Download Abl Family Kinases in Development and Disease by Anthony Koleske PDF

By Anthony Koleske

Abl relatives Kinases in improvement and ailment presents an summary of the capabilities of Abl family members kinases in improvement and illness. This new identify discusses the biochemical, genetic, and telephone organic information that elucidate the mobile roles for those kinases in those processes.

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Additional resources for Abl Family Kinases in Development and Disease

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Activated nuclear ABL can exit to the cytoplasm and stimulate cell death by transcription-independent mechanism. BCR-ABL-transformed cells, supporting the nuclear requirement for activated ABL kinase in inducing cell death. In recent unpublished studies, we have examined the pro-death function of Abl proteins that are either exclusively cytoplasmic (NLS-mutated), exclusively nuclear (Nuc), or shuttling (wild type). ^ W h e n expressed in an appropriate cell context, dimerization of wild type or Abl-Nuk is sufficient to activate programmed cell death (XD Huang and JYJ Wang, unpublished).

J Clin Invest 1997; 100(l):46-57. 23. Hurley RW, McCarthy JB, Verfaillie C M . Direct adhesion to bone marrow stroma via fibronectin receptors inhibits hematopoietic progenitor proliferation. J Clin Invest 1995; 96(1):511-519. 24. Lundell BI, McCarthy JB, Kovach N L et al. Activation-dependent alpha5betal integrin-mediated adhesion to fibronectin decreases proliferation of chronic myelogenous leukemia progenitors and K562 cells. Blood 1996; 87(6):2450-2458. 25. Renshaw M W , McWhirter JR, W a n g JY.

Sini P, Cannas A, Koleske AJ et al. Abl-dependent tyrosine phosphorylation of Sos-1 mediates growth-factor-induced Rac activation. N a t Cell Biol 2004; 6(3):268-274. 69. Wisniewski D , Strife A, Wojciechowicz D et al. A 62-kilodalton tyrosine phosphoprotein constitutively present in primary chronic phase chronic myelogenous leukemia enriched lineage negative blast populations. Leukemia 1994; 8(4):688-693. 70. Carpino N , Wisniewski D , Strife A et al. p62(dok): a constitutively tyrosine-phosphorylated, GAP-associated protein in chronic myelogenous leukemia progenitor cells.

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