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  • 11
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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
    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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    A role for thrombin receptor signaling in endothelial cells during embryonic development (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-05
    Description: The coagulation protease thrombin triggers fibrin formation, platelet activation, and other cellular responses at sites of tissue injury. We report a role for PAR1, a protease-activated G protein-coupled receptor for thrombin, in embryonic development. Approximately half of Par1-/- mouse embryos died at midgestation with bleeding from multiple sites. PAR1 is expressed in endothelial cells, and a PAR1 transgene driven by an endothelial-specific promoter prevented death of Par1-/- embryos. Our results suggest that the coagulation cascade and PAR1 modulate endothelial cell function in developing blood vessels and that thrombin's actions on endothelial cells-rather than on platelets, mesenchymal cells, or fibrinogen-contribute to vascular development and hemostasis in the mouse embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, C T -- Srinivasan, Y -- Zheng, Y W -- Huang, W -- Coughlin, S R -- HL44907/HL/NHLBI NIH HHS/ -- HL65590/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2001 Aug 31;293(5535):1666-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Institute, University of California at San Francisco (UCSF), San Francisco, California 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11533492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Coagulation ; Blood Coagulation Factors/physiology ; Blood Vessels/*embryology/metabolism ; Calcium/metabolism ; Crosses, Genetic ; *Embryonic and Fetal Development ; Endocardium/embryology/metabolism ; Endothelium, Vascular/cytology/*embryology/metabolism ; Factor V/genetics/physiology ; Female ; Fibrinogen/genetics/physiology ; Fibroblasts/metabolism ; Hemorrhage/embryology ; Hemostasis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Transgenic ; *Neovascularization, Physiologic ; Phenotype ; Prothrombin/genetics/physiology ; Receptor, PAR-1 ; Receptors, Thrombin/deficiency/genetics/*physiology ; *Signal Transduction ; Thrombin/physiology ; Thromboplastin/genetics/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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  • 13
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    A p53 amino-terminal nuclear export signal inhibited by DNA damage-induced phosphorylation (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-09
    Description: The p53 protein is present in low amounts in normally growing cells and is activated in response to physiological insults. MDM2 regulates p53 either through inhibiting p53's transactivating function in the nucleus or by targeting p53 degradation in the cytoplasm. We identified a previously unknown nuclear export signal (NES) in the amino terminus of p53, spanning residues 11 to 27 and containing two serine residues phosphorylated after DNA damage, which was required for p53 nuclear export in colloboration with the carboxyl-terminal NES. Serine-15-phosphorylated p53 induced by ultraviolet irradiation was not exported. Thus, DNA damage-induced phosphorylation may achieve optimal p53 activation by inhibiting both MDM2 binding to, and the nuclear export of, p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Y -- Xiong, Y -- CA65572/CA/NCI NIH HHS/ -- K01 CA087580/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Jun 8;292(5523):1910-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, Department of Biochemistry and Biophysics, and Program in Molecular Biology and Biotechnology, University of North Carolina at Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11397945" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Amino Acid Sequence ; Animals ; Cell Fusion ; Cell Line ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cytoplasm/metabolism ; *DNA Damage ; Mice ; Molecular Sequence Data ; Mutation ; *Nuclear Proteins ; Phosphorylation ; Phosphoserine/metabolism ; *Protein Sorting Signals ; Protein Structure, Tertiary ; Proteins/genetics/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2 ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p14ARF ; Tumor Suppressor Protein p53/*chemistry/genetics/*metabolism ; Ubiquitins/metabolism ; Ultraviolet Rays
    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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    Positive regulation of T cell activation and integrin adhesion by the adapter Fyb/Slap (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-22
    Description: The molecular adapter Fyb/Slap regulates signaling downstream of the T cell receptor (TCR), but whether it plays a positive or negative role is controversial. We demonstrate that Fyb/Slap-deficient T cells exhibit defective proliferation and cytokine production in response to TCR stimulation. Fyb/Slap is also required in vivo for T cell-dependent immune responses. Functionally, Fyb/Slap has no apparent role in the activation of known TCR signaling pathways, F-actin polymerization, or TCR clustering. Rather, Fyb/Slap regulates TCR-induced integrin clustering and adhesion. Thus, Fyb/Slap is the first molecular adapter to be identified that couples TCR stimulation to the avidity modulation of integrins governing T cell adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffiths, E K -- Krawczyk, C -- Kong, Y Y -- Raab, M -- Hyduk, S J -- Bouchard, D -- Chan, V S -- Kozieradzki, I -- Oliveira-Dos-Santos, A J -- Wakeham, A -- Ohashi, P S -- Cybulsky, M I -- Rudd, C E -- Penninger, J M -- New York, N.Y. -- Science. 