ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Publication Date: 2011-08-18
    Description: Pavlovian olfactory learning in Drosophila produces two genetically distinct forms of intermediate-term memories: anesthesia-sensitive memory, which requires the amnesiac gene, and anesthesia-resistant memory (ARM), which requires the radish gene. Here, we report that ARM is specifically enhanced or inhibited in flies with elevated or reduced serotonin (5HT) levels, respectively. The requirement for 5HT was additive with the memory defect of the amnesiac mutation but was occluded by the radish mutation. This result suggests that 5HT and Radish protein act on the same pathway for ARM formation. Three supporting lines of evidence indicate that ARM formation requires 5HT released from only two dorsal paired medial (DPM) neurons onto the mushroom bodies (MBs), the olfactory learning and memory center in Drosophila: (i) DPM neurons were 5HT-antibody immunopositive; (ii) temporal inhibition of 5HT synthesis or release from DPM neurons, but not from other serotonergic neurons, impaired ARM formation; (iii) knocking down the expression of d5HT1A serotonin receptors in α/β MB neurons, which are innervated by DPM neurons, inhibited ARM formation. Thus, in addition to the Amnesiac peptide required for anesthesia-sensitive memory formation, the two DPM neurons also release 5HT acting on MB neurons for ARM formation.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2001-03-10
    Description: Familial advanced sleep phase syndrome (FASPS) is an autosomal dominant circadian rhythm variant; affected individuals are "morning larks" with a 4-hour advance of the sleep, temperature, and melatonin rhythms. Here we report localization of the FASPS gene near the telomere of chromosome 2q. A strong candidate gene (hPer2), a human homolog of the period gene in Drosophila, maps to the same locus. Affected individuals have a serine to glycine mutation within the casein kinase Iepsilon (CKIepsilon) binding region of hPER2, which causes hypophosphorylation by CKIepsilon in vitro. Thus, a variant in human sleep behavior can be attributed to a missense mutation in a clock component, hPER2, which alters the circadian period.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toh, K L -- Jones, C R -- He, Y -- Eide, E J -- Hinz, W A -- Virshup, D M -- Ptacek, L J -- Fu, Y H -- HL/HD 59596/HL/NHLBI NIH HHS/ -- M01-RR00064/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2001 Feb 9;291(5506):1040-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Utah, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11232563" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Biological Clocks/*genetics ; Casein Kinases ; Chromosome Mapping ; Chromosomes, Human, Pair 2/genetics ; Circadian Rhythm/*genetics ; Exons ; Female ; Genetic Linkage ; Glycine ; Humans ; Male ; Molecular Sequence Data ; Mutation, Missense ; Nuclear Proteins/chemistry/*genetics/*metabolism ; Pedigree ; Period Circadian Proteins ; Phosphorylation ; Polymorphism, Single-Stranded Conformational ; Protein Kinases/metabolism ; Proteins/chemistry/*genetics/*metabolism ; Serine ; Sleep Disorders, Circadian Rhythm/*genetics/physiopathology ; Transcription Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2015-09-30
    Description: Earlier spring leaf unfolding is a frequently observed response of plants to climate warming. Many deciduous tree species require chilling for dormancy release, and warming-related reductions in chilling may counteract the advance of leaf unfolding in response to warming. Empirical evidence for this, however, is limited to saplings or twigs in climate-controlled chambers. Using long-term in situ observations of leaf unfolding for seven dominant European tree species at 1,245 sites, here we show that the apparent response of leaf unfolding to climate warming (ST, expressed in days advance of leaf unfolding per degrees C warming) has significantly decreased from 1980 to 2013 in all monitored tree species. Averaged across all species and sites, ST decreased by 40% from 4.0 +/- 1.8 days degrees C(-1) during 1980-1994 to 2.3 +/- 1.6 days degrees C(-1) during 1999-2013. The declining ST was also simulated by chilling-based phenology