- Chien, Y -- Wilson, I A -- AI33431/AI/NIAID NIH HHS/ -- CA58896/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 14;287(5451):310-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10634787" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Binding Sites ; Crystallography, X-Ray ; Glycosylation ; Histocompatibility Antigens Class I/*chemistry ; Hydrogen Bonding ; Ligands ; Mice ; Models, Molecular ; Point Mutation ; Protein Conformation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Proteins/*chemistry/immunology/metabolism ; Receptors, Antigen, T-Cell, gamma-delta/immunology/*metabolism ; Surface Properties ; beta 2-Microglobulin/chemistry
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    Treatment of murine colitis by Lactococcus lactis secreting interleukin-10 (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-08-26
    Description: The cytokine interleukin-10 (IL-10) has shown promise in clinical trials for treatment of inflammatory bowel disease (IBD). Using two mouse models, we show that the therapeutic dose of IL-10 can be reduced by localized delivery of a bacterium genetically engineered to secrete the cytokine. Intragastric administration of IL-10-secreting Lactococcus lactis caused a 50% reduction in colitis in mice treated with dextran sulfate sodium and prevented the onset of colitis in IL-10(-/-) mice. This approach may lead to better methods for cost-effective and long-term management of IBD in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steidler, L -- Hans, W -- Schotte, L -- Neirynck, S -- Obermeier, F -- Falk, W -- Fiers, W -- Remaut, E -- New York, N.Y. -- Science. 2000 Aug 25;289(5483):1352-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Ghent University and Flanders Interuniversity Institute for Biotechnology, K. L. Ledeganckstraat 35, 9000 Gent, Belgium. lothar.steidler@dmb.rug.ac.be〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10958782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Colitis/immunology/pathology/prevention & control/therapy ; Colon/immunology/metabolism/microbiology/pathology ; Dextran Sulfate ; Inflammatory Bowel Diseases/immunology/pathology/prevention & control/*therapy ; Interleukin-10/*administration & dosage/*biosynthesis/genetics/metabolism ; Intestinal Mucosa/metabolism/pathology ; Lactococcus lactis/*genetics/immunology/*metabolism ; Mice ; Probiotics/*therapeutic use ; Recombinant Proteins/administration & dosage/biosynthesis/metabolism
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    Involvement of cellular caveolae in bacterial entry into mast cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: Caveolae are subcellular structures implicated in the import and transcytosis of macromolecules and in transmembrane signaling. To date, evidence for the existence of caveolae in hematopoietic cells has been ambiguous. Caveolae were detected in the microvilli and intracellular vesicles of cultured mouse bone marrow-derived mast cells (BMMCs). CD48, a receptor for FimH-expressing (type 1 fimbriated) Escherichia coli, was specifically localized to plasmalemmal caveolae in BMMCs. The involvement of caveolae in bacterial entry into BMMCs was indicated because caveolae-disrupting and -usurping agents specifically blocked E. coli entry, and markers of caveolae were actively recruited to sites of bacterial entry. The formation of bacteria-encapsulating caveolar chambers in BMMCs represents a distinct mechanism of microbial entry into phagocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, J S -- Gao, Z -- Abraham, S N -- AI 35678/AI/NIAID NIH HHS/ -- CA 14236/CA/NCI NIH HHS/ -- DK 50814/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Aug 4;289(5480):785-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10926542" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*metabolism ; *Adhesins, Escherichia coli ; Animals ; Antigens, CD/analysis/*metabolism ; Bacterial Adhesion ; Caveolin 1 ; *Caveolins ; Cell Fractionation ; Cell Membrane/chemistry/*metabolism/microbiology/ultrastructure ; Cholera Toxin/pharmacology ; Cyclodextrins/pharmacology ; *Endocytosis ; Escherichia coli/*metabolism/pathogenicity ; *Fimbriae Proteins ; Glycosylphosphatidylinositols/analysis ; Mast Cells/*metabolism/*microbiology/ultrastructure ; Membrane Proteins/analysis ; Mice ; Microscopy, Confocal ; Microscopy, Fluorescence ; Microscopy, Immunoelectron
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    Intellectual property. NIH cuts deal on use of OncoMouse (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 2000 Jan 28;287(5453):567.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691532" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; *Mice, Transgenic ; *National Institutes of Health (U.S.) ; *Neoplasms, Experimental ; *Patents as Topic ; Research Support as Topic ; United States
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    Lipid research. Possible new way to lower cholesterol (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-09-19
    Description: Clinicians may soon be able to mount a multipronged attack against cholesterol, the artery-clogging lipid whose buildup in the body is a major contributor to heart attacks and other cardiovascular diseases. In work reported on page 1524, a team has pinpointed a biological master switch in mice that controls three pathways that work together to both rid the body of excess cholesterol and prevent its absorption from the intestine. The work suggests a new mechanism for reducing cholesterol, for example, with drugs that turn up the activity of the master switch, a protein known as the retinoid X receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1446-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10991725" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/*metabolism ; Animals ; Bile Acids and Salts ; Biological Transport/drug effects ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; DNA-Binding Proteins/metabolism ; Glycoproteins/*metabolism ; Humans ; Intestinal Absorption/drug effects ; Intestines/drug effects/*metabolism ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Orphan Nuclear Receptors ; *Receptors, Cytoplasmic and Nuclear ; Receptors, Retinoic Acid/*metabolism ; Receptors, Thyroid Hormone/metabolism ; Retinoid X Receptors ; Transcription Factors/*metabolism
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    Immunology. A touch of antibody class (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-06-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stavnezer, J -- New York, N.Y. -- Science. 2000 May 12;288(5468):984-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue N., Worcester, MA 01655, USA. Janet.Stavnezer@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10841719" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Cytokines/immunology ; DNA/genetics/*metabolism ; Genes, Immunoglobulin ; *Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/genetics ; *Immunoglobulin Switch Region ; Mice ; Mice, Transgenic ; Models, Genetic ; *Nucleic Acid Hybridization ; RNA/genetics/*metabolism ; RNA Splicing ; Recombination, Genetic ; Ribonuclease H/genetics/metabolism ; Templates, Genetic ; Transcription, Genetic
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    Regulation of cell fate decision of undifferentiated spermatogonia by GDNF (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-02-26
