Oncogenic E17K mutation in the pleckstrin homology domain of AKT1 promotes v-Abl-mediated pre-B-cell transformation and survival of Pim-deficient cells

Oncogene

Volumn 29, Issue 26, 2010, Pages 3845-3853

  Guo, G ^a   Qiu, X ^a   Wang, S ^a   Chen, Y ^a,c   Rothman, P B ^b   Wang, Z ^c   Wang, G ^d   Chen, J L ^a  

^a INSTITUTE OF MICROBIOLOGY   (China)

^b UNIVERSITY OF IOWA   (United States)

^c CHINA AGRICULTURAL UNIVERSITY   (China)

^d LOUISIANA STATE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

AKT1; cancer; mutation; Pim; v Abl

Indexed keywords

ABELSON KINASE; IMATINIB; PROTEIN AKT1; PROTEIN BAD; PROTEIN BCL 2; PROTEIN KINASE; PROTEIN KINASE B; PROTEIN KINASE PIM 1; PROTEIN KINASE PIM 2; UNCLASSIFIED DRUG;

ANIMAL CELL; APOPTOSIS; ARTICLE; CARCINOGENESIS; CELL SURVIVAL; CONTROLLED STUDY; GENE MUTATION; LYMPHOCYTE CLONE; LYMPHOCYTE TRANSFORMATION; MOUSE; MUTANT; NONHUMAN; PRE B LYMPHOCYTE; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN LOCALIZATION; PROTEIN PHOSPHORYLATION; WILD TYPE;

ANIMALS; B-LYMPHOCYTES; BLOOD PROTEINS; CELL SURVIVAL; CELL TRANSFORMATION, NEOPLASTIC; HUMANS; MICE; MUTATION; ONCOGENES; PHOSPHOPROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; PROTO-ONCOGENE PROTEINS C-PIM-1;

MUS;

EID: 77954242428     PISSN: 09509232     EISSN: 14765594     Source Type: Journal    
DOI: 10.1038/onc.2010.149     Document Type: Article

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