models, albeit with a weaker decline (24-30%) than observed in situ. The reduction in ST is likely to be partly attributable to reduced chilling. Nonetheless, other mechanisms may also have a role, such as 'photoperiod limitation' mechanisms that may become ultimately limiting when leaf unfolding dates occur too early in the season. Our results provide empirical evidence for a declining ST, but also suggest that the predicted strong winter warming in the future may further reduce ST and therefore result in a slowdown in the advance of tree spring phenology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Yongshuo H -- Zhao, Hongfang -- Piao, Shilong -- Peaucelle, Marc -- Peng, Shushi -- Zhou, Guiyun -- Ciais, Philippe -- Huang, Mengtian -- Menzel, Annette -- Penuelas, Josep -- Song, Yang -- Vitasse, Yann -- Zeng, Zhenzhong -- Janssens, Ivan A -- England -- Nature. 2015 Oct 1;526(7571):104-7. doi: 10.1038/nature15402. Epub 2015 Sep 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sino-French Institute for Earth System Science, College of Urban and Environmental Sciences, Peking University, Beijing 100871, China. ; Centre of Excellence PLECO (Plant and Vegetation Ecology), Department of Biology, University of Antwerp, Universiteitsplein 1, B-2610 Wilrijk, Belgium. ; Key Laboratory of Alpine Ecology and Biodiversity, Institute of Tibetan Plateau Research, Chinese Academy of Sciences, Beijing 100085, China. ; Center for Excellence in Tibetan Earth Science, Chinese Academy of Sciences, Beijing 100085, China. ; Laboratoire des Sciences du Climat et de l'Environnement, CEA CNRS UVSQ, Gif-sur-Yvette 91190, France. ; School of Resources and Environment, University of Electronic Science and Technology of China, Chengdu 611731, China. ; Ecoclimatology, Technische Universitat Munchen, Freising 85354, Germany. ; Technische Universitat Munchen, Institute for Advanced Study, Lichtenbergstrasse 2a, 85748 Garching, Germany. ; CREAF, Cerdanyola del Valles, Barcelona 08193, Catalonia, Spain. ; CSIC, Global Ecology Unit CREAF-CSIC-UAB, Cerdanyola del Valles, Barcelona 08193, Catalonia, Spain. ; Department of Atmospheric Sciences, University of Illinois, Urbana, Illinois 61801, USA. ; University of Neuchatel, Institute of Geography, Neuchatel 2000, Switzerland. ; WSL Swiss Federal Institute for Forest, Snow and Landscape Research, Neuchatel 2000, Switzerland. ; WSL Institute for Snow and Avalanche Research SLF, Group Mountain Ecosystems, Davos 7260, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26416746" target="_blank"〉PubMed〈/a〉
    Keywords: Cold Temperature ; Europe ; *Global Warming ; Models, Biological ; Photoperiod ; Plant Leaves/*growth & development ; *Seasons ; Time Factors ; Trees/*growth & development
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-05-18
    Description: Triplet repeats are the sites of mutation in three human heritable disorders, spinal and bulbar muscular atrophy (SBMA), fragile X syndrome, and myotonic dystrophy (DM). These repeats are GC-rich and highly polymorphic in the normal population. Fragile X syndrome and DM are examples of diseases in which premutation alleles cause little or no disease in the individual, but give rise to significantly amplified repeats in affected progeny. This newly identified mechanism of mutation has, so far, been identified in two of the most common heritable disorders, fragile X syndrome and DM, and one rare disease, SBMA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caskey, C T -- Pizzuti, A -- Fu, Y H -- Fenwick, R G Jr -- Nelson, D L -- 1R01HD29256/HD/NICHD NIH HHS/ -- P30-HG00210/HG/NHGRI NIH HHS/ -- P30HD24064/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1992 May 8;256(5058):784-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589758" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Fragile X Syndrome/*genetics/physiopathology ; Genetic Diseases, Inborn/*genetics/physiopathology ; Humans ; Male ; Muscular Atrophy, Spinal/*genetics/physiopathology ; *Mutation ; Myotonic Dystrophy/*genetics/physiopathology ; Pedigree ; Repetitive Sequences, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2009-08-15