    Description: The molecular control of self-renewal and differentiation of stem cells has remained enigmatic. Transgenic loss-of-function and overexpression models now show that the dosage of glial cell line-derived neurotrophic factor (GDNF), produced by Sertoli cells, regulates cell fate decisions of undifferentiated spermatogonial cells that include the stem cells for spermatogenesis. Gene-targeted mice with one GDNF-null allele show depletion of stem cell reserves, whereas mice overexpressing GDNF show accumulation of undifferentiated spermatogonia. They are unable to respond properly to differentiation signals and undergo apoptosis upon retinoic acid treatment. Nonmetastatic testicular tumors are regularly formed in older GDNF-overexpressing mice. Thus, GDNF contributes to paracrine regulation of spermatogonial self-renewal and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meng, X -- Lindahl, M -- Hyvonen, M E -- Parvinen, M -- de Rooij, D G -- Hess, M W -- Raatikainen-Ahokas, A -- Sainio, K -- Rauvala, H -- Lakso, M -- Pichel, J G -- Westphal, H -- Saarma, M -- Sariola, H -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1489-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Programs of Developmental Biology, Molecular Neurobiology, Electron Microscopy Unit, Institute of Biotechnology, Viikki Biocenter, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Cell Cycle ; Cell Differentiation/drug effects ; Cobalt/metabolism ; *Drosophila Proteins ; Female ; Gene Expression ; Gene Targeting ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Male ; Mice ; Mice, Transgenic ; Mitosis ; *Nerve Growth Factors ; Nerve Tissue Proteins/genetics/*physiology ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Receptor Protein-Tyrosine Kinases/genetics/metabolism ; Sertoli Cells/cytology/physiology ; *Spermatogenesis ; Spermatogonia/*cytology/drug effects ; Stem Cells/*cytology ; Testicular Neoplasms/pathology ; Testis/anatomy & histology ; Vitamin A/pharmacology
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    Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
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    Induction and maintenance of the neuronal cholinergic phenotype in the central nervous system by BMP-9 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: Bone morphogenetic proteins (BMPs) have multiple functions in the developing nervous system. A member of this family, BMP-9, was found to be highly expressed in the embryonic mouse septum and spinal cord, indicating a possible role in regulating the cholinergic phenotype. In cultured neurons, BMP-9 directly induced the expression of the cholinergic gene locus encoding choline acetyltransferase and the vesicular acetylcholine transporter and up-regulated acetylcholine synthesis. The effect was reversed upon withdrawal of BMP-9. Intracerebroventricular injection of BMP-9 increased acetylcholine levels in vivo. Although certain other BMPs also up-regulated the cholinergic phenotype in vitro, they were less effective than BMP-9. These data indicate that BMP-9 is a differentiating factor for cholinergic central nervous system neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Coviella, I -- Berse, B -- Krauss, R -- Thies, R S -- Blusztajn, J K -- P01 AG09525/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894782" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/biosynthesis ; Animals ; Bone Morphogenetic Proteins/*physiology ; Carrier Proteins/genetics ; Cells, Cultured ; Central Nervous System ; Choline O-Acetyltransferase/genetics ; Embryo, Mammalian/metabolism ; Fibroblast Growth Factor 2/physiology ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Enzymologic ; Growth Differentiation Factor 2 ; *Membrane Transport Proteins ; Mice ; Neurons/metabolism ; Phenotype ; RNA, Messenger/metabolism ; Septum of Brain/embryology/metabolism ; Spinal Cord/embryology/metabolism ; Up-Regulation ; Vesicular Acetylcholine Transport Proteins ; *Vesicular Transport Proteins
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    Transgenic mouse model of stunned myocardium (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: Stunned myocardium is a syndrome of reversible contractile failure that frequently complicates coronary artery disease. Cardiac excitation is uncoupled from contraction at the level of the myofilaments. Selective proteolysis of the thin filament protein troponin I has been correlated with stunned myocardium. Here, transgenic mice expressing the major degradation product of troponin I (TnI1-193) in the heart were found to develop ventricular dilatation, diminished contractility, and reduced myofilament calcium responsiveness, recapitulating the phenotype of stunned myocardium. Proteolysis of troponin I also occurs in ischemic human cardiac muscle. Thus, troponin I proteolysis underlies the pathogenesis of a common acquired form of heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, A M -- Kogler, H -- Georgakopoulos, D -- McDonough, J L -- Kass, D A -- Van Eyk, J E -- Marban, E -- HL 44065/HL/NHLBI NIH HHS/ -- HL 63038/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):488-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Johns Hopkins University School of Medicine, Ross Building 1144, 720 Rutland Avenue, Baltimore, MD 21205, USA. murphy@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642551" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Adrenergic beta-Agonists/pharmacology ; Animals ; Calcium/metabolism ; Cardiomegaly/pathology ; Dilatation, Pathologic ; *Disease Models, Animal ; Heart Rate ; Heart Ventricles/pathology ; Humans ; Isoproterenol/pharmacology ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Myocardial Contraction ; Myocardial Stunning/*metabolism/pathology/physiopathology ; Myocardium/*metabolism/pathology ; Myofibrils/metabolism ; Troponin I/genetics/*metabolism ; Ventricular Function, Left
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    Perspectives: drug delivery. Regulating export of ER cargo (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aridor, M -- Balch, W E -- New York, N.Y. -- Science. 2000 Feb 4;287(5454):816-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Cell Line ; Drug Delivery Systems ; Endoplasmic Reticulum/*metabolism/secretion ; Golgi Apparatus/metabolism ; Growth Hormone/chemistry/metabolism/secretion ; Immunophilins/chemistry/metabolism ; Insulin/chemistry/metabolism/secretion ; Ligands ; Mice ; Models, Biological ; Protein Conformation ; Protein Engineering ; Protein Folding ; Recombinant Fusion Proteins/*chemistry/*metabolism/secretion ; Tacrolimus Binding Proteins
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    Role of the enteric nervous system in the fluid and electrolyte secretion of rotavirus diarrhea (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: The mechanism underlying the intestinal fluid loss in rotavirus diarrhea, which often afflicts children in developing countries, is not known. One hypothesis is that the rotavirus evokes intestinal fluid and electrolyte secretion by activation of the nervous system in the intestinal wall, the enteric nervous system (ENS). Four different drugs that inhibit ENS functions were used to obtain experimental evidence for this hypothesis in mice in vitro and in vivo. The involvement of the ENS in rotavirus diarrhea indicates potential sites of action for drugs in the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lundgren, O -- Peregrin, A T -- Persson, K -- Kordasti, S -- Uhnoo, I -- Svensson, L -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):491-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Goteborg University, Box 432, S-405 30 Goteborg, Sweden. ove.lundgren@fysiologi.gu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Body Water/*secretion ; Diarrhea/drug therapy/*physiopathology ; Electrolytes/*metabolism ; Enteric Nervous System/drug effects/*physiopathology ; Hexamethonium/pharmacology ; In Vitro Techniques ; Intestinal Mucosa/drug effects/*secretion ; Intestine, Small/innervation ; Lidocaine/pharmacology ; Mecamylamine/pharmacology ; Mice ; Mice, Inbred BALB C ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Rotavirus Infections/drug therapy/*physiopathology ; Synaptic Transmission/drug effects ; Tetrodotoxin/pharmacology ; Theophylline/pharmacology
