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  • 1
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    Chondrocytes in Mig-6-deficient {jnodot}oint disorder [Developmental Biology] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-02-19
    Description: A deficiency of mitogen-inducible gene-6 (Mig-6) in mice leads to the development of an early-onset, osteoarthritis (OA)-like disorder in multiple synovial joints, underlying its importance in maintaining joint homeostasis. Here we determined what joint tissues Mig-6 is expressed in and what role chondrocytes play in the Mig-6–deficient OA-like disorder. A...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    The product of the mos proto-oncogene as a candidate "initiator" for oocyte maturation (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-11
    Description: The endogenous c-mos product, pp39mos, is required for progesterone-induced meiotic maturation in Xenopus oocytes. Treatment of oocytes with progesterone induced a rapid increase in pp39mos that preceded both the activation of maturation promoting factor (MPF) and germinal vesicle breakdown (GVBD). Microinjection of synthetic mos RNA into oocytes activated MPF and induced GVBD in the absence of progesterone. Thus, the mos proto-oncogene product may qualify as a candidate "initiator" protein of MPF and is at least one of the "triggers" for G2 to M transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sagata, N -- Daar, I -- Oskarsson, M -- Showalter, S D -- Vande Woude, G F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 Aug 11;245(4918):643-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BRI-Basic Research Program, National Cancer Institute, Frederick Cancer Research Facility, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2474853" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cycloheximide/pharmacology ; Female ; Growth Substances/physiology ; Kinetics ; Maturation-Promoting Factor ; Meiosis/drug effects ; Microinjections ; Oocytes/*physiology ; Progesterone/pharmacology ; Protein Biosynthesis ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-mos ; RNA/genetics ; Transcription, Genetic ; Transfection ; Xenopus
    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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  • 3
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    Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-15
    Description: Hepatocyte growth factor (HGF) is a plasminogen-like protein thought to be a humoral mediator of liver regeneration. A 145-kilodalton tyrosyl phosphoprotein observed in rapid response to HGF treatment of intact target cells was identified by immunoblot analysis as the beta subunit of the c-met proto-oncogene product, a membrane-spanning tyrosine kinase. Covalent cross-linking of 125I-labeled ligand to cellular proteins of appropriate size that were recognized by antibodies to c-met directly established the c-met product as the cell-surface receptor for HGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bottaro, D P -- Rubin, J S -- Faletto, D L -- Chan, A M -- Kmiecik, T E -- Vande Woude, G F -- Aaronson, S A -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):802-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846706" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cross-Linking Reagents ; Growth Substances/*metabolism/physiology ; Hepatocyte Growth Factor ; Humans ; Molecular Weight ; Phosphorylation ; Precipitin Tests ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-met ; Receptors, Cell Surface/*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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  • 4
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    Ability of the c-mos product to associate with and phosphorylate tubulin (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-08
    Description: The mos proto-oncogene product, pp39mos, is a protein kinase and has been equated with cytostatic factor (CSF), an activity in unfertilized eggs that is thought to be responsible for the arrest of meiosis at metaphase II. The biochemical properties and potential substrates of pp39mos were examined in unfertilized eggs and in transformed cells in order to study how the protein functions both as CSF and in transformation. The pp39mos protein associated with polymers under conditions that favor tubulin oligomerization and was present in an approximately 500-kilodalton "core" complex under conditions that favor depolymerization. beta-Tubulin was preferentially coprecipitated in pp39mos immunoprecipitates and was the major phosphorylated product in a pp39mos-dependent immune complex kinase assay. Immunofluorescence analysis of NIH 3T3 cells transformed with Xenopus c-mos showed that pp39mos colocalizes with tubulin in the spindle during metaphase and in the midbody and asters during telophase. Disruption of microtubules with nocodazole affected tubulin and pp39mos organization in the same way. It therefore appears that pp39mos is a tubulin-associated protein kinase and may thus participate in the modification of microtubules and contribute to the formation of the spindle. This activity expressed during interphase in somatic cells may be responsible for the transforming activity of pp39mos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, R P -- Oskarsson, M -- Paules, R S -- Schulz, N -- Cleveland, D -- Vande Woude, G F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 8;251(4994):671-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1825142" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Phosphoproteins/metabolism ; Precipitin Tests ; Protein Binding ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-mos ; Tubulin/*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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  • 5
