Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/38092
DC FieldValueLanguage
dc.contributor.authorLiu, G.Y.en_US
dc.contributor.author洪慧芝zh_TW
dc.contributor.authorLiao, Y.F.en_US
dc.contributor.authorChang, W.H.en_US
dc.contributor.authorLiu, C.C.en_US
dc.contributor.authorHsieh, M.C.en_US
dc.contributor.authorHsu, P.C.en_US
dc.contributor.authorTsay, G.en_US
dc.contributor.authorHung, H.C.en_US
dc.date2006zh_TW
dc.date.accessioned2014-06-06T08:00:30Z-
dc.date.available2014-06-06T08:00:30Z-
dc.identifier.issn1360-8185zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/38092-
dc.description.abstractPeptidylarginine deiminases (PADIs) convert peptidylarginine into citrulline via posttranslational modification. One member of the family, PADI4, plays an important role in immune cell differentiation and cell death. To elucidate the participation of PADI4 in haematopoietic cell death, we examine whether inducible overexpression of PADI4 enhances the apoptotic cell death. PADI4 reduced the viability in a dose- and time-dependent manner of human leukemia HL-60 cells and human acute T leukemia Jurkat cells. The apoptosis-inducing activities were determined by nuclear condensation, DNA fragmentation, sub-G1 appearance, loss of mitochondrial membrane potential (Delta psi(m)), release of mitochondrial cytochrome c into cytoplasm and proteolytic activation of caspase 9 and 3. Following PADI4 overexpression, cells arrest in G1 phase significantly before their entrance into apoptotic cell death. PADI4 increases tumor suppressor p53 and its downstream p21 to control cell cycle. In the detections of protein expression and kinase activity, all protein levels of cyclin-dependent kinases (CDKs) and cyclins are not reduced except cyclin D, however, CDK2 (G1 entry S phase) and CDK1 (G2 entry M phase) enzyme activities are inhibited by conditionally inducible PADI4. p53 also expands its other downstream Bax to induce cytochrome c release from mitochondria. According to these data, we suggest that PADI4 induces apoptosis mainly through cell cycle arrest and mitochondria-mediated pathway. Furthermore, p53 features in PADI4-induced apoptosis by increasing intracellular p21 to control cell cycle and by Bax accumulation to decline Bcl-2 function, destroy Delta psi(m), release cytochrome c to cytoplasm and activate the caspase cascade.en_US
dc.language.isoen_USzh_TW
dc.relationApoptosisen_US
dc.relation.ispartofseriesApoptosis, Volume 11, Issue 2, Page(s) 183-196.en_US
dc.relation.urihttp://dx.doi.org/10.1007/s10495-006-3715-4en_US
dc.subjectapoptosisen_US
dc.subjectBaxen_US
dc.subjectBcl-2en_US
dc.subjectp21en_US
dc.subjectp53en_US
dc.subjectPADIsen_US
dc.subjectPADI4en_US
dc.subjectrheumatoid-arthritisen_US
dc.subjectornithine-decarboxylaseen_US
dc.subjectp53 proteinen_US
dc.subjecthuman skinen_US
dc.subjectdevelopmentally immatureen_US
dc.subjectintermediate-filamentsen_US
dc.subjectarginine methylationen_US
dc.subjecthistone deiminationen_US
dc.subjectmultiple-sclerosisen_US
dc.subjecthl-60 granulocytesen_US
dc.titleOverexpression of peptidylarginine deiminase IV features in apoptosis of haematopoietic cellsen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1007/s10495-006-3715-4zh_TW
item.fulltextno fulltext-
item.languageiso639-1en_US-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
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