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Cloning of a transcriptionally active human TATA binding factor (1990)

C. C. Kao ; P. M. Lieberman ; M. C. Schmidt ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 248(4963): 1646-50.

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Publication Date: 1990-06-29

Description: Transcription factor IID (TFIID) binds to the TATA box promoter element and regulates the expression of most eukaryotic genes transcribed by RNA polymerase II. Complementary DNA (cDNA) encoding a human TFIID protein has been cloned. The human TFIID polypeptide has 339 amino acids and a molecular size of 37,745 daltons. The carboxyl-terminal 181 amino acids of the human TFIID protein shares 80% identity with the TFIID protein from Saccharomyces cerevisiae. The amino terminus contains an unusual repeat of 38 consecutive glutamine residues and an X-Thr-Pro repeat. Expression of DNA in reticulocyte lysates or in Escherichia coli yielded a protein that was competent for both DNA binding and transcription activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kao, C C -- Lieberman, P M -- Schmidt, M C -- Zhou, Q -- Pei, R -- Berk, A J -- CA25235/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1646-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Molecular Biology Institute, University of California, Los Angeles 90024-1570.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2194289" target="_blank"〉PubMed〈/a〉

Keywords: Amino Acid Sequence ; Cloning, Molecular ; Escherichia coli/genetics ; Gene Expression ; HeLa Cells/metabolism ; Humans ; Molecular Sequence Data ; *Promoter Regions, Genetic ; Recombinant Proteins/metabolism ; Reticulocytes/metabolism ; Saccharomyces cerevisiae/*genetics ; Sequence Homology, Nucleic Acid ; Transcription Factor TFIID ; Transcription Factors/*genetics/metabolism ; *Transcription, Genetic

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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Rapid identification of subtype-selective agonists of the somatostatin receptor through combinatorial chemistry (1998)

S. P. Rohrer ; E. T. Birzin ; R. T. Mosley ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 282(5389): 737-40.

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Publication Date: 1998-10-23

Description: Nonpeptide agonists of each of the five somatostatin receptors were identified in combinatorial libraries constructed on the basis of molecular modeling of known peptide agonists. In vitro experiments using these selective compounds demonstrated the role of the somatostatin subtype-2 receptor in inhibition of glucagon release from mouse pancreatic alpha cells and the somatostatin subtype-5 receptor as a mediator of insulin secretion from pancreatic beta cells. Both receptors regulated growth hormone release from the rat anterior pituitary gland. The availability of high-affinity, subtype-selective agonists for each of the somatostatin receptors provides a direct approach to defining their physiological functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohrer, S P -- Birzin, E T -- Mosley, R T -- Berk, S C -- Hutchins, S M -- Shen, D M -- Xiong, Y -- Hayes, E C -- Parmar, R M -- Foor, F -- Mitra, S W -- Degrado, S J -- Shu, M -- Klopp, J M -- Cai, S J -- Blake, A -- Chan, W W -- Pasternak, A -- Yang, L -- Patchett, A A -- Smith, R G -- Chapman, K T -- Schaeffer, J M -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biochemistry and Physiology, Merck Research Laboratories, Post Office Box 2000, Rahway, NJ 07065, USA. susanvrohrer@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784130" target="_blank"〉PubMed〈/a〉

Keywords: Amides/metabolism/*pharmacology ; Amino Acid Sequence ; Animals ; Cell Line ; Cells, Cultured ; Cricetinae ; Drug Design ; Glucagon/secretion ; Growth Hormone/secretion ; Insulin/secretion ; Islets of Langerhans/drug effects/secretion ; Ligands ; Membrane Proteins ; Mice ; Models, Chemical ; Molecular Sequence Data ; Pituitary Gland, Anterior/drug effects/metabolism ; Rats ; Receptors, Somatostatin/*agonists/physiology

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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Transcription control by E1A and MAP kinase pathway via Sur2 mediator subunit (2002)

J. L. Stevens ; G. T. Cantin ; G. Wang ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 296(5568): 755-8. doi: 10.1126/science.1068943.

