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  • 1
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    Requirement of tissue-selective TBP-associated factor TAFII105 in ovarian development (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-15
    Description: Transcription factor TFIID, composed of TBP and TAFII subunits, is a central component of the RNA polymerase II machinery. Here, we report that the tissue-selective TAFII105 subunit of TFIID is essential for proper development and function of the mouse ovary. Female mice lacking TAFII105 are viable but infertile because of a defect in folliculogenesis correlating with restricted expression of TAFII105 in the granulosa cells of the ovarian follicle. Gene expression profiling has uncovered a defective inhibin-activin signaling pathway in TAFII105-deficient ovaries. Together, these studies suggest that TAFII105 mediates the transcription of a subset of genes required for proper folliculogenesis in the ovary and establishes TAFII105 as a cell type-specific component of the mammalian transcriptional machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freiman, R N -- Albright, S R -- Zheng, S -- Sha, W C -- Hammer, R E -- Tjian, R -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2084-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California at Berkeley, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11557891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Binding Proteins/genetics/*metabolism ; Down-Regulation ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Granulosa Cells/metabolism/*physiology ; In Situ Hybridization ; Infertility, Female ; Male ; Mice ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; Organ Size ; Organ Specificity ; Ovarian Follicle/*growth & development ; Ovary/cytology/growth & development/metabolism/*physiology ; Ovulation ; Protein Subunits ; Signal Transduction ; *TATA-Binding Protein Associated Factors ; Transcription Factor TFIID ; Transcription Factors/genetics/*metabolism ; Transcription Factors, TFII/metabolism ; *Transcription, 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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  • 2
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    Synaptic assembly of the brain in the absence of neurotransmitter secretion (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-05
    Description: Brain function requires precisely orchestrated connectivity between neurons. Establishment of these connections is believed to require signals secreted from outgrowing axons, followed by synapse formation between selected neurons. Deletion of a single protein, Munc18-1, in mice leads to a complete loss of neurotransmitter secretion from synaptic vesicles throughout development. However, this does not prevent normal brain assembly, including formation of layered structures, fiber pathways, and morphologically defined synapses. After assembly is completed, neurons undergo apoptosis, leading to widespread neurodegeneration. Thus, synaptic connectivity does not depend on neurotransmitter secretion, but its maintenance does. Neurotransmitter secretion probably functions to validate already established synaptic connections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verhage, M -- Maia, A S -- Plomp, J J -- Brussaard, A B -- Heeroma, J H -- Vermeer, H -- Toonen, R F -- Hammer, R E -- van den Berg, T K -- Missler, M -- Geuze, H J -- Sudhof, T C -- New York, N.Y. -- Science. 2000 Feb 4;287(5454):864-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neuroscience, Rudolf Magnus Institute, University of Utrecht Medical Centre, Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10657302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Brain/cytology/*embryology/*physiology ; Cell Differentiation ; Cell Division ; Gene Deletion ; Growth Cones/physiology ; Mice ; Mice, Knockout ; Munc18 Proteins ; Nerve Degeneration ; Nerve Tissue Proteins/genetics/*physiology ; Neural Pathways ; Neuromuscular Junction/embryology/physiology ; Neurons/cytology/physiology ; Neurotransmitter Agents/*metabolism ; Patch-Clamp Techniques ; Synapses/*physiology/ultrastructure ; Synaptic Transmission ; Synaptic Vesicles/metabolism/ultrastructure ; *Vesicular Transport Proteins
    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
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    Genetic engineering of livestock (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-16
