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  • 1
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    A cytoplasmic inhibitor of the JNK signal transduction pathway (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-01
    Description: The c-Jun amino-terminal kinase (JNK) is a member of the stress-activated group of mitogen-activated protein (MAP) kinases that are implicated in the control of cell growth. A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned. JIP-1 caused cytoplasmic retention of JNK and inhibition of JNK-regulated gene expression. In addition, JIP-1 suppressed the effects of the JNK signaling pathway on cellular proliferation, including transformation by the Bcr-Abl oncogene. This analysis identifies JIP-1 as a specific inhibitor of the JNK signal transduction pathway and establishes protein targeting as a mechanism that regulates signaling by stress-activated MAP kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickens, M -- Rogers, J S -- Cavanagh, J -- Raitano, A -- Xia, Z -- Halpern, J R -- Greenberg, M E -- Sawyers, C L -- Davis, R J -- CA43855/CA/NCI NIH HHS/ -- CA65861/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 1;277(5326):693-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, 373 Plantation Street, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235893" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 2 ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/chemistry/*metabolism ; Cell Nucleus/metabolism ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cloning, Molecular ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cytoplasm/metabolism ; Fusion Proteins, bcr-abl/metabolism ; Gene Expression Regulation ; JNK Mitogen-Activated Protein Kinases ; Mitogen-Activated Protein Kinase 9 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transcription Factors/metabolism ; Transcriptional Activation ; Transfection
    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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  • 2
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    Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-24
    Description: Apoptosis plays an important role during neuronal development, and defects in apoptosis may underlie various neurodegenerative disorders. To characterize molecular mechanisms that regulate neuronal apoptosis, the contributions to cell death of mitogen-activated protein (MAP) kinase family members, including ERK (extracellular signal-regulated kinase), JNK (c-JUN NH2-terminal protein kinase), and p38, were examined after withdrawal of nerve growth factor (NGF) from rat PC-12 pheochromocytoma cells. NGF withdrawal led to sustained activation of the JNK and p38 enzymes and inhibition of ERKs. The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells. Therefore, the dynamic balance between growth factor-activated ERK and stress-activated JNK-p38 pathways may be important in determining whether a cell survives or undergoes apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xia, Z -- Dickens, M -- Raingeaud, J -- Davis, R J -- Greenberg, M E -- CA43855/CA/NCI NIH HHS/ -- CA65861/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 24;270(5240):1326-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7481820" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/pharmacology ; Animals ; *Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/*antagonists & ; inhibitors/genetics/*metabolism ; Cell Differentiation ; Enzyme Activation ; Genes, jun ; *JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 1 ; MAP Kinase Kinase 3 ; MAP Kinase Kinase 4 ; MAP Kinase Kinase Kinases ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Nerve Growth Factors/pharmacology ; Neurons/*cytology/enzymology ; PC12 Cells ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/genetics/metabolism ; Rats ; *Signal Transduction ; Staurosporine ; Sympathetic Nervous System/cytology ; p38 Mitogen-Activated Protein Kinases
    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)
    Location Call Number Expected Availability
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