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Publication Date: 2002-04-06

Description: Sur2 is a metazoan Mediator subunit that interacts with the adenovirus E1A protein and functions in a mitogen-activated protein kinase pathway required for vulva development in Caenorhabditis elegans. We generated sur2-/- embryonic stem cells to analyze its function as a mammalian Mediator component. Our results show that Sur2 forms a subcomplex of the Mediator with two other subunits, TRAP/Med100 and 95. Knock-out of Sur2 prevents activation by E1A-CR3 and the mitogen-activated protein kinase-regulated ETS transcription factor Elk-1, but not by multiple other transcription factors. These results imply that specific activation domains stimulate transcription by binding to distinct Mediator subunits. Activation by E1A and Elk-1 requires recruitment of Mediator to a promoter by binding to its Sur2 subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, Jennitte L -- Cantin, Greg T -- Wang, Gang -- Shevchenko, Andrej -- Shevchenko, Anna -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- GM07185/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):755-8. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, 611 Charles Young Drive East, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934987" target="_blank"〉PubMed〈/a〉

Keywords: Adenovirus E1A Proteins/*metabolism ; Adenoviruses, Human/physiology ; Animals ; Carrier Proteins/genetics/*metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; Genes, Immediate-Early ; HeLa Cells ; Humans ; *MAP Kinase Signaling System ; Mediator Complex ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/metabolism ; Stem Cells/*metabolism ; *Trans-Activators ; Transcription Factors/metabolism ; *Transcription, Genetic ; *Transcriptional Activation ; Transfection ; ets-Domain Protein Elk-1

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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Apolipoprotein E controls cerebrovascular integrity via cyclophilin A (2012)

R. D. Bell ; E. A. Winkler ; I. Singh ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 485(7399): 512-6. doi: 10.1038/nature11087.

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Publication Date: 2012-05-25

Description: Human apolipoprotein E has three isoforms: APOE2, APOE3 and APOE4. APOE4 is a major genetic risk factor for Alzheimer's disease and is associated with Down's syndrome dementia and poor neurological outcome after traumatic brain injury and haemorrhage. Neurovascular dysfunction is present in normal APOE4 carriers and individuals with APOE4-associated disorders. In mice, lack of Apoe leads to blood-brain barrier (BBB) breakdown, whereas APOE4 increases BBB susceptibility to injury. How APOE genotype affects brain microcirculation remains elusive. Using different APOE transgenic mice, including mice with ablation and/or inhibition of cyclophilin A (CypA), here we show that expression of APOE4 and lack of murine Apoe, but not APOE2 and APOE3, leads to BBB breakdown by activating a proinflammatory CypA-nuclear factor-kappaB-matrix-metalloproteinase-9 pathway in pericytes. This, in turn, leads to neuronal uptake of multiple blood-derived neurotoxic proteins, and microvascular and cerebral blood flow reductions. We show that the vascular defects in Apoe-deficient and APOE4-expressing mice precede neuronal dysfunction and can initiate neurodegenerative changes. Astrocyte-secreted APOE3, but not APOE4, suppressed the CypA-nuclear factor-kappaB-matrix-metalloproteinase-9 pathway in pericytes through a lipoprotein receptor. Our data suggest that CypA is a key target for treating APOE4-mediated neurovascular injury and the resulting neuronal dysfunction and degeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047116/" 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/PMC4047116/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, Robert D -- Winkler, Ethan A -- Singh, Itender -- Sagare, Abhay P -- Deane, Rashid -- Wu, Zhenhua -- Holtzman, David M -- Betsholtz, Christer -- Armulik, Annika -- Sallstrom, Jan -- Berk, Bradford C -- Zlokovic, Berislav V -- R01 AG039452/AG/NIA NIH HHS/ -- R01 NS034467/NS/NINDS NIH HHS/ -- R01AG039452/AG/NIA NIH HHS/ -- R37 AG013956/AG/NIA NIH HHS/ -- R37 AG023084/AG/NIA NIH HHS/ -- R37 NS034467/NS/NINDS NIH HHS/ -- R37AG13956/AG/NIA NIH HHS/ -- R37AG23084/AG/NIA NIH HHS/ -- R37NS34467/NS/NINDS NIH HHS/ -- England -- Nature. 2012 May 16;485(7399):512-6. doi: 10.1038/nature11087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, New York 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22622580" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Apolipoprotein E2/deficiency/genetics/metabolism ; Apolipoprotein E3/deficiency/genetics/metabolism ; Apolipoprotein E4/deficiency/genetics/metabolism ; Apolipoproteins E/deficiency/genetics/*metabolism ; Blood-Brain Barrier/drug effects/*physiology/physiopathology ; Cerebrovascular Circulation/*physiology ; Cyclophilin A/antagonists & inhibitors/deficiency/*metabolism ; Hippocampus/metabolism/pathology ; Humans ; Matrix Metalloproteinase 9/metabolism ; Mice ; Mice, Transgenic ; Microcirculation ; NF-kappa B/metabolism ; Neurodegenerative Diseases/metabolism/pathology ; Neurons/metabolism/pathology ; Pericytes/metabolism

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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5