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    Regulation of antigen-specific CD8+ T cell homeostasis by perforin and interferon-gamma (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-18
    Description: T cell memory depends on factors that regulate expansion and death of these cells after antigenic stimulation. Mice deficient in perforin and interferon-gamma (IFN-gamma) exhibited increased expansion, altered immunodominance, and decreased death of antigen-specific CD8+ T cells after infection with an attenuated strain of Listeria monocytogenes, which was cleared from these mice. Expansion of CD8+ T cells was controlled by perforin, whereas IFN-gamma regulated immunodominance and the death phase. Thus, perforin and IFN-gamma regulate distinct elements of CD8+ T cell homeostasis independently of their role as antimicrobial effector molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Badovinac, V P -- Tvinnereim, A R -- Harty, J T -- AI36864/AI/NIAID NIH HHS/ -- AI42767/AI/NIAID NIH HHS/ -- T32AI07511/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1354-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11082062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, Bacterial/immunology ; Apoptosis ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Homeostasis ; Immunodominant Epitopes/*immunology ; *Immunologic Memory ; Interferon-gamma/*physiology ; Listeria monocytogenes/immunology ; Listeriosis/*immunology ; Lymphocytic Choriomeningitis/immunology ; Membrane Glycoproteins/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Perforin ; Pore Forming Cytotoxic Proteins
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    Inhibition of experimental liver cirrhosis in mice by telomerase gene delivery (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Accelerated telomere loss has been proposed to be a factor leading to end-stage organ failure in chronic diseases of high cellular turnover such as liver cirrhosis. To test this hypothesis directly, telomerase-deficient mice, null for the essential telomerase RNA (mTR) gene, were subjected to genetic, surgical, and chemical ablation of the liver. Telomere dysfunction was associated with defects in liver regeneration and accelerated the development of liver cirrhosis in response to chronic liver injury. Adenoviral delivery of mTR into the livers of mTR(-/-) mice with short dysfunctional telomeres restored telomerase activity and telomere function, alleviated cirrhotic pathology, and improved liver function. These studies indicate that telomere dysfunction contributes to chronic diseases of continual cellular loss-replacement and encourage the evaluation of "telomerase therapy" for such diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rudolph, K L -- Chang, S -- Millard, M -- Schreiber-Agus, N -- DePinho, R A -- K08 AG001019/AG/NIA NIH HHS/ -- R01HD28317/HD/NICHD NIH HHS/ -- R01HD34880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1253-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Adult Oncology, Medicine and Genetics, Dana-Farber Cancer Institute, 44 Binney Street (M413), and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678830" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apoptosis ; Carbon Tetrachloride/toxicity ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Hepatectomy ; Liver/enzymology/*pathology ; Liver Cirrhosis, Experimental/enzymology/pathology/physiopathology/*therapy ; *Liver Regeneration ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mitosis ; Spleen/enzymology ; Telomerase/*genetics/metabolism ; Telomere/physiology/ultrastructure ; Transforming Growth Factor beta/metabolism
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    CD95/CD95 ligand interactions on epithelial cells in host defense to Pseudomonas aeruginosa (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: Pseudomonas aeruginosa causes severe infections, particularly of the lung, that are life threatening. Here, we show that P. aeruginosa infection induces apoptosis of lung epithelial cells by activation of the endogenous CD95/CD95 ligand system. Deficiency of CD95 or CD95 ligand on epithelial cells prevented apoptosis of lung epithelial cells in vivo as well as in vitro. The importance of CD95/CD95 ligand-mediated lung epithelial cell apoptosis was demonstrated by the rapid development of sepsis in CD95- or CD95 ligand-deficient mice, but not in normal mice, after P. aeruginosa infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grassme, H -- Kirschnek, S -- Riethmueller, J -- Riehle, A -- von Kurthy, G -- Lang, F -- Weller, M -- Gulbins, E -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):527-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Tuebingen, Gmelinstrasse 5, 72076 Tuebingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039936" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/genetics/*metabolism ; *Apoptosis ; Bone Marrow Transplantation ; Cell Line ; Epithelial Cells/*immunology/microbiology/pathology ; Fas Ligand Protein ; Humans ; In Situ Nick-End Labeling ; Lung/*immunology/microbiology/pathology ; Lung Diseases/*immunology/microbiology/pathology ; Membrane Glycoproteins/genetics/*metabolism ; Mice ; Mice, Inbred C3H ; Pseudomonas Infections/*immunology/microbiology/pathology ; Pseudomonas aeruginosa/immunology/*pathogenicity ; Sepsis/microbiology ; Spleen/microbiology
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    Spongiform disease. Experts downplay new vCJD fears (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1663-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11001722" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Domestic ; Carrier State/*veterinary ; Cattle ; Creutzfeldt-Jakob Syndrome/epidemiology/prevention & control/*transmission ; Cricetinae ; Encephalopathy, Bovine Spongiform/epidemiology/prevention & control/*transmission ; Great Britain/epidemiology ; Humans ; Mice ; Prion Diseases/*transmission ; Species Specificity
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    Biomedicine. Protein loss in cancer cachexia (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tisdale, M J -- New York, N.Y. -- Science. 2000 Sep 29;289(5488):2293-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmaceutical Sciences Research Institute, Aston University, Birmingham B4 7ET, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11041796" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Proteins/metabolism ; Cachexia/drug therapy/etiology/*metabolism/pathology ; Cell Differentiation ; Cysteine Endopeptidases/genetics/metabolism ; Cytokines/pharmacology ; Homeostasis ; Humans ; Interferon-gamma/pharmacology ; Mice ; Multienzyme Complexes/genetics/metabolism ; Muscle Proteins/*metabolism ; Muscle, Skeletal/cytology/*metabolism/pathology ; MyoD Protein/genetics/metabolism ; Myosins/genetics/metabolism ; NF-kappa B/*metabolism ; Neoplasms/*complications ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex ; Proteoglycans ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/pharmacology ; Ubiquitins/metabolism
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    A primitive T cell-independent mechanism of intestinal mucosal IgA responses to commensal bacteria (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-24