    Description: Genetic engineering of livestock is expected to have a major effect on the agricultural industry. However, accurate assessment of the consequences of transgene expression is impossible without multigenerational studies. A systematic study of the beneficial and adverse consequences of long-term elevations in the plasma levels of bovine growth hormone (bGH) was conducted on two lines of transgenic pigs. Two successive generations of pigs expressing the bGH gene showed significant improvements in both daily weight gain and feed efficiency and exhibited changes in carcass composition that included a marked reduction in subcutaneous fat. However, long-term elevation of bGH was generally detrimental to health: the pigs had a high incidence of gastric ulcers, arthritis, cardiomegaly, dermatitis, and renal disease. The ability to produce pigs exhibiting only the beneficial, growth-promoting effects of growth hormone by a transgenic approach may require better control of transgene expression, a different genetic background, or a modified husbandry regimen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pursel, V G -- Pinkert, C A -- Miller, K F -- Bolt, D J -- Campbell, R G -- Palmiter, R D -- Brinster, R L -- Hammer, R E -- HD-09172/HD/NICHD NIH HHS/ -- HD-19018/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1281-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Agriculture, Beltsville, MD 20705.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2499927" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; Animals, Domestic/*genetics/growth & development ; *Animals, Genetically Modified ; Body Weight ; Female ; *Genetic Engineering ; Growth Hormone/genetics ; Growth Hormone-Releasing Hormone/genetics ; Insulin-Like Growth Factor I/genetics ; Mice ; Organ Size ; Swine/genetics/growth & development ; *Transfection
    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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    Diet-induced hypercholesterolemia in mice: prevention by overexpression of LDL receptors (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: The current studies were designed to determine whether chronic overexpression of low density lipoprotein (LDL) receptors in the liver would protect mice from the increase in plasma LDL-cholesterol that is induced by high-fat diets. A line of transgenic mice was studied that express the human LDL receptor gene in the liver under control of the transferrin promoter. When fed a diet containing cholesterol, saturated fat, and bile acids for 3 weeks, the transgenic mice, in contrast to normal mice, did not develop a detectable increase in plasma LDL. The current data indicate that unregulated overexpression of LDL receptors can protect against diet-induced hypercholesterolemia in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokode, M -- Hammer, R E -- Ishibashi, S -- Brown, M S -- Goldstein, J L -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1273-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholesterol, Dietary/adverse effects ; Cholesterol, LDL/*blood ; Dietary Fats/*adverse effects ; Exons ; *Gene Expression ; Humans ; Hypercholesterolemia/etiology/*prevention & control ; Introns ; Lipoproteins/blood ; Lipoproteins, HDL/blood ; Lipoproteins, IDL ; Lipoproteins, VLDL/blood ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nucleic Acid Hybridization ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics ; Receptors, LDL/*genetics ; Transferrin/genetics
    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
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    A neuroligin-3 mutation implicated in autism increases inhibitory synaptic transmission in mice (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-08
    Description: Autism spectrum disorders (ASDs) are characterized by impairments in social behaviors that are sometimes coupled to specialized cognitive abilities. A small percentage of ASD patients carry mutations in genes encoding neuroligins, which are postsynaptic cell-adhesion molecules. We introduced one of these mutations into mice: the Arg451--〉Cys451 (R451C) substitution in neuroligin-3. R451C mutant mice showed impaired social interactions but enhanced spatial learning abilities. Unexpectedly, these behavioral changes were accompanied by an increase in inhibitory synaptic transmission with no apparent effect on excitatory synapses. Deletion of neuroligin-3, in contrast, did not cause such changes, indicating that the R451C substitution represents a gain-of-function mutation. These data suggest that increased inhibitory synaptic transmission may contribute to human ASDs and that the R451C knockin mice may be a useful model for studying autism-related behaviors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235367/" 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/PMC3235367/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tabuchi, Katsuhiko -- Blundell, Jacqueline -- Etherton, Mark R -- Hammer, Robert E -- Liu, Xinran -- Powell, Craig M -- Sudhof, Thomas C -- AS1264/Autism Speaks/ -- K08 MH065975/MH/NIMH NIH HHS/ -- K08 MH065975-04/MH/NIMH NIH HHS/ -- K08 MH065975-05/MH/NIMH NIH HHS/ -- R01 MH081164/MH/NIMH NIH HHS/ -- R37 MH52804-08/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2007 Oct 5;318(5847):71-6. Epub 2007 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17823315" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Autistic Disorder/*genetics ; Brain/anatomy & histology/metabolism/*physiology ; Cell Adhesion Molecules, Neuronal ; *Disease Models, Animal ; Female ; Gene Targeting ; Hippocampus/physiology ; Humans ; Male ; Maze Learning ; Membrane Proteins/*genetics/metabolism ; Memory ; Mice ; Mice, Knockout ; *Mutation ; Nerve Tissue Proteins/*genetics/metabolism ; Social Behavior ; Somatosensory Cortex/physiology ; Synapses/*physiology ; *Synaptic Transmission ; Vesicular Glutamate Transport Protein 1/metabolism ; Vesicular Inhibitory Amino Acid Transport Proteins/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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  • 6