2001 Sep 21;293(5538):2260-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11567140" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD/metabolism ; Antigens, CD3/metabolism ; Antigens, Differentiation, T-Lymphocyte/metabolism ; B-Lymphocytes/immunology ; Carrier Proteins/genetics/*physiology ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Chimera ; Gene Targeting ; Humans ; Immunization ; Immunoglobulin G/biosynthesis ; Integrins/*metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis/pharmacology ; Lectins, C-Type ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Mice ; Phosphoproteins/genetics/*physiology ; Receptors, Antigen, T-Cell/immunology/metabolism ; Receptors, Interleukin-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/metabolism/*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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  • 15
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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
    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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    Asef, a link between the tumor suppressor APC and G-protein signaling (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-19
    Description: The adenomatous polyposis coli gene (APC) is mutated in familial adenomatous polyposis and in sporadic colorectal tumors. Here the APC gene product is shown to bind through its armadillo repeat domain to a Rac-specific guanine nucleotide exchange factor (GEF), termed Asef. Endogenous APC colocalized with Asef in mouse colon epithelial cells and neuronal cells. Furthermore, APC enhanced the GEF activity of Asef and stimulated Asef-mediated cell flattening, membrane ruffling, and lamellipodia formation in MDCK cells. These results suggest that the APC-Asef complex may regulate the actin cytoskeletal network, cell morphology and migration, and neuronal function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawasaki, Y -- Senda, T -- Ishidate, T -- Koyama, R -- Morishita, T -- Iwayama, Y -- Higuchi, O -- Akiyama, T -- New York, N.Y. -- Science. 2000 Aug 18;289(5482):1194-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Genetic Information, Institute for Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10947987" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Brain/metabolism ; Cell Line ; Cell Membrane/ultrastructure ; Cell Size ; Colon/cytology/metabolism ; Cytoplasm/metabolism ; Cytoskeletal Proteins/*metabolism ; Guanine Nucleotide Exchange Factors/chemistry/genetics/*metabolism ; Guanosine Diphosphate/metabolism ; Humans ; Immunoblotting ; Intestinal Mucosa/cytology/metabolism ; Mice ; Molecular Sequence Data ; Neurons/metabolism ; Precipitin Tests ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Recombinant Fusion Proteins/metabolism ; Rho Guanine Nucleotide Exchange Factors ; Signal Transduction ; *Trans-Activators ; Transfection ; Two-Hybrid System Techniques ; beta Catenin ; rac GTP-Binding 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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  • 17
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    Requirement of DNase II for definitive erythropoiesis in the mouse fetal liver (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-26
    Description: Mature erythrocytes in mammals have no nuclei, although they differentiate from nucleated precursor cells. The mechanism by which enucleation occurs is not well understood. Here we show that deoxyribonuclease II (DNase II) is indispensable for definitive erythropoiesis in mouse fetal liver. No live DNase II-null mice were born, owing to severe anemia. When mutant fetal liver cells were transferred into lethally irradiated wild-type mice, mature red blood cells were generated from the mutant cells, suggesting that DNase II functions in a non-cell-autonomous manner. Histochemical analyses indicated that the critical cellular sources of DNase II are macrophages present at the site of definitive erythropoiesis in the fetal liver. Thus, DNase II in macrophages appears to be responsible for destroying the nuclear DNA expelled from erythroid precursor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawane, K -- Fukuyama, H -- Kondoh, G -- Takeda, J -- Ohsawa, Y -- Uchiyama, Y -- Nagata, S -- New York, N.Y. -- Science. 2001 May 25;292(5521):1546-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Osaka University Medical School, and Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11375492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Differentiation ; Cell Transplantation ; DNA/analysis/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Endodeoxyribonucleases/genetics/*metabolism ; Erythroblasts/cytology/metabolism ; Erythroid Precursor Cells/cytology/metabolism ; *Erythropoiesis ; Fetus/enzymology ; Gene Targeting ; Globins/genetics/metabolism ; *Hematopoiesis, Extramedullary ; Kruppel-Like Transcription Factors ; Liver/cytology/*embryology/enzymology/*physiology ; Lysosomes/enzymology ; Macrophages/chemistry/*enzymology/ultrastructure ; Mice ; Mice, Knockout ; Mutation ; RNA, Messenger/genetics/metabolism ; Transcription Factors/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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  • 18
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    Treatment of ischemic brain damage by perturbing NMDA receptor- PSD-95 protein interactions (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-26