    Description: The immunoglobulin A (IgA) is produced to defend mucosal surfaces from environmental organisms, but host defenses against the very heavy load of intestinal commensal microorganisms are poorly understood. The IgA against intestinal commensal bacterial antigens was analyzed; it was not simply "natural antibody" but was specifically induced and responded to antigenic changes within an established gut flora. In contrast to IgA responses against exotoxins, a significant proportion of this specific anti-commensal IgA induction was through a pathway that was independent of T cell help and of follicular lymphoid tissue organization, which may reflect an evolutionarily primitive form of specific immune defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macpherson, A J -- Gatto, D -- Sainsbury, E -- Harriman, G R -- Hengartner, H -- Zinkernagel, R M -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2222-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Immunology, Universitatsspital, Schmelzbergstrasse 12, CH8091, Zurich, Switzerland. amacpher@pathol.unizh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity ; Antigens, Bacterial/immunology ; B-Lymphocytes/*immunology ; Bacterial Proteins/immunology ; Enterobacter cloacae/*immunology ; Escherichia coli/*immunology ; Genes, T-Cell Receptor ; Germ-Free Life ; *Immunity, Mucosal ; Immunoglobulin A, Secretory/*biosynthesis/immunology ; Intestinal Mucosa/*immunology/microbiology ; Lipopolysaccharides/immunology ; Mice ; Mice, Inbred C57BL ; Peritoneum/cytology ; Plasma Cells/immunology ; Porins/immunology ; Specific Pathogen-Free Organisms ; T-Lymphocytes/*immunology
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    Genetics. Was Lamarck just a little bit right? (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 2000 Apr 7;288(5463):38.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10766632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *DNA Methylation ; France ; *Gene Expression Regulation ; Gene Silencing ; Hair Color/genetics ; History, 18th Century ; History, 19th Century ; Mice ; *Mutation ; Plants/genetics
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    Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tournier, C -- Hess, P -- Yang, D D -- Xu, J -- Turner, T K -- Nimnual, A -- Bar-Sagi, D -- Jones, S N -- Flavell, R A -- Davis, R J -- New York, N.Y. -- Science. 2000 May 5;288(5467):870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry & Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Cell Division ; Cells, Cultured ; Cytochrome c Group/*metabolism ; DNA Fragmentation ; Enzyme Activation ; Fibroblasts ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Methyl Methanesulfonate/pharmacology ; Mice ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; NF-kappa B/metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
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    Structural mechanism for STI-571 inhibition of abelson tyrosine kinase (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-16
    Description: The inadvertent activation of the Abelson tyrosine kinase (Abl) causes chronic myelogenous leukemia (CML). A small-molecule inhibitor of Abl (STI-571) is effective in the treatment of CML. We report the crystal structure of the catalytic domain of Abl, complexed to a variant of STI-571. Critical to the binding of STI-571 is the adoption by the kinase of an inactive conformation, in which a centrally located "activation loop" is not phosphorylated. The conformation of this loop is distinct from that in active protein kinases, as well as in the inactive form of the closely related Src kinases. These results suggest that compounds that exploit the distinctive inactivation mechanisms of individual protein kinases can achieve both high affinity and high specificity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schindler, T -- Bornmann, W -- Pellicena, P -- Miller, W T -- Clarkson, B -- Kuriyan, J -- GM29362/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 15;289(5486):1938-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratories of Molecular Biophysics and Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10988075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/chemistry/*pharmacology ; Benzamides ; Catalytic Domain ; Crystallography, X-Ray ; Enzyme Activation ; Enzyme Inhibitors/chemistry/*pharmacology ; Humans ; Imatinib Mesylate ; Mice ; Models, Molecular ; Phosphorylation ; *Piperazines ; Protein Conformation ; Proto-Oncogene Proteins c-abl/*antagonists & inhibitors/chemistry/metabolism ; Pyrimidines/chemistry/*pharmacology ; Recombinant Fusion Proteins ; Structure-Activity Relationship
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A structural framework for deciphering the link between I-Ag7 and autoimmune diabetes (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: Susceptibility to murine and human insulin-dependent diabetes mellitus correlates strongly with major histocompatibility complex (MHC) class II I-A or HLA-DQ alleles that lack an aspartic acid at position beta57. I-Ag7 lacks this aspartate and is the only class II allele expressed by the nonobese diabetic mouse. The crystal structure of I-Ag7 was determined at 2.6 angstrom resolution as a complex with a high-affinity peptide from the autoantigen glutamic acid decarboxylase (GAD) 65. I-Ag7 has a substantially wider peptide-binding groove around beta57, which accounts for distinct peptide preferences compared with other MHC class II alleles. Loss of Asp(beta57) leads to an oxyanion hole in I-Ag7 that can be filled by peptide carboxyl residues or, perhaps, through interaction with the T cell receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corper, A L -- Stratmann, T -- Apostolopoulos, V -- Scott, C A -- Garcia, K C -- Kang, A S -- Wilson, I A -- Teyton, L -- CA58896/CA/NCI NIH HHS/ -- DK55037/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):505-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10775108" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Aspartic Acid/chemistry ; Crystallography, X-Ray ; Diabetes Mellitus, Type 1/*immunology ; Drosophila melanogaster ; *Genes, MHC Class II ; Glutamate Decarboxylase/metabolism ; Histocompatibility Antigens Class II/*chemistry/genetics/metabolism ; Humans ; Hydrogen Bonding ; Mice ; Mice, Inbred NOD ; Models, Molecular ; Molecular Sequence Data ; Peptide Library ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell/metabolism ; Recombinant Proteins/chemistry/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Development of CD8alpha-positive dendritic cells from a common myeloid progenitor (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Dendritic cells (DCs) are critical in both initiating adaptive immune responses and maintaining tolerance to self antigens. These apparently contradictory roles have been suggested to depend on different subsets of DCs that arise from either myeloid or lymphoid hematopoietic origins, respectively. Although DC expression of CD8alpha is attributed to a lymphoid origin, here we show that both CD8alpha+ and CD8alpha- DCs can arise from clonogenic common myeloid progenitors in both thymus and spleen. Thus, expression of CD8alpha is not indicative of a lymphoid origin, and phenotypic and functional differences among DC subsets are likely to reflect maturation status rather than ontogeny.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Traver, D -- Akashi, K -- Manz, M -- Merad, M -- Miyamoto, T -- Engleman, E G -- Weissman, I L -- 5T32 AI-07290/AI/NIAID NIH HHS/ -- CA42551/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2152-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD8/*analysis ; B-Lymphocytes/cytology/immunology ; Cell Lineage ; Dendritic Cells/*cytology/*immunology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology ; Immunophenotyping ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/transplantation ; Spleen/*cytology/immunology ; T-Lymphocytes/cytology/immunology ; Thymus Gland/*cytology/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 81