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    The ras oncoprotein and M-phase activity (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-05
    Description: The endogenous mos proto-oncogene product (Mos) is required for meiotic maturation. In Xenopus oocytes, the ras oncogene product (Ras) can induce meiotic maturation and high levels of M-phase--promoting factor (MPF) independent of endogenous Mos, indicating that a parallel pathway to metaphase exists. In addition, Ras, like Mos and cytostatic factor, can arrest Xenopus embryonic cell cleavage in mitosis and maintain high levels of MPF. Thus, in the Xenopus oocyte and embryo systems Ras functions in the M phase of the cell cycle. The embryonic cleavage arrest assay is a rapid and sensitive test for Ras function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daar, I -- Nebreda, A R -- Yew, N -- Sass, P -- Paules, R -- Santos, E -- Wigler, M -- Vande Woude, G F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):74-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1829549" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; In Vitro Techniques ; Maturation-Promoting Factor/*metabolism ; Meiosis/*drug effects ; Oncogene Protein p21(ras)/*pharmacology ; Oncogene Proteins v-mos ; Oogenesis/*drug effects ; Progesterone/pharmacology ; Retroviridae Proteins, Oncogenic/pharmacology ; Xenopus laevis
    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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    Proteolytic inactivation of MAP-kinase-kinase by anthrax lethal factor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: Anthrax lethal toxin, produced by the bacterium Bacillus anthracis, is the major cause of death in animals infected with anthrax. One component of this toxin, lethal factor (LF), is suspected to be a metalloprotease, but no physiological substrates have been identified. Here it is shown that LF is a protease that cleaves the amino terminus of mitogen-activated protein kinase kinases 1 and 2 (MAPKK1 and MAPKK2) and that this cleavage inactivates MAPKK1 and inhibits the MAPK signal transduction pathway. The identification of a cleavage site for LF may facilitate the development of LF inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duesbery, N S -- Webb, C P -- Leppla, S H -- Gordon, V M -- Klimpel, K R -- Copeland, T D -- Ahn, N G -- Oskarsson, M K -- Fukasawa, K -- Paull, K D -- Vande Woude, G F -- New York, N.Y. -- Science. 1998 May 1;280(5364):734-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Advanced BioScience Laboratories-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Post Office Box B, Frederick, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9563949" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Bacterial ; *Bacillus anthracis/enzymology ; Bacterial Toxins/metabolism/*toxicity ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cell Line, Transformed ; Enzyme Activation ; Enzyme Inhibitors/toxicity ; Humans ; MAP Kinase Kinase 1 ; MAP Kinase Kinase 2 ; Metalloendopeptidases/metabolism/toxicity ; Mice ; *Mitogen-Activated Protein Kinase Kinases ; Myelin Basic Protein/metabolism ; Oocytes/physiology ; Phosphorylation ; Protein-Serine-Threonine Kinases/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/chemistry/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Signal Transduction ; Xenopus laevis
    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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    The Met proto-oncogene mesenchymal to epithelial cell conversion (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-07
    Description: Coexpression of the human Met receptor and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), in NIH 3T3 fibroblasts causes the cells to become tumorigenic in nude mice. The resultant tumors display lumen-like morphology, contain carcinoma-like focal areas with intercellular junctions resembling desmosomes, and coexpress epithelial (cytokeratin) and mesenchymal (vimentin) cytoskeletal markers. The tumor cells also display enhanced expression of desmosomal and tight-junction proteins. The apparent mesenchymal to epithelial conversion of the tumor cells mimics the conversion that occurs during embryonic kidney development, suggesting that Met-HGF/SF signaling plays a role in this process as well as in tumors that express both epithelial and mesenchymal markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsarfaty, I -- Rong, S -- Resau, J H -- Rulong, S -- da Silva, P P -- Vande Woude, G F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):98-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute (NCI)-Frederick Cancer Research and Development Center, MD 21702-1201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7505952" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Cell Transformation, Neoplastic ; Desmosomes/ultrastructure ; Epithelial Cells ; Hepatocyte Growth Factor/metabolism/pharmacology ; Keratins/biosynthesis ; Kidney/embryology/metabolism ; Mesoderm/cytology ; Mice ; Mice, Nude ; Neoplasms, Experimental/metabolism/*pathology ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-met ; *Proto-Oncogenes ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Signal Transduction ; Transfection ; Vimentin/biosynthesis
