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dc.contributor.authorKhar, Ashok-
dc.contributor.authorKumari, A Leela-
dc.contributor.authorPardhasaradhi, B V V-
dc.contributor.authorVaralakshmi, Ch-
dc.contributor.authorRangaraj, Nandini-
dc.date.accessioned2009-11-18T07:39:28Z-
dc.date.available2009-11-18T07:39:28Z-
dc.date.issued2006-10-
dc.identifier.issn0975-1009 (Online); 0019-5189 (Print)-
dc.identifier.urihttp://hdl.handle.net/123456789/6616-
dc.description802-808en_US
dc.description.abstract BC-8, a rat histiocytoma undergoes apoptosis after heat shock, which is due to lack of an effective heat shock response. Heat shock induced generation of free radicals, which in turn are involved in the induction of apoptotic death in BC-8 cells. Treatment of BC-8 cells with N-acetylcysteine partially inhibited the heat induced apoptosis. Introduction of Bcl-2 gene in these cells did not protect them from apoptotic death, whereas transfection with hsp-70 gene did render these cells resistant to heat induced apoptosis transiently. Heat shock also downregulated the expression of Bcl-2 and p53 in these cells. These observations suggested that the heat shock induced apoptosis was mediated through reactive oxygen species and controlled upstream of Bcl-2 check point. en_US
dc.language.isoen_USen_US
dc.publisherCSIRen_US
dc.sourceIJEB Vol.44(10) [October 2006]en_US
dc.subjectAK-5 tumoren_US
dc.subjectApoptosisen_US
dc.subjectBcl-2en_US
dc.subjectHeat shocken_US
dc.subjectROSen_US
dc.titleHeat stress induced apoptosis in BC-8 cells derived from AK-5 tumor involves downregulation of Bcl-2 and generation of reactive oxygen speciesen_US
dc.typeArticleen_US
Appears in Collections:IJEB Vol.44(10) [October 2006]

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