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    Obesity. Enzyme blocker prompts mice to shed weight (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: A multidisciplinary team may have discovered an important new weapon in the battle of the bulge. On page 2379 of this issue, the team reports that a molecule that is needed for fat synthesis in the body may play a key role in appetite signaling in the brain. Moreover, the investigators produced a synthetic inhibitor of this molecule that spurred a dramatic drop in appetite and weight in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2299-300.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917820" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite/drug effects ; Appetite Depressants/*pharmacology ; Brain/metabolism ; Enzyme Inhibitors/*pharmacology ; Fasting ; Fatty Acid Synthases/*antagonists & inhibitors ; Humans ; Liver/drug effects/metabolism ; Malonyl Coenzyme A/metabolism ; Mice ; Neuropeptide Y/genetics/metabolism ; Obesity/*drug therapy ; RNA, Messenger/genetics/metabolism ; Weight Loss/*drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
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    Circadian rhythms. Two feedback loops run mammalian clock (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 2000 May 12;288(5468):943-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10841707" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/genetics/*physiology ; CLOCK Proteins ; Cell Cycle Proteins ; Cell Nucleus/metabolism ; Circadian Rhythm/genetics/*physiology ; Cryptochromes ; Drosophila/metabolism ; *Drosophila Proteins ; *Eye Proteins ; Feedback ; Flavoproteins/genetics/*metabolism ; *Gene Expression Regulation ; Mice ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 83
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    Transport of peptide-MHC class II complexes in developing dendritic cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: Major histocompatibility complex class II (MHC II) molecules capture peptides within the endocytic pathway to generate T cell receptor (TCR) ligands. Immature dendritic cells (DCs) sequester intact antigens in lysosomes, processing and converting antigens into peptide-MHC II complexes upon induction of DC maturation. The complexes then accumulate in distinctive, nonlysosomal MHC II+ vesicles that appear to migrate to the cell surface. Although the vesicles exclude soluble lysosomal contents and antigen-processing machinery, many contain MHC I and B7 costimulatory molecules. After arrival at the cell surface, the MHC and costimulatory molecules remain clustered. Thus, transport of peptide-MHC II complexes by DCs not only accomplishes transfer from late endocytic compartments to the plasma membrane, but does so in a manner that selectively concentrates TCR ligands and costimulatory molecules for T cell contact.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turley, S J -- Inaba, K -- Garrett, W S -- Ebersold, M -- Unternaehrer, J -- Steinman, R M -- Mellman, I -- AI-13013/AI/NIAID NIH HHS/ -- AI-34098/AI/NIAID NIH HHS/ -- AI-39672/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):522-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Section of Immunobiology, Ludwig Institute for Cancer Research, Yale University School of Medicine, 333 Cedar Street, Post Office Box 208002, New Haven, CT 06520-8002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10775112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Antigen Presentation ; Antigens, CD/immunology/metabolism ; Antigens, CD86 ; B-Lymphocytes/immunology/metabolism ; Bicyclo Compounds, Heterocyclic/pharmacology ; Biological Transport ; Cell Membrane/immunology/metabolism ; Cells, Cultured ; Dendritic Cells/*immunology/*metabolism ; Endocytosis ; Endosomes/immunology/metabolism ; Histocompatibility Antigens Class I/immunology/metabolism ; Histocompatibility Antigens Class II/immunology/*metabolism ; Kinetics ; Ligands ; Lipopolysaccharides/immunology ; Lysosomes/immunology/metabolism ; Membrane Glycoproteins/immunology/metabolism ; Mice ; Mice, Inbred C3H ; Muramidase/immunology/*metabolism ; Peptide Fragments/immunology/*metabolism ; Receptors, Antigen, T-Cell/metabolism ; Thiazoles/pharmacology ; Thiazolidines
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Angiogenesis research. Cancer drugs found to work in new way (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):245.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10777399" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inhibitors/*administration & dosage/therapeutic use/toxicity ; Animals ; Antineoplastic Combined Chemotherapy Protocols/*administration & ; dosage/therapeutic use/toxicity ; Clinical Trials as Topic ; Cyclohexanes ; Humans ; Mice ; Neoplasms/*drug therapy/pathology ; Neoplasms, Experimental/drug therapy/pathology ; Neovascularization, Pathologic/*drug therapy/pathology ; Sesquiterpenes/administration & dosage/therapeutic use
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Family of bitter taste receptors found (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2133-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10744529" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chemoreceptor Cells/*physiology ; Humans ; Mice ; Multigene Family ; Receptors, Cell Surface/genetics/*physiology ; *Taste ; Taste Buds/*physiology ; Transducin/biosynthesis
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    NF-kappaB-induced loss of MyoD messenger RNA: possible role in muscle decay and cachexia (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-29
    Description: MyoD regulates skeletal muscle differentiation (SMD) and is essential for repair of damaged tissue. The transcription factor nuclear factor kappa B (NF-kappaB) is activated by the cytokine tumor necrosis factor (TNF), a mediator of skeletal muscle wasting in cachexia. Here, the role of NF-kappaB in cytokine-induced muscle degeneration was explored. In differentiating C2C12 myocytes, TNF-induced activation of NF-kappaB inhibited SMD by suppressing MyoD mRNA at the posttranscriptional level. In contrast, in differentiated myotubes, TNF plus interferon-gamma (IFN-gamma) signaling was required for NF-kappaB-dependent down-regulation of MyoD and dysfunction of skeletal myofibers. MyoD mRNA was also down-regulated by TNF and IFN-gamma expression in mouse muscle in vivo. These data elucidate a possible mechanism that may underlie the skeletal muscle decay in cachexia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guttridge, D C -- Mayo, M W -- Madrid, L V -- Wang, C Y -- Baldwin, A S Jr -- AI35098/AI/NIAID NIH HHS/ -- CA72771/CA/NCI NIH HHS/ -- K01 CA78595/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 29;289(5488):2363-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, Curriculum in Genetics and Molecular Biology, Department of Biology, University of North Carolina, Chapel Hill, Mason Farm Road, Campus Box 7295, Chapel Hill, NC, 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11009425" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Cachexia/*etiology/metabolism/pathology ; Cell Differentiation ; Cell Line ; Cricetinae ; DNA-Binding Proteins/genetics/metabolism ; Down-Regulation ; *I-kappa B Proteins ; Interferon-gamma/pharmacology ; Interleukins/pharmacology ; Mice ; Mice, Inbred Strains ; Mice, Nude ; Muscle, Skeletal/*cytology/*metabolism/pathology ; MyoD Protein/*genetics/metabolism ; NF-kappa B/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Transcription Factor RelA ; Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
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    Allosteric effects of Pit-1 DNA sites on long-term repression in cell type specification (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-10