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    White fat progenitor cells reside in the adipose vasculature (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: White adipose (fat) tissues regulate metabolism, reproduction, and life span. Adipocytes form throughout life, with the most marked expansion of the lineage occurring during the postnatal period. Adipocytes develop in coordination with the vasculature, but the identity and location of white adipocyte progenitor cells in vivo are unknown. We used genetically marked mice to isolate proliferating and renewing adipogenic progenitors. We found that most adipocytes descend from a pool of these proliferating progenitors that are already committed, either prenatally or early in postnatal life. These progenitors reside in the mural cell compartment of the adipose vasculature, but not in the vasculature of other tissues. Thus, the adipose vasculature appears to function as a progenitor niche and may provide signals for adipocyte development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597101/" 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/PMC2597101/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wei -- Zeve, Daniel -- Suh, Jae Myoung -- Bosnakovski, Darko -- Kyba, Michael -- Hammer, Robert E -- Tallquist, Michelle D -- Graff, Jonathan M -- 1R01DK064261/DK/NIDDK NIH HHS/ -- 1R01DK066556/DK/NIDDK NIH HHS/ -- R01 DK064261/DK/NIDDK NIH HHS/ -- R01 DK064261-01/DK/NIDDK NIH HHS/ -- R01 DK064261-02/DK/NIDDK NIH HHS/ -- R01 DK064261-03/DK/NIDDK NIH HHS/ -- R01 DK064261-04/DK/NIDDK NIH HHS/ -- R01 DK064261-05/DK/NIDDK NIH HHS/ -- R01 DK066556/DK/NIDDK NIH HHS/ -- R01 DK066556-01/DK/NIDDK NIH HHS/ -- R01 DK066556-02/DK/NIDDK NIH HHS/ -- R01 DK066556-03/DK/NIDDK NIH HHS/ -- R01 DK066556-04/DK/NIDDK NIH HHS/ -- R01 DK066556-05/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 24;322(5901):583-6. doi: 10.1126/science.1156232. Epub 2008 Sep 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18801968" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes, White/*cytology/metabolism ; Adipogenesis ; Adipose Tissue/*blood supply/cytology ; Animals ; Antigens, CD/metabolism ; Blood Vessels/*cytology ; Cell Lineage ; Cell Proliferation ; Cell Separation ; Cells, Cultured ; Doxycycline/pharmacology ; Gene Expression Profiling ; Mice ; Mice, Transgenic ; Multipotent Stem Cells/*cytology/metabolism ; PPAR gamma/genetics/metabolism ; Stromal Cells/*cytology/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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  • 7
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    Conformational switch of syntaxin-1 controls synaptic vesicle fusion (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: During synaptic vesicle fusion, the soluble N-ethylmaleimide-sensitive factor-attachment protein receptor (SNARE) protein syntaxin-1 exhibits two conformations that both bind to Munc18-1: a "closed" conformation outside the SNARE complex and an "open" conformation in the SNARE complex. Although SNARE complexes containing open syntaxin-1 and Munc18-1 are essential for exocytosis, the function of closed syntaxin-1 is unknown. We generated knockin/knockout mice that expressed only open syntaxin-1B. Syntaxin-1B(Open) mice were viable but succumbed to generalized seizures at 2 to 3 months of age. Binding of Munc18-1 to syntaxin-1 was impaired in syntaxin-1B(Open) synapses, and the size of the readily releasable vesicle pool was decreased; however, the rate of synaptic vesicle fusion was dramatically enhanced. Thus, the closed conformation of syntaxin-1 gates the initiation of the synaptic vesicle fusion reaction, which is then mediated by SNARE-complex/Munc18-1 assemblies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235364/" 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/PMC3235364/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerber, Stefan H -- Rah, Jong-Cheol -- Min, Sang-Won -- Liu, Xinran -- de Wit, Heidi -- Dulubova, Irina -- Meyer, Alexander C -- Rizo, Josep -- Arancillo, Marife -- Hammer, Robert E -- Verhage, Matthijs -- Rosenmund, Christian -- Sudhof, Thomas C -- NS051262/NS/NINDS NIH HHS/ -- NS37200/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1507-10. doi: 10.1126/science.1163174. Epub 2008 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703708" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Epilepsy/etiology ; Excitatory Postsynaptic Potentials ; Membrane Fusion ; Mice ; Mice, Knockout ; Munc18 Proteins/metabolism ; Mutation ; Protein Conformation ; Protein Structure, Tertiary ; SNARE Proteins/metabolism ; Sucrose/metabolism ; Synapses/physiology ; Synaptic Vesicles/*physiology/ultrastructure ; Syntaxin 1/*chemistry/genetics/*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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  • 8
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    Metallothionein-human GH fusion genes stimulate growth of mice (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-11-18
