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  • Animals  (6)
  • *Genes, Homeobox  (1)
  • American Association for the Advancement of Science (AAAS)  (6)
  • 1
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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
    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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  • 2
    Publication Date: 2002-07-20
    Description: The mammalian protein MBD4 contains a methyl-CpG binding domain and can enzymatically remove thymine (T) or uracil (U) from a mismatched CpG site in vitro. These properties suggest that MBD4 might function in vivo to minimize the mutability of 5-methylcytosine by removing its deamination product from DNA. We tested this hypothesis by analyzing Mbd4-/- mice and found that the frequency of of C --〉 T transitions at CpG sites was increased by a factor of three. On a cancer-susceptible Apc(Min/+) background, Mbd4-/- mice showed accelerated tumor formation with CpG --〉 TpG mutations in the Apc gene. Thus MBD4 suppresses CpG mutability and tumorigenesis in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millar, Catherine B -- Guy, Jacky -- Sansom, Owen J -- Selfridge, Jim -- MacDougall, Eilidh -- Hendrich, Brian -- Keightley, Peter D -- Bishop, Stefan M -- Clarke, Alan R -- Bird, Adrian -- New York, N.Y. -- Science. 2002 Jul 19;297(5580):403-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Cell Biology, The King's Buildings, Edinburgh University, Edinburgh EH9 3JR, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12130785" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Alleles ; Amino Acid Sequence ; Animals ; Base Pair Mismatch ; Cytosine/*analogs & derivatives/metabolism ; DNA Methylation ; DNA Repair ; Deamination ; Dinucleoside Phosphates/*genetics ; Endodeoxyribonucleases/*genetics/*physiology ; Female ; Gene Targeting ; Genes, APC ; Genetic Predisposition to Disease ; Intestinal Neoplasms/etiology/*genetics ; Intestine, Large ; Loss of Heterozygosity ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Point Mutation ; Suppression, Genetic
    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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  • 3
    Publication Date: 2002-07-06
    Description: Pharmacological inactivation of oncogenes is being investigated as a possible therapeutic strategy for cancer. One potential drawback is that cessation of such therapy may allow reactivation of the oncogene and tumor regrowth. We used a conditional transgenic mouse model for MYC-induced tumorigenesis to demonstrate that brief inactivation of MYC results in the sustained regression of tumors and the differentiation of osteogenic sarcoma cells into mature osteocytes. Subsequent reactivation of MYC did not restore the cells' malignant properties but instead induced apoptosis. Thus, brief MYC inactivation appears to cause epigenetic changes in tumor cells that render them insensitive to MYC-induced tumorigenesis. These results raise the possibility that transient inactivation of MYC may be an effective therapy for certain cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jain, Meenakshi -- Arvanitis, Constadina -- Chu, Kenneth -- Dewey, William -- Leonhardt, Edith -- Trinh, Maxine -- Sundberg, Christopher D -- Bishop, J Michael -- Felsher, Dean W -- K08-CA75967-01/CA/NCI NIH HHS/ -- R01-CA85610/CA/NCI NIH HHS/ -- R01-CA89305-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):102-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305-5151, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/administration & dosage/therapeutic use ; Apoptosis ; Cell Differentiation ; Cell Division ; Doxycycline/pharmacology ; Gene Expression/drug effects ; *Gene Silencing ; *Genes, myc ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Osteocytes/cytology ; Osteosarcoma/drug therapy/*genetics/*pathology ; Phenotype ; Transgenes ; Tumor Cells, Cultured
    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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  • 4
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-06-04
    Description: Homologous recombination was used to introduce a nominally transforming mutation into an endogenous H-ras1 gene in Rat1 fibroblasts. Although both the mutant and the remaining normal allele were expressed equally, the heterozygous cells were not neoplastically transformed. Instead, spontaneously transformed cells arose from the heterozygotes at a low frequency, and the majority of these cells had amplified the mutant allele. Thus, the activated H-ras1 allele was not by itself dominant over the normal allele but predisposed cells to transformation by independent events, such as amplification of the mutant allele.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finney, R E -- Bishop, J M -- CA 44338/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1524-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉George Williams Hooper Foundation, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8502998" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Cell Division/genetics ; Cell Line ; Cell Line, Transformed ; Cell Transformation, Neoplastic/*genetics ; Genes, ras/*genetics ; Mice ; Mice, Nude ; Molecular Sequence Data ; Neoplasm Transplantation ; Point Mutation ; Rats ; Recombination, Genetic
    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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  • 5
    Publication Date: 2015-01-17
    Description: The physiological and biomechanical requirements of flight at high altitude have been the subject of much interest. Here, we uncover a steep relation between heart rate and wingbeat frequency (raised to the exponent 3.5) and estimated metabolic power and wingbeat frequency (exponent 7) of migratory bar-headed geese. Flight costs increase more rapidly than anticipated as air density declines, which overturns prevailing expectations that this species should maintain high-altitude flight when traversing the Himalayas. Instead, a "roller coaster" strategy, of tracking the underlying terrain and discarding large altitude gains only to recoup them later in the flight with occasional benefits from orographic lift, is shown to be energetically advantageous for flights over the Himalayas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, C M -- Spivey, R J -- Hawkes, L A -- Batbayar, N -- Chua, B -- Frappell, P B -- Milsom, W K -- Natsagdorj, T -- Newman, S H -- Scott, G R -- Takekawa, J Y -- Wikelski, M -- Butler, P J -- BB/FO15615/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):250-4. doi: 10.1126/science.1258732.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, Bangor University, Bangor, Gwynedd, UK. ; School of Biological Sciences, Bangor University, Bangor, Gwynedd, UK. c.bishop@bangor.ac.uk l.hawkes@exeter.ac.uk. ; Wildlife Science and Conservation Center of Mongolia, Ulaanbataar, Mongolia. ; Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada. ; Office of the Dean of Graduate Research, University of Tasmania, Tasmania, Australia. ; Mongolian Academy of Sciences, Ulaanbataar, Mongolia. ; Emergency Prevention System(EMPRES) Wildlife and Ecology Unit, Food and Agriculture Organization of the United Nations (FAO), Rome, Italy. ; Department of Biology, McMaster University, Ontario, Ontario, Canada. ; San Francisco Bay Estuary Field Station, Western Ecological Research Center, U.S. Geological Survey, Vallejo, CA 94592 USA. ; Max Planck Institut fur Ornithologie, Radolfzell, Germany. Department of Biology, University of Konstanz, Konstanz, Germany. ; School of Biosciences, University of Birmingham, Birmingham, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25593180" target="_blank"〉PubMed〈/a〉
    Keywords: *Altitude ; *Animal Migration ; Animals ; Biomechanical Phenomena ; Body Temperature ; Body Weight ; *Energy Metabolism ; Flight, Animal/*physiology ; Geese/*physiology ; Heart Rate ; Tibet ; Wings, Animal/*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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  • 6
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-01-16
    Description: The search for genetic damage in neoplastic cells now occupies a central place in cancer research. Diverse examples of such damage are in hand, and they in turn hint at biochemical explanations for neoplastic growth. The way may be open to solve the riddles of how normal cells govern their replication and why cancer cells do not.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, J M -- CA12705/CA/NCI NIH HHS/ -- SO7 RR05355/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):305-11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3541204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Chromosome Deletion ; DNA Damage ; DNA, Neoplasm/genetics ; Gene Amplification ; Humans ; Mutation ; Neoplasms/*genetics/pathology ; *Oncogenes ; *Proto-Oncogenes ; Retroviridae/genetics ; Translocation, Genetic
    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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