    Description: N-methyl-D-aspartate receptors (NMDARs) mediate ischemic brain damage but also mediate essential neuronal excitation. To treat stroke without blocking NMDARs, we transduced neurons with peptides that disrupted the interaction of NMDARs with the postsynaptic density protein PSD-95. This procedure dissociated NMDARs from downstream neurotoxic signaling without blocking synaptic activity or calcium influx. The peptides, when applied either before or 1 hour after an insult, protected cultured neurons from excitotoxicity, reduced focal ischemic brain damage in rats, and improved their neurological function. This approach circumvents the negative consequences associated with blocking NMDARs and may constitute a practical stroke therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aarts, Michelle -- Liu, Yitao -- Liu, Lidong -- Besshoh, Shintaro -- Arundine, Mark -- Gurd, James W -- Wang, Yu-Tian -- Salter, Michael W -- Tymianski, Michael -- NS 39060/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 25;298(5594):846-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Toronto Western Hospital Research Institute, 11-416 MC-PAV, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12399596" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/*drug effects/metabolism ; Brain Ischemia/*drug therapy/metabolism ; Calcium/metabolism ; Cells, Cultured ; Cerebral Infarction/*drug therapy/metabolism ; Cyclic GMP/metabolism ; Guanylate Kinase ; In Vitro Techniques ; Intracellular Signaling Peptides and Proteins ; Male ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; N-Methylaspartate/pharmacology ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurons/drug effects/physiology ; Patch-Clamp Techniques ; Peptides/administration & dosage/*pharmacology/therapeutic use ; Protein Binding ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/*chemistry/*metabolism ; Recombinant Fusion Proteins/administration & dosage/pharmacology/therapeutic use ; Signal Transduction ; Synaptic Transmission/drug effects
    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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  • 19
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    A subclass of Ras proteins that regulate the degradation of IkappaB (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-05
    Description: Small guanosine triphosphatases, typified by the mammalian Ras proteins, play major roles in the regulation of numerous cellular pathways. A subclass of evolutionarily conserved Ras-like proteins was identified, members of which differ from other Ras proteins in containing amino acids at positions 12 and 61 that are similar to those present in the oncogenic forms of Ras. These proteins, kappaB-Ras1 and kappaB-Ras2, interact with the PEST domains of IkappaBalpha and IkappaBbeta [inhibitors of the transcription factor nuclear factor kappa B (NF-kappaB)] and decrease their rate of degradation. In cells, kappaB-Ras proteins are associated only with NF-kappaB:IkappaBbeta complexes and therefore may provide an explanation for the slower rate of degradation of IkappaBbeta compared with IkappaBalpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fenwick, C -- Na, S Y -- Voll, R E -- Zhong, H -- Im, S Y -- Lee, J W -- Ghosh, S -- New York, N.Y. -- Science. 2000 Feb 4;287(5454):869-73.〈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/10657303" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; Guanosine Triphosphate/metabolism ; Humans ; I-kappa B Proteins/*metabolism ; Mice ; Molecular Sequence Data ; NF-kappa B/metabolism ; Phosphorylation ; Recombinant Fusion Proteins/chemistry/metabolism ; Signal Transduction ; Transcription Factor RelA ; Transfection ; Tumor Necrosis Factor-alpha/metabolism/pharmacology ; Two-Hybrid System Techniques ; ras 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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  • 20
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    DNA damage-induced activation of p53 by the checkpoint kinase Chk2 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: Chk2 is a protein kinase that is activated in response to DNA damage and may regulate cell cycle arrest. We generated Chk2-deficient mouse cells by gene targeting. Chk2-/- embryonic stem cells failed to maintain gamma-irradiation-induced arrest in the G2 phase of the cell cycle. Chk2-/- thymocytes were resistant to DNA damage-induced apoptosis. Chk2-/- cells were defective for p53 stabilization and for induction of p53-dependent transcripts such as p21 in response to gamma irradiation. Reintroduction of the Chk2 gene restored p53-dependent transcription in response to gamma irradiation. Chk2 directly phosphorylated p53 on serine 20, which is known to interfere with Mdm2 binding. This provides a mechanism for increased stability of p53 by prevention of ubiquitination in response to DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirao, A -- Kong, Y Y -- Matsuoka, S -- Wakeham, A -- Ruland, J -- Yoshida, H -- Liu, D -- Elledge, S J -- Mak, T W -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1824-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Amgen Institute, Ontario Cancer Institute, and Departments of Medical Biophysics and Immunology, University of Toronto, 620 University Avenue, Suite 706, Toronto, Ontario, M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; Checkpoint Kinase 2 ; *DNA Damage ; DNA-Binding Proteins ; G1 Phase ; G2 Phase ; Gamma Rays ; Gene Expression Regulation ; Gene Targeting ; Genes, Tumor Suppressor ; Genes, p53 ; Humans ; *Interphase ; Mice ; *Nuclear Proteins ; Phosphorylation ; Phosphoserine/metabolism ; *Protein Kinases ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2 ; Stem Cells/cytology/metabolism ; T-Lymphocytes/cytology ; Transcription, Genetic ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins
    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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