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Article

Functional cooperation among Ras, STAT5, and phosphatidylinositol 3-kinase is required for full oncogenic activities of BCR/ABL in K562 cells.

The Journal of biological chemistry - 8 Mar 2002

Sonoyama Junko, Matsumura Itaru, Ezoe Sachiko, Satoh Yusuke, Zhang Xian, Kataoka Yoshihisa, Takai Emi, Mizuki Masao, Machii Takashi, Wakao Hiroshi, Kanakura Yuzuru

Abstract excerpt

BCR/ABL tyrosine kinase generated from the chromosomal translocation t(9;22) causes chronic myelogenous leukemia and acute lymphoblastic leukemia. To examine the roles of BCR/ABL-activated individual signaling molecules and their cooperation in leukemogenesis, we inducibly expressed a dominant negative (DN) form of Ras, phosphatidylinositol 3-kinase, and STAT5 alone or in combination in p210 BCR/ABL-positive K562...

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PMID: 11779872
DOI: 10.1074/jbc.M111501200

Genes

BCR

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Functional cooperation among Ras, STAT5, and phosphatidylinositol 3-kinase is required for full oncogenic activities of BCR/ABL in K562 cells.PMID 11779872Read ↗

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