    Description: Sleep deprivation can impair human health and performance. Habitual total sleep time and homeostatic sleep response to sleep deprivation are quantitative traits in humans. Genetic loci for these traits have been identified in model organisms, but none of these potential animal models have a corresponding human genotype and phenotype. We have identified a mutation in a transcriptional repressor (hDEC2-P385R) that is associated with a human short sleep phenotype. Activity profiles and sleep recordings of transgenic mice carrying this mutation showed increased vigilance time and less sleep time than control mice in a zeitgeber time- and sleep deprivation-dependent manner. These mice represent a model of human sleep homeostasis that provides an opportunity to probe the effect of sleep on human physical and mental health.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884988/" 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/PMC2884988/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Ying -- Jones, Christopher R -- Fujiki, Nobuhiro -- Xu, Ying -- Guo, Bin -- Holder, Jimmy L Jr -- Rossner, Moritz J -- Nishino, Seiji -- Fu, Ying-Hui -- HL059596/HL/NHLBI NIH HHS/ -- MH074924/MH/NIMH NIH HHS/ -- R01 HL059596/HL/NHLBI NIH HHS/ -- R01 HL059596-09/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 14;325(5942):866-70. doi: 10.1126/science.1174443.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California at San Francisco, Mission Bay, 1550 Fourth Street, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19679812" target="_blank"〉PubMed〈/a〉
    Keywords: Activity Cycles/genetics ; Adolescent ; Adult ; Aged ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Animals, Genetically Modified ; Basic Helix-Loop-Helix Transcription Factors/chemistry/*genetics/physiology ; Child ; Circadian Rhythm/genetics ; Drosophila/genetics ; Electroencephalography ; Electromyography ; Female ; Homeostasis ; Humans ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Molecular Sequence Data ; Pedigree ; Point Mutation ; Sleep/*genetics/physiology ; Sleep Deprivation ; Sleep, REM/genetics/physiology ; Transcription Factors/chemistry/genetics/physiology ; Wakefulness
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 1992-03-16
    Description: Synthetic oligonucleotides containing GC-rich triplet sequences were used in a scanning strategy to identify unstable genetic sequences at the myotonic dystrophy (DM) locus. A highly polymorphic GCT repeat was identified and found to be unstable, with an increased number of repeats occurring in DM patients. In the case of severe congenital DM, the paternal triplet allele was inherited unaltered while the maternal, DM-associated allele was unstable. These studies suggest that the mutational mechanism leading to DM is triplet amplification, similar to that occurring in the fragile X syndrome. The triplet repeat sequence is within a gene (to be referred to as myotonin-protein kinase), which has a sequence similar to protein kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Y H -- Pizzuti, A -- Fenwick, R G Jr -- King, J -- Rajnarayan, S -- Dunne, P W -- Dubel, J -- Nasser, G A -- Ashizawa, T -- de Jong, P -- 5-M01-RR00350/RR/NCRR NIH HHS/ -- P30-HG00210/HG/NHGRI NIH HHS/ -- P50HL42267-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 6;255(5049):1256-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546326" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Chromosomes, Human, Pair 19 ; Cloning, Molecular ; DNA/chemistry ; Humans ; Molecular Sequence Data ; Mutation ; Myotonic Dystrophy/*genetics ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; Polymorphism, Genetic ; *Repetitive Sequences, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 1993-04-09
