Rac2 stimulates Akt activation affecting BAD/Bcl-XL expression while mediating survival and actin function in primary mast cells

Feng Chun Yang, Reuben Kapur, Alastair J. King, Wen Tao, Chaekyun Kim, Jovencio Borneo, Robert Breese, Mark Marshall, Mary C. Dinauer, David A. Williams

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138 Scopus citations

Abstract

Mast cells generated from Rac2-deficient ((-/-)) mice demonstrated defective actin-based functions, including adhesion, migration, and degranulation. Rac2(-/-) mast cells generated lower numbers and less mast cell colonies in response to growth factors and were deficient in vivo. Rac2(-/-) mast cells demonstrated a significant reduction in growth factor-induced survival, which correlated with the lack of activation of Akt and significant changes in the expression of the Bcl-2 family members BAD and Bcl-X(L), in spite of a 3-fold induction of Rac1 protein. These results suggest that Rac2 plays a unique role in multiple cellular functions and describe an essential role for Rac2 in growth factor-dependent survival and expression of BAD/Bcl-X(L).

Original languageEnglish (US)
Pages (from-to)557-568
Number of pages12
JournalImmunity
Volume12
Issue number5
DOIs
StatePublished - Jan 1 2000

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Cite this

Yang, F. C., Kapur, R., King, A. J., Tao, W., Kim, C., Borneo, J., Breese, R., Marshall, M., Dinauer, M. C., & Williams, D. A. (2000). Rac2 stimulates Akt activation affecting BAD/Bcl-XL expression while mediating survival and actin function in primary mast cells. Immunity, 12(5), 557-568. https://doi.org/10.1016/S1074-7613(00)80207-1