    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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  • 8
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    Abnormal centrosome amplification in the absence of p53 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukasawa, K -- Choi, T -- Kuriyama, R -- Rulong, S -- Vande Woude, G F -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1744-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Cells, Cultured ; Centrosome/*metabolism ; Culture Media ; Fibroblasts ; Genes, Retinoblastoma ; Genes, p53 ; *Interphase ; Mice ; *Mitosis ; Spindle Apparatus/metabolism/ultrastructure ; Tumor Suppressor Protein p53/*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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  • 9
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    Transformation of mammalian cells by constitutively active MAP kinase kinase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: Mitogen-activated protein (MAP) kinase kinase (MAPKK) activates MAP kinase in a signal transduction pathway that mediates cellular responses to growth and differentiation factors. Oncogenes such as ras, src, raf, and mos have been proposed to transform cells by prolonging the activated state of MAPKK and of components downstream in the signaling pathway. To test this hypothesis, constitutively active MAPKK mutants were designed that had basal activities up to 400 times greater than that of the unphosphorylated wild-type kinase. Expression of these mutants in mammalian cells activated AP-1-regulated transcription. The cells formed transformed foci, grew efficiently in soft agar, and were highly tumorigenic in nude mice. These findings indicate that constitutive activation of MAPKK is sufficient to promote cell transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mansour, S J -- Matten, W T -- Hermann, A S -- Candia, J M -- Rong, S -- Fukasawa, K -- Vande Woude, G F -- Ahn, N G -- GM48521/GM/NIGMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):966-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052857" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; Enzyme Activation ; Genes, mos ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase Kinases ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Protein Kinases/genetics/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Signal Transduction ; 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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  • 10
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    The met proto-oncogene receptor and lumen formation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: The met proto-oncogene product (Met) and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), have been implicated in cell mitogenic response, cell motility, and the promotion of the ordered spatial arrangement of tissue. By means of confocal laser-scanning microscopy, it was shown that Met is expressed in cells bordering lumen-like structures that resemble ducts in the human mammary cell line T47D. In human breast tissue biopsies, Met staining was intense in normal cells bordering mammary ducts but was reduced in adjacent tumor tissue. Met staining in lumen-forming organs colocalizes with staining of antibody to phosphotyrosine, which suggests that the Met receptor and its substrates may be activated in lumen structures or ducts. HGF/SF treatment of human epithelial carcinoma cell lines resulted in the formation of lumen-like structures in vitro. Reduced expression of Met could be related to the extent of tumor cell differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsarfaty, I -- Resau, J H -- Rulong, S -- Keydar, I -- Faletto, D L -- Vande Woude, G F -- N01-C0-74101/PHS HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1258-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1387731" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/metabolism/pathology ; Animals ; Breast Neoplasms/metabolism/pathology ; Cell Differentiation/genetics ; Chromosomes, Human, Pair 7 ; Colonic Neoplasms/chemically induced/metabolism/pathology ; Digestive System/metabolism ; Dose-Response Relationship, Drug ; Growth Substances/pharmacology/*physiology ; Hepatocyte Growth Factor ; Humans ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Microscopy, Immunoelectron ; Proto-Oncogene Proteins/*physiology ; Proto-Oncogene Proteins c-met
    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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