rdf:type |
|
lifeskim:mentions |
|
pubmed:dateCreated |
2011-3-3
|
pubmed:abstractText |
The cysteine protease caspase-8 is an essential executioner of the death receptor (DR) apoptotic pathway. The physiological function of its homologue caspase-10 remains poorly understood, and the ability of caspase-10 to substitute for caspase-8 in the DR apoptotic pathway is still controversial. Here, we analysed the particular contribution of caspase-10 isoforms to DR-mediated apoptosis in neuroblastoma (NB) cells characterised by their resistance to DR signalling. Silencing of caspase-8 in tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-sensitive NB cells resulted in complete resistance to TRAIL, which could be reverted by overexpression of caspase-10A or -10D. Overexpression experiments in various caspase-8-expressing tumour cells also demonstrated that caspase-10A and -10D isoforms strongly increased TRAIL and FasL sensitivity, whereas caspase-10B or -10G had no effect or were weakly anti-apoptotic. Further investigations revealed that the unique C-terminal end of caspase-10B was responsible for its degradation by the ubiquitin-proteasome pathway and for its lack of pro-apoptotic activity compared with caspase-10A and -10D. These data highlight in several tumour cell types, a differential pro- or anti-apoptotic role for the distinct caspase-10 isoforms in DR signalling, which may be relevant for fine tuning of apoptosis initiation.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-10187817,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-10647931,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-10802708,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-10969767,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-11048727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-11245427,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-11583996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-11593392,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-11973654,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12010809,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12010812,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12037669,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12184808,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12198154,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12384554,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12612655,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12615731,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12620239,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12700660,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-12902978,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-15094781,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-15452117,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-15767684,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-15772077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-15886205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-16186808,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-16502263,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-16767158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-17822854,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-17952061,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-19111387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-19331667,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-20795673,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-4747985,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-8938368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-9045686,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-9087414,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21368896-9931493
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:issn |
2041-4889
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:volume |
2
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
e125
|
pubmed:meshHeading |
pubmed-meshheading:21368896-Amino Acid Motifs,
pubmed-meshheading:21368896-Apoptosis,
pubmed-meshheading:21368896-Caspase 10,
pubmed-meshheading:21368896-Caspase 8,
pubmed-meshheading:21368896-Cell Line, Tumor,
pubmed-meshheading:21368896-Humans,
pubmed-meshheading:21368896-Isoenzymes,
pubmed-meshheading:21368896-Neuroblastoma,
pubmed-meshheading:21368896-Receptors, Death Domain,
pubmed-meshheading:21368896-Receptors, TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:21368896-TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:21368896-Tumor Necrosis Factor-alpha
|
pubmed:year |
2011
|
pubmed:articleTitle |
Individual caspase-10 isoforms play distinct and opposing roles in the initiation of death receptor-mediated tumour cell apoptosis.
|
pubmed:affiliation |
Department of Paediatrics, Paediatric Oncology Research, University Hospital CHUV, CH-1011 Lausanne, Switzerland. Annick.Muhlethaler@chuv.ch
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|