    Description: The myotonic dystrophy mutation has recently been identified; however, the molecular mechanism of the disease is still unknown. The sequence of the myotonin-protein kinase gene was determined, and messenger RNA spliced forms were identified in various tissues. Antisera were developed for analytical studies. Quantitative reverse transcription-polymerase chain reaction and radioimmunoassay were used to demonstrate that decreased levels of the messenger RNA and protein expression are associated with the adult form of myotonic dystrophy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Y H -- Friedman, D L -- Richards, S -- Pearlman, J A -- Gibbs, R A -- Pizzuti, A -- Ashizawa, T -- Perryman, M B -- Scarlato, G -- Fenwick, R G Jr -- P30-HG00210/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 9;260(5105):235-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469976" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alternative Splicing ; Amino Acid Sequence ; Base Sequence ; Gene Expression ; Humans ; Molecular Sequence Data ; Molecular Weight ; Muscles/chemistry/*metabolism ; Myotonic Dystrophy/*genetics/metabolism ; Myotonin-Protein Kinase ; Polymerase Chain Reaction ; Protein Kinases/biosynthesis/chemistry/*genetics ; *Protein-Serine-Threonine Kinases ; RNA, Messenger/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 1996-04-12
    Description: Werner's syndrome (WS) is an inherited disease with clinical symptoms resembling premature aging. Early susceptibility to a number of major age-related diseases is a key feature of this disorder. The gene responsible for WS (known as WRN) was identified by positional cloning. The predicted protein is 1432 amino acids in length and shows significant similarity to DNA helicases. Four mutations in WS patients were identified. Two of the mutations are splice-junction mutations, with the predicted result being the exclusion of exons from the final messenger RNA. One of the these mutations, which results in a frameshift and a predicted truncated protein, was found in the homozygous state in 60 percent of Japanese WS patients examined. The other two mutations are nonsense mutations. The identification of a mutated putative helicase as the gene product of the WS gene suggests that defective DNA metabolism is involved in the complex process of aging in WS patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, C E -- Oshima, J -- Fu, Y H -- Wijsman, E M -- Hisama, F -- Alisch, R -- Matthews, S -- Nakura, J -- Miki, T -- Ouais, S -- Martin, G M -- Mulligan, J -- Schellenberg, G D -- P01 AG01751/AG/NIA NIH HHS/ -- R01 AG12019/AG/NIA NIH HHS/ -- T32 AG00057/AG/NIA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Apr 12;272(5259):258-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle Division, WA 98108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602509" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics ; Amino Acid Sequence ; Base Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 8/*genetics ; *Cloning, Molecular ; Codon, Terminator ; DNA/metabolism ; DNA Helicases/chemistry/*genetics ; DNA, Complementary/genetics ; Disease Susceptibility ; Exodeoxyribonucleases ; Exons/genetics ; Female ; Frameshift Mutation ; Heterozygote ; Homozygote ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neoplasms/etiology/genetics ; RecQ Helicases ; Sequence Alignment ; Werner Syndrome/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Molecular microbiology 15 (1995), S. 0 
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The expression of the structural genes nit-3 and nit-6, which encode the nitrate assimilatory enzymes nitrate reductase and nitrite reductase, respectively, is highly regulated by the global-acting NIT2 regulatory protein. These structural genes are also controlled by nitrogen catabolite repression and by specific induction via nitrate. A pathway-specific regulatory protein, NIT4, appears to mediate nitrate induction of nit-3 and of nit-6. The NIT4 protein, composed of 1090 amino acids, contains a putative GAL4-like Cys-6 zinc cluster DNA-binding motif, which is joined by a short segment to a stretch of amino acids that appear to constitute a coiled-coil dimerization domain. Chemical crosslinking studies demonstrated that a truncated form of NIT4 forms homodimers. Mobility-shift and DNA-footprinting experiments have identified two NIT4-binding sites of significantly different strengths in the promoter region of the nit-3 gene. The stronger binding site contains a symmetrical octameric sequence, TCCGCGGA, whereas the weaker site has a related sequence. Sequences related to this palindromic element can be found upstream of the nit-6 gene.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 10
    Publication Date: 1990-07-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...