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Mismatch repair deficiency in phenotypically normal human cells (1995)

R. Parsons ; G. M. Li ; M. Longley ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 268(5211): 738-40.

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Publication Date: 1995-05-05

Description: Tumor cells in patients with hereditary nonpolyposis colorectal cancer (HNPCC) are characterized by a genetic hypermutability caused by defects in DNA mismatch repair. A subset of HNPCC patients was found to have widespread mutations not only in their tumors, but also in their non-neoplastic cells. Although these patients had numerous mutations in all tissues examined, they had very few tumors. The hypermutability was associated with a profound defect in mismatch repair at the biochemical level. These results have implications for the relation between mutagenesis and carcinogenesis, and they suggest that mismatch repair deficiency is compatible with normal human development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, R -- Li, G M -- Longley, M -- Modrich, P -- Liu, B -- Berk, T -- Hamilton, S R -- Kinzler, K W -- Vogelstein, B -- CA35494/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM45190/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 May 5;268(5211):738-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7632227" target="_blank"〉PubMed〈/a〉

Keywords: Base Sequence ; Cell Line, Transformed ; Clone Cells ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics ; DNA Repair/*genetics ; DNA, Satellite/analysis ; Humans ; Intestinal Mucosa/chemistry ; Lymphocytes/chemistry ; Molecular Sequence Data ; Mutation ; Phenotype ; 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

Published by American Association for the Advancement of Science (AAAS)

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6

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Transcription of class III genes activated by viral immediate early proteins (1985)

R. B. Gaynor ; L. T. Feldman ; A. J. Berk

American Association for the Advancement of Science (AAAS)

In: Science. 230(4724): 447-50.

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Publication Date: 1985-10-25

Description: The adenovirus EIA and pseudorabies virus immediate early (IE) proteins induce transcription from transfected viral and nonviral genes transcribed by RNA polymerase II (class II genes). These proteins have now been shown also to activate transcription of transfected genes transcribed by RNA polymerase III (class III genes). As previously observed for class II genes, this stimulation of class III gene transcription was much greater for transfected genes than for the major endogenous cellular class III genes. Extracts made from cell lines stably expressing a transfected pseudorabies virus IE gene were 10 to 20 times more active in the in vitro transcription of exogenously added class III genes than extracts of the parental cell line. These results indicate that the E1A and IE proteins stimulate the expression of class III genes by a mechanism similar to the mechanism for stimulation of class II gene transcription by these proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gaynor, R B -- Feldman, L T -- Berk, A J -- CA 25235/CA/NCI NIH HHS/ -- CA 30981/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):447-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996135" target="_blank"〉PubMed〈/a〉

Keywords: Adenoviridae/genetics ; Animals ; Drosophila/genetics ; *Genes, Viral ; HeLa Cells ; Herpesvirus 1, Suid/genetics ; Humans ; RNA, Transfer/genetics ; Rabbits ; Rats ; *Transcription, Genetic ; Viral Proteins/*genetics

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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7

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Vasoconstriction: a new activity for platelet-derived growth factor (1986)

B. C. Berk ; R. W. Alexander ; T. A. Brock ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 232(4746): 87-90.

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Publication Date: 1986-04-04

Description: Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells that has been implicated in the pathogenesis of atherosclerosis. The potential role of PDGF in the altered vasoreactivity of atherosclerotic vessels has been studied through an examination of its effects on contractility in the rat aorta. PDGF caused a concentration-dependent contraction of aortic strips and was significantly more potent on a molar basis than the classic vasoconstrictor peptide angiotensin II. Furthermore, PDGF increased the cytosolic free calcium concentration in cultured rat aortic smooth muscle cells. These observations suggest a new biological activity for PDGF that may contribute to the enhanced vasoreactivity of certain atherosclerotic vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berk, B C -- Alexander, R W -- Brock, T A -- Gimbrone, M A Jr -- Webb, R C -- HL20054/HL/NHLBI NIH HHS/ -- HL22602/HL/NHLBI NIH HHS/ -- HL35013/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):87-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3485309" target="_blank"〉PubMed〈/a〉

Keywords: Aminoquinolines ; Angiotensin II/pharmacology ; Animals ; Aorta/*drug effects/metabolism/physiology ; Calcium/metabolism ; Cytosol/metabolism ; Dose-Response Relationship, Drug ; Epidermal Growth Factor/pharmacology ; Fluorescent Dyes ; Homeostasis/drug effects ; Humans ; In Vitro Techniques ; Kinetics ; Platelet-Derived Growth Factor/*pharmacology ; Rats ; Vasoconstriction/*drug effects

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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