    Description: Reciprocal gene activation and restriction during cell type differentiation from a common lineage is a hallmark of mammalian organogenesis. A key question, then, is whether a critical transcriptional activator of cell type-specific gene targets can also restrict expression of the same genes in other cell types. Here, we show that whereas the pituitary-specific POU domain factor Pit-1 activates growth hormone gene expression in one cell type, the somatotrope, it restricts its expression from a second cell type, the lactotrope. This distinction depends on a two-base pair spacing in accommodation of the bipartite POU domains on a conserved growth hormone promoter site. The allosteric effect on Pit-1, in combination with other DNA binding factors, results in the recruitment of a corepressor complex, including nuclear receptor corepressor N-CoR, which, unexpectedly, is required for active long-term repression of the growth hormone gene in lactotropes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scully, K M -- Jacobson, E M -- Jepsen, K -- Lunyak, V -- Viadiu, H -- Carriere, C -- Rose, D W -- Hooshmand, F -- Aggarwal, A K -- Rosenfeld, M G -- R01 DK18477/DK/NIDDK NIH HHS/ -- R01 DK54802/DK/NIDDK NIH HHS/ -- R01 GM49327/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 10;290(5494):1127-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Endocrinology and Metabolism, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11073444" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Animals ; Base Sequence ; Binding Sites ; Cell Line ; Conserved Sequence ; Crystallization ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Female ; *Gene Expression Regulation ; Genes, Reporter ; Growth Hormone/*genetics ; Male ; Mice ; Mice, Transgenic ; Models, Molecular ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Nuclear Receptor Co-Repressor 1 ; Pituitary Gland/cytology/*metabolism ; Prolactin/*genetics ; Promoter Regions, Genetic ; Protein Conformation ; Protein Structure, Tertiary ; Rats ; Repressor Proteins/chemistry/genetics/*metabolism ; Transcription Factor Pit-1 ; Transcription Factors/chemistry/genetics/*metabolism ; Transcriptional Activation
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  • 88
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    Requirement for DARPP-32 in progesterone-facilitated sexual receptivity in female rats and mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-11
    Description: DARPP-32, a dopamine- and adenosine 3',5'-monophosphate (cAMP)-regulated phosphoprotein (32 kilodaltons in size), is an obligate intermediate in progesterone (P)-facilitated sexual receptivity in female rats and mice. The facilitative effect of P on sexual receptivity in female rats was blocked by antisense oligonucleotides to DARPP-32. Homozygous mice carrying a null mutation for the DARPP-32 gene exhibited minimal levels of P-facilitated sexual receptivity when compared to their wild-type littermates. P significantly increased hypothalamic cAMP levels and cAMP-dependent protein kinase activity. These increases were not inhibited by a D1 subclass dopamine receptor antagonist. P also enhanced phosphorylation of DARPP-32 on threonine 34 in the hypothalamus of mice. DARPP-32 activation is thus an obligatory step in progestin receptor regulation of sexual receptivity in rats and mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mani, S K -- Fienberg, A A -- O'Callaghan, J P -- Snyder, G L -- Allen, P B -- Dash, P K -- Moore, A N -- Mitchell, A J -- Bibb, J -- Greengard, P -- O'Malley, B W -- MH49662/MH/NIMH NIH HHS/ -- MH57442/MH/NIMH NIH HHS/ -- NS 35457/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):1053-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. smani@bcm.tmc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10669419" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; Animals ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dopamine/pharmacology ; Dopamine Agonists/pharmacology ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; Female ; Hypothalamus/metabolism ; Injections, Intraventricular ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; *Nerve Tissue Proteins ; Oligonucleotides, Antisense/pharmacology ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Posture ; Progesterone/*pharmacology ; Proteins/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Progesterone/metabolism ; Serotonin/pharmacology ; Sexual Behavior, Animal/*drug effects ; Signal Transduction
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    Perspectives: signal transduction. Signals to move cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dekker, L V -- Segal, A W -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):982-3, 985.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Molecular Medicine, University College London, London, UK. rmhalvd@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691572" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Chemotaxis/*physiology ; Chemotaxis, Leukocyte/*physiology ; Enzyme Activation ; GTP Phosphohydrolases/metabolism ; Heterotrimeric GTP-Binding Proteins/metabolism ; Isoenzymes/metabolism ; Leukocytes/physiology ; Macrophages/physiology ; Mice ; Mice, Knockout ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphatidylinositol Phosphates/metabolism ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Receptors, Formyl Peptide ; Receptors, Immunologic/metabolism ; Receptors, Interleukin/metabolism ; Receptors, Interleukin-8A ; Receptors, Peptide/metabolism ; *Signal Transduction ; rac GTP-Binding Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    In silico mapping of mouse quantitative trait loci (2002)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2002-02-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darvasi, A -- New York, N.Y. -- Science. 2001 Dec 21;294(5551):2423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Evolution Systematicsand Ecology, The Hebrew University of Jerusalem, Jerusalem 91904, Israel. arield@cc.huji.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11865449" target="_blank"〉PubMed〈/a〉
    Keywords: *Algorithms ; Animals ; Chromosome Mapping/*methods ; Genetic Variation ; Genotype ; Mice ; Mice, Inbred Strains ; Phenotype ; Polymorphism, Single Nucleotide ; *Quantitative Trait, Heritable
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    Medulloblastoma growth inhibition by hedgehog pathway blockade (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-31
    Description: Constitutive Hedgehog (Hh) pathway activity is associated with initiation of neoplasia, but its role in the continued growth of established tumors is unclear. Here, we investigate the therapeutic efficacy of the Hh pathway antagonist cyclopamine in preclinical models of medulloblastoma, the most common malignant brain tumor in children. Cyclopamine treatment of murine medulloblastoma cells blocked proliferation in vitro and induced changes in gene expression consistent with initiation of neuronal differentiation and loss of neuronal stem cell-like character. This compound also caused regression of murine tumor allografts in vivo and induced rapid death of cells from freshly resected human medulloblastomas, but not from other brain tumors, thus establishing a specific role for Hh pathway activity in medulloblastoma growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berman, David M -- Karhadkar, Sunil S -- Hallahan, Andrew R -- Pritchard, Joel I -- Eberhart, Charles G -- Watkins, D Neil -- Chen, James K -- Cooper, Michael K -- Taipale, Jussi -- Olson, James M -- Beachy, Philip A -- New York, N.Y. -- Science. 2002 Aug 30;297(5586):1559-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12202832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*therapeutic use ; Bicuculline/*therapeutic use ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cerebellar Neoplasms/*drug therapy ; Disease Models, Animal ; Hedgehog Proteins ; Humans ; Medulloblastoma/*drug therapy ; Membrane Proteins/genetics ; Mice ; Mice, Nude ; Receptors, Cell Surface ; Signal Transduction/drug effects ; Trans-Activators/*antagonists & inhibitors/metabolism ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Molecular hydrogen as an energy source for Helicobacter pylori (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-03
