4.5 Article

Multifunctional Abl kinases in health and disease

Journal

JOURNAL OF CELL SCIENCE
Volume 129, Issue 1, Pages 9-16

Publisher

COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.175521

Keywords

Abelson kinases; Cytoskeletal reorganization; Cell motility; Polarity; Adhesion; Endocytosis; Microbial pathogens; Cancer; Inflammation

Categories

Funding

  1. National Institutes of Health (NIH) [R01CA195549, CA155160, AI056266]
  2. [F30HL126448]
  3. [T32 GM007171F30]
  4. NATIONAL CANCER INSTITUTE [R01CA195549, R01CA155160] Funding Source: NIH RePORTER
  5. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [F30HL126448] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI056266] Funding Source: NIH RePORTER
  7. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007171] Funding Source: NIH RePORTER

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The Abelson tyrosine kinases were initially identified as drivers of leukemia in mice and humans. The Abl family kinases Abl1 and Abl2 regulate diverse cellular processes during development and normal homeostasis, and their functions are subverted during inflammation, cancer and other pathologies. Abl kinases can be activated by multiple stimuli leading to cytoskeletal reorganization required for cell morphogenesis, motility, adhesion and polarity. Depending on the cellular context, Abl kinases regulate cell survival and proliferation. Emerging data support important roles for Abl kinases in pathologies linked to inflammation. Among these are neurodegenerative diseases and inflammatory pathologies. Unexpectedly, Abl kinases have also been identified as important players in mammalian host cells during microbial pathogenesis. Thus, the use of Abl kinase inhibitors might prove to be effective in the treatment of pathologies beyond leukemia and solid tumors. In this Cell Science at a Glance article and in the accompanying poster, we highlight the emerging roles of Abl kinases in the regulation of cellular processes in normal cells and diverse pathologies ranging from cancer to microbial pathogenesis.

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