The additional loss of Bak and not the lack of the protein tyrosine kinase p56/Lck in one JCaM1.6 subclone caused pronounced apoptosis resistance in response to stimuli of the intrinsic pathway

Apoptosis

Volumn 14, Issue 5, 2009, Pages 711-720

  Rudner, J ^a   Mueller, A C ^a   Matzner, N ^a   Huber, S M ^a   Handrick, R ^a,b   Belka, C ^a   Jendrossek, V ^a,b  

^a UNIVERSITY OF TÜBINGEN   (Germany)

^b UNIVERSITY OF DUISBURG ESSEN   (Germany)

Author keywords

Apoptosis; Bak; Celecoxib; Hypoxia; Ionising radiation; P56 Lck

Indexed keywords

CELECOXIB; PROTEIN BAK; PROTEIN KINASE LCK; PYRAZOLE DERIVATIVE; SULFONAMIDE;

APOPTOSIS; ARTICLE; CELL CLONE; DRUG EFFECT; GENE SILENCING; HUMAN; IONIZING RADIATION; METABOLISM; RADIATION EXPOSURE; SIGNAL TRANSDUCTION; TUMOR CELL LINE;

APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; CELL LINE, TUMOR; CLONE CELLS; GENE SILENCING; HUMANS; LYMPHOCYTE SPECIFIC PROTEIN TYROSINE KINASE P56(LCK); PYRAZOLES; RADIATION, IONIZING; SIGNAL TRANSDUCTION; SULFONAMIDES;

EID: 77955069880     PISSN: 13608185     EISSN: 1573675X     Source Type: Journal    
DOI: 10.1007/s10495-009-0342-x     Document Type: Article

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