    Description: The gastric pathogen Helicobacter pylori is known to be able to use molecular hydrogen as a respiratory substrate when grown in the laboratory. We found that hydrogen is available in the gastric mucosa of mice and that its use greatly increased the stomach colonization by H. pylori. Hydrogenase activity in H. pylori is constitutive but increased fivefold upon incubation with hydrogen. Hydrogen concentrations measured in the stomachs of live mice were found to be 10 to 50 times as high as the H. pylori affinity for hydrogen. A hydrogenase mutant strain is much less efficient in its colonization of mice. Therefore, hydrogen present in animals as a consequence of normal colonic flora is an energy-yielding substrate that can facilitate the maintenance of a pathogenic bacterium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Jonathan W -- Maier, Robert J -- New York, N.Y. -- Science. 2002 Nov 29;298(5599):1788-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Georgia, Athens, GA 30602, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12459589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catechol 2,3-Dioxygenase ; Colon/metabolism/microbiology ; *Dioxygenases ; Energy Metabolism ; Fermentation ; Gastric Mucosa/*metabolism/*microbiology ; Gene Expression Regulation, Bacterial ; Genes, Reporter ; Helicobacter pylori/growth & development/*metabolism ; Hydrogen/*metabolism ; Hydrogenase/genetics/*metabolism ; Kinetics ; Mice ; Mutation ; Oxidation-Reduction ; Oxygenases/genetics/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
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    An essential role of N-terminal arginylation in cardiovascular development (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-06
    Description: The enzymatic conjugation of arginine to the N-termini of proteins is a part of the ubiquitin-dependent N-end rule pathway of protein degradation. In mammals, three N-terminal residues-aspartate, glutamate, and cysteine-are substrates for arginylation. The mouse ATE1 gene encodes a family of Arg-tRNA-protein transferases (R-transferases) that mediate N-terminal arginylation. We constructed ATE1-lacking mouse strains and found that ATE1-/- embryos die with defects in heart development and in angiogenic remodeling of the early vascular plexus. Through biochemical analyses, we show that N-terminal cysteine, in contrast to N-terminal aspartate and glutamate, is oxidized before its arginylation by R-transferase, suggesting that the arginylation branch of the N-end rule pathway functions as an oxygen sensor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Yong Tae -- Kashina, Anna S -- Davydov, Ilia V -- Hu, Rong-Gui -- An, Jee Young -- Seo, Jai Wha -- Du, Fangyong -- Varshavsky, Alexander -- GM31530/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):96-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, 147-75, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098698" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylation ; Aminoacyltransferases/*genetics/*metabolism ; Animals ; Aorta/embryology ; Arginine/*metabolism ; Aspartic Acid/metabolism ; Blood Vessels/*embryology ; Cell Line ; Cysteic Acid/metabolism ; Cysteine/metabolism ; Female ; Glutamic Acid/metabolism ; Heart/*embryology ; Heart Defects, Congenital/embryology ; Heart Septal Defects/embryology ; Hypoxia-Inducible Factor 1, alpha Subunit ; Male ; Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic ; Oxidation-Reduction ; Proteins/*metabolism ; Pulmonary Artery/embryology ; RGS Proteins/metabolism ; Recombinant Proteins/metabolism ; Sulfinic Acids/metabolism ; Transcription Factors/metabolism ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    MAP kinase phosphatase as a locus of flexibility in a mitogen-activated protein kinase signaling network (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-10
    Description: Intracellular signaling networks receive and process information to control cellular machines. The mitogen-activated protein kinase (MAPK) 1,2/protein kinase C (PKC) system is one such network that regulates many cellular machines, including the cell cycle machinery and autocrine/paracrine factor synthesizing machinery. We used a combination of computational analysis and experiments in mouse NIH-3T3 fibroblasts to understand the design principles of this controller network. We find that the growth factor-stimulated signaling network containing MAPK 1, 2/PKC can operate with one (monostable) or two (bistable) stable states. At low concentrations of MAPK phosphatase, the system exhibits bistable behavior, such that brief stimulus results in sustained MAPK activation. The MAPK-induced increase in the amounts of MAPK phosphatase eliminates the prolonged response capability and moves the network to a monostable state, in which it behaves as a proportional response system responding acutely to stimulus. Thus, the MAPK 1, 2/PKC controller network is flexibly designed, and MAPK phosphatase may be critical for this flexible response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhalla, Upinder S -- Ram, Prahlad T -- Iyengar, Ravi -- CA-79134/CA/NCI NIH HHS/ -- CA-81050/CA/NCI NIH HHS/ -- GM-54508/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):1018-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Biological Sciences, Bangalore 560065 India. bhalla@ncbs.res.in〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12169734" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adaptation, Physiological ; Animals ; *Cell Cycle Proteins ; Computer Simulation ; Dose-Response Relationship, Drug ; Dual Specificity Phosphatase 1 ; *Feedback, Physiological ; Immediate-Early Proteins/*metabolism ; *MAP Kinase Signaling System ; Mathematics ; Mice ; Mitogen-Activated Protein Kinase 1/*metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases/*metabolism ; Models, Biological ; Phospholipases A/antagonists & inhibitors/metabolism ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Protein Kinase C/metabolism ; Protein Phosphatase 1 ; Protein Tyrosine Phosphatases/*metabolism
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  • 95
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    BRCA2 function in DNA binding and recombination from a BRCA2-DSS1-ssDNA structure (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-14
    Description: Mutations in the BRCA2 (breast cancer susceptibility gene 2) tumor suppressor lead to chromosomal instability due to defects in the repair of double-strand DNA breaks (DSBs) by homologous recombination, but BRCA2's role in this process has been unclear. Here, we present the 3.1 angstrom crystal structure of a approximately 90-kilodalton BRCA2 domain bound to DSS1, which reveals three oligonucleotide-binding (OB) folds and a helix-turn-helix (HTH) motif. We also (i) demonstrate that this BRCA2 domain binds single-stranded DNA, (ii) present its 3.5 angstrom structure bound to oligo(dT)9, (iii) provide data that implicate the HTH motif in dsDNA binding, and (iv) show that BRCA2 stimulates RAD51-mediated recombination in vitro. These findings establish that BRCA2 functions directly in homologous recombination and provide a structural and biochemical basis for understanding the loss of recombination-mediated DSB repair in BRCA2-associated cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Haijuan -- Jeffrey, Philip D -- Miller, Julie -- Kinnucan, Elspeth -- Sun, Yutong -- Thoma, Nicolas H -- Zheng, Ning -- Chen, Phang-Lang -- Lee, Wen-Hwa -- Pavletich, Nikola P -- New York, N.Y. -- Science. 2002 Sep 13;297(5588):1837-48.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Sloan-Kettering Division, Joan and Sanford I. Weill Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12228710" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; BRCA2 Protein/*chemistry/genetics/*metabolism ; Binding Sites ; Crystallography, X-Ray ; DNA/metabolism ; *DNA Repair ; DNA, Single-Stranded/*metabolism ; DNA-Binding Proteins/metabolism ; Genes, BRCA2 ; Helix-Turn-Helix Motifs ; Humans ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Mice ; Molecular Sequence Data ; Mutation ; Proteasome Endopeptidase Complex ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Proteins/chemistry/*metabolism ; Rad51 Recombinase ; Rats ; *Recombination, Genetic
