https://scholars.lib.ntu.edu.tw/handle/123456789/473869
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Wang W.-J. | en_US |
dc.contributor.author | Kuo J.-C. | en_US |
dc.contributor.author | Ku W. | en_US |
dc.contributor.author | Lee Y.-R. | en_US |
dc.contributor.author | Lin F.-C. | en_US |
dc.contributor.author | YIH-LEONG CHANG | en_US |
dc.contributor.author | Lin Y.-M. | en_US |
dc.contributor.author | Chen C.-H. | en_US |
dc.contributor.author | Huang Y.-P. | en_US |
dc.contributor.author | Chiang M.-J. | en_US |
dc.contributor.author | Yeh S.-W. | en_US |
dc.contributor.author | Wu P.-R. | en_US |
dc.contributor.author | Shen C.-H. | en_US |
dc.contributor.author | CHEN-TU WU | en_US |
dc.contributor.author | Chen R.-H. | en_US |
dc.creator | Wang W.-J.;Kuo J.-C.;Ku W.;Lee Y.-R.;Lin F.-C.;Yih-Leong Chang;Lin Y.-M.;Chen C.-H.;Huang Y.-P.;Chiang M.-J.;Yeh S.-W.;Wu P.-R.;Shen C.-H.;Wu C.-T.;Chen R.-H. | - |
dc.date.accessioned | 2020-03-07T06:56:48Z | - |
dc.date.available | 2020-03-07T06:56:48Z | - |
dc.date.issued | 2007 | - |
dc.identifier.issn | 1097-2765 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-34548249520&doi=10.1016%2fj.molcel.2007.06.037&partnerID=40&md5=73b82ed317c111691d7f66ea7ec463ea | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/473869 | - |
dc.description.abstract | Death-associated protein kinase (DAPK) is a calmodulin-regulated serine/threonine kinase and elicits tumor suppression function through inhibiting cell adhesion/migration and promoting apoptosis. Despite these biological functions, the signaling mechanisms through which DAPK is regulated remain largely elusive. Here, we show that the leukocyte common antigen-related (LAR) tyrosine phosphatase dephosphorylates DAPK at pY491/492 to stimulate the catalytic, proapoptotic, and antiadhesion/antimigration activities of DAPK. Conversely, Src phosphorylates DAPK at Y491/492, which induces DAPK intra-/intermolecular interaction and inactivation. Upon EGF stimulation, a rapid Src activation leads to subsequent LAR downregulation, and these two events act in synergism to inactivate DAPK, thereby facilitating tumor cell migration and invasion toward EGF. Finally, DAPK Y491/492 hyperphosphorylation is found in human cancers in which Src activity is aberrantly elevated. These results identify LAR and Src as a DAPK regulator through their reciprocal modification of DAPK Y491/492 residues and establish a functional link of this DAPK-regulatory circuit to tumor progression. ? 2007 Elsevier Inc. All rights reserved. | - |
dc.relation.ispartof | Molecular Cell | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | CD45 antigen; death associated protein kinase; phosphatase; protein tyrosine kinase; small interfering RNA; tumor suppressor protein; tyrosine kinase src; unclassified drug; amino acid sequence; animal cell; apoptosis; article; cancer inhibition; catabolism; cell adhesion; cell differentiation; cell growth; controlled study; dephosphorylation; enzyme activation; enzyme activity; enzyme assay; enzyme regulation; human; human cell; immunoblotting; in vitro study; in vivo study; leukocyte migration inhibition test; nonhuman; protein expression; protein function; protein phosphorylation; protein protein interaction; signal transduction; tumor cell; Apoptosis Regulatory Proteins; Calcium-Calmodulin-Dependent Protein Kinases; Cell Line, Tumor; Epidermal Growth Factor; Humans; Neoplasms; Nerve Tissue Proteins; Phosphorylation; Protein Tyrosine Phosphatases; Proto-Oncogene Proteins pp60(c-src); Receptor-Like Protein Tyrosine Phosphatases, Class 2; Receptors, Cell Surface; Signal Transduction; Tumor Suppressor Proteins | - |
dc.title | The Tumor Suppressor DAPK Is Reciprocally Regulated by Tyrosine Kinase Src and Phosphatase LAR | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1016/j.molcel.2007.06.037 | - |
dc.identifier.pmid | 17803936 | - |
dc.identifier.scopus | 2-s2.0-34548249520 | - |
dc.relation.pages | 701-716 | - |
dc.relation.journalvolume | 27 | - |
dc.relation.journalissue | 5 | - |
item.fulltext | no fulltext | - |
item.grantfulltext | none | - |
item.openairetype | journal article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Pathology | - |
crisitem.author.dept | Pathology-NTUH | - |
crisitem.author.dept | Pathology-NTUCC | - |
crisitem.author.dept | Pathology | - |
crisitem.author.dept | Pathology-NTUH | - |
crisitem.author.orcid | 0000-0001-5309-0554 | - |
crisitem.author.orcid | 0000-0001-8458-4119 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Cancer Center (NTUCC) | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
顯示於: | 病理學科所 |
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