The PIM-1 serine kinase prolongs survival and inhibits apoptosis-related mitochondrial dysfunction in part through a bcl-2-dependent pathway

Oncogene

Volumn 18, Issue 27, 1999, Pages 4022-4031

  Lilly, Michael ^a,d   Sandholm, Jouko ^b   Cooper, John J ^a   Koskinen, Päivi J ^b   Kraft, Andrew ^c  

^a UNIVERSITY OF WASHINGTON   (United States)

^b UNIVERSITY OF TURKU   (Finland)

^c UNIVERSITY OF COLORADO   (United States)

^d LOMA LINDA UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Apoptosis; bcl 2; FDCP1; IL 3; Mitochondria; pim 1

Indexed keywords

CATALASE; COMPLEMENTARY DNA; COMPLEMENTARY RNA; GLUTATHIONE; INTERLEUKIN 3; MESSENGER RNA; PROTEIN BCL 2; PROTEIN SERINE KINASE; REACTIVE OXYGEN METABOLITE; SUPEROXIDE DISMUTASE;

ANIMAL CELL; APOPTOSIS; ARTICLE; CELL SURVIVAL; CONTROLLED STUDY; FLOW CYTOMETRY; HEMATOPOIETIC CELL; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MITOCHONDRION; MOUSE; NONHUMAN; PRIORITY JOURNAL;

ANIMALS; APOPTOSIS; BCL-2-ASSOCIATED X PROTEIN; CELL LINE; CELL SURVIVAL; GENES, DOMINANT; GROWTH SUBSTANCES; INTERLEUKIN-3; MICE; MITOCHONDRIA; MOLECULAR WEIGHT; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; PROTO-ONCOGENE PROTEINS C-PIM-1; RNA, MESSENGER; SEQUENCE DELETION; SIGNAL TRANSDUCTION;

EID: 0033536203     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1202741     Document Type: Article

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