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    Immunology. Plant a few cells, sprout a thymus (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2002 Jun 21;296(5576):2120-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12077376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transplantation ; Epithelial Cells/cytology/transplantation ; Kidney ; Mice ; Mice, Nude ; Stem Cell Transplantation ; Stem Cells/*physiology ; T-Lymphocytes/cytology/*immunology ; Thymus Gland/*cytology/growth & development/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Toll-like receptor 4-dependent activation of dendritic cells by beta-defensin 2 (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-02
    Description: beta-Defensins are small antimicrobial peptides of the innate immune system produced in response to microbial infection of mucosal tissue and skin. We demonstrate that murine beta-defensin 2 (mDF2beta) acts directly on immature dendritic cells as an endogenous ligand for Toll-like receptor 4 (TLR-4), inducing up-regulation of costimulatory molecules and dendritic cell maturation. These events, in turn, trigger robust, type 1 polarized adaptive immune responses in vivo, suggesting that mDF2beta may play an important role in immunosurveillance against pathogens and, possibly, self antigens or tumor antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biragyn, Arya -- Ruffini, Pier Adelchi -- Leifer, Cynthia A -- Klyushnenkova, Elena -- Shakhov, Alexander -- Chertov, Oleg -- Shirakawa, Aiko K -- Farber, Joshua M -- Segal, David M -- Oppenheim, Joost J -- Kwak, Larry W -- N0L-CO-12400/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 1;298(5595):1025-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Transplantation and Immunology Branch, National Cancer Institute, Bethesda, MD 20892, USA. arya@mail.ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12411706" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; Cancer Vaccines/immunology ; Cell Line ; Cytokines/biosynthesis ; Dendritic Cells/*immunology ; *Drosophila Proteins ; Female ; Humans ; Interferon-alpha/physiology ; Ligands ; Lipopolysaccharides/immunology/pharmacology ; Lymphocyte Culture Test, Mixed ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Neoplasms/immunology/therapy ; Receptors, CCR6 ; Receptors, Cell Surface/genetics/*physiology ; Receptors, Chemokine/metabolism ; Recombinant Fusion Proteins/pharmacology ; Signal Transduction ; Toll-Like Receptor 4 ; Toll-Like Receptors ; Transfection ; beta-Defensins/pharmacology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Lymphatic metastasis in the absence of functional intratumor lymphatics (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-27
    Description: Lymphatic metastasis contributes to mortality from solid tumors. Whether metastasizing cancer cells reach lymph nodes via intratumor lymphatic vessels is unknown. Here, we examine functional lymphatics associated with mouse tumors expressing normal or elevated levels of vascular endothelial growth factor-C (VEGF-C), a molecule that stimulates lymphangiogenesis. Although VEGF-C overexpression increased lymphatic surface area in the tumor margin and lymphatic metastasis, these tumors contained no functional lymphatics, as assessed by four independent functional assays and immunohistochemical staining. These findings suggest that the functional lymphatics in the tumor margin alone are sufficient for lymphatic metastasis and should be targeted therapeutically.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Padera, Timothy P -- Kadambi, Ananth -- di Tomaso, Emmanuelle -- Carreira, Carla Mouta -- Brown, Edward B -- Boucher, Yves -- Choi, Noah C -- Mathisen, Douglas -- Wain, John -- Mark, Eugene J -- Munn, Lance L -- Jain, Rakesh K -- R24-CA85140/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 7;296(5574):1883-6. Epub 2002 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉E. L. Steele Laboratory, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, 100 Blossom Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976409" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/chemistry/pathology ; Animals ; Antigens, Surface/analysis ; Endothelial Growth Factors/metabolism ; Extracellular Space/physiology ; Fibrosarcoma/metabolism/*pathology/physiopathology/secondary ; Glycoproteins/analysis ; Humans ; Immunohistochemistry ; Lung Neoplasms/chemistry/pathology/physiopathology/secondary ; *Lymphatic Metastasis ; Lymphatic System/chemistry/*pathology/physiology ; Lymphography ; Melanoma, Experimental/metabolism/*pathology/physiopathology/secondary ; Mice ; Mice, Inbred C3H ; Mice, Nude ; Microscopy/methods ; Neoplasm Transplantation ; Neoplasms/metabolism/*pathology/physiopathology ; Pressure ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor C ; Vesicular Transport Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Protein structure. Harmless proteins twist into troublemakers (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2002 Apr 5;296(5565):28-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934996" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid beta-Peptides/chemistry ; Animals ; Humans ; Mice ; Protein Conformation ; *Protein Folding ; *Protein Structure, Quaternary ; Proteins/*chemistry ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Effect of p53 status on tumor response to antiangiogenic therapy (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-23
    Description: The p53 tumor suppressor gene is inactivated in the majority of human cancers. Tumor cells deficient in p53 display a diminished rate of apoptosis under hypoxic conditions, a circumstance that might reduce their reliance on vascular supply, and hence their responsiveness to antiangiogenic therapy. Here, we report that mice bearing tumors derived from p53(-/-) HCT116 human colorectal cancer cells were less responsive to antiangiogenic combination therapy than mice bearing isogenic p53(+/+) tumors. Thus, although antiangiogenic therapy targets genetically stable endothelial cells in the tumor vasculature, genetic alterations that decrease the vascular dependence of tumor cells can influence the therapeutic response of tumors to this therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Joanne L -- Rak, Janusz W -- Coomber, Brenda L -- Hicklin, Daniel J -- Kerbel, Robert S -- CA-41233/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Feb 22;295(5559):1526-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sunnybrook and Women's College Health Sciences Centre, Molecular and Cellular Biology Research, Room S-218, 2075 Bayview Avenue, Toronto, Ontario, Canada M4N 3M5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11859195" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inhibitors/pharmacology/*therapeutic use ; Animals ; Antibodies/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/pharmacology/*therapeutic use ; Apoptosis ; *Cell Hypoxia ; Cell Survival ; Colorectal Neoplasms ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics/metabolism ; Gene Deletion ; *Gene Silencing ; *Genes, p53 ; Humans ; In Situ Nick-End Labeling ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Neoplasms, Experimental/blood supply/*drug therapy/*genetics/pathology ; Receptor Protein-Tyrosine Kinases/immunology ; Receptors, Growth Factor/immunology ; Receptors, Vascular Endothelial Growth Factor ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/metabolism ; Vinblastine/therapeutic use
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