    Description: The promoter or regulatory region of the mouse gene for metallothionein-I was fused to the structural gene coding for human growth hormone. These fusion genes were introduced into mice by microinjection of fertilized eggs. Twenty-three (70 percent) of the mice that stably incorporated the fusion genes showed high concentrations of human growth hormone in their serum and grew significantly larger than control mice. Synthesis of human growth hormone was induced further by cadmium or zinc, which normally induce metallothionein gene expression. Transgenic mice that expressed human growth hormone also showed increased concentrations of insulin-like growth factor I in their serum. Histology of their pituitaries suggests dysfunction of the cells that normally synthesize growth hormone. The fusion genes were expressed in all tissues examined, but the ratio of human growth hormone messenger RNA to endogenous metallothionein-I messenger RNA varied among different tissues and different animals, suggesting that expression of the foreign genes is influenced by site of integration and tissue environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palmiter, R D -- Norstedt, G -- Gelinas, R E -- Hammer, R E -- Brinster, R L -- HD-07155/HD/NICHD NIH HHS/ -- HD-09172/HD/NICHD NIH HHS/ -- HD-17321/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Nov 18;222(4625):809-14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6356363" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadmium/pharmacology ; DNA, Recombinant ; Gene Expression Regulation/drug effects ; Genetic Engineering ; Growth Hormone/*genetics ; Metallothionein/*genetics ; Mice/*growth & development ; Operon ; RNA, Messenger/genetics ; Tissue Distribution ; Transcription, Genetic ; Zinc/pharmacology
    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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  • 9
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    Gonadotroph-specific expression of metallothionein fusion genes in pituitaries of transgenic mice (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-28
    Description: Transgenic mice expressing a metallothionein-somatostatin fusion gene contain high concentrations of somatostatin in the anterior pituitary gland, a tissue that does not normally produce somatostatin. Immunoreactive somatostatin within the anterior pituitaries was found exclusively within gonadotrophs. Similarly, a metallothionein-human growth-hormone fusion gene was also expressed selectively in gonadotrophs. It is proposed that sequences common to the two fusion genes are responsible for the gonadotroph-specific expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Low, M J -- Lechan, R M -- Hammer, R E -- Brinster, R L -- Habener, J F -- Mandel, G -- Goodman, R H -- AM 01313/AM/NIADDK NIH HHS/ -- AM 30457/AM/NIADDK NIH HHS/ -- AM 31400/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):1002-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2868526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Recombinant/metabolism ; Genes ; Genetic Engineering ; Humans ; Immunoenzyme Techniques ; Luteinizing Hormone/metabolism ; Metallothionein/*genetics ; Mice ; Pituitary Gland, Anterior/*metabolism ; Rats ; Somatostatin/*genetics/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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  • 10
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    Pancreatic neoplasia induced by SV40 T-antigen expression in acinar cells of transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-09
    Description: Three lines of transgenic mice were produced that develop pancreatic neoplasms as a consequence of expression of an elastase I-SV40 T-antigen fusion gene in the acinar cells. A developmental analysis suggests at least a two-stage process in the ontogeny of this disease. The first stage is a T antigen-induced, preneoplastic state characterized by a progression from hyperplasia to dysplasia of the exocrine pancreas, by an increased percentage of tetraploid cells, and by an arrest in acinar cell differentiation. The second stage is characterized by the formation of tumor nodules that appear to be monoclonal, because they have discrete aneuploid DNA contents. The cells within the nodules as compared to normal pancreatic tissue have less total RNA by a factor of 5, less pancreas-specific messenger RNA by a factor of about 50, and increased levels of T-antigen messenger RNA. A tumor cell line has been derived that retains both pancreatic and neoplastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ornitz, D M -- Hammer, R E -- Messing, A -- Palmiter, R D -- Brinster, R L -- GM-07266/GM/NIGMS NIH HHS/ -- HD-09172/HD/NICHD NIH HHS/ -- NS-00956/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):188-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratory, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821617" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/*genetics ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Genes ; Genes, Viral ; Mice ; Mice, Transgenic ; Pancreatic Elastase/genetics ; Pancreatic Neoplasms/genetics/*microbiology/pathology ; Protein Kinases/*genetics ; RNA, Messenger/genetics ; Simian virus 40/*genetics
    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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