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

doi:10.1016/S1074-7613(00)80207-1

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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145 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 language	English
Pages (from-to)	557-568
Number of pages	12
Journal	Immunity
Volume	12
Issue number	5
DOIs	https://doi.org/10.1016/S1074-7613(00)80207-1
State	Published - 2000

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@article{8958dd9d5cc24d7e9d4012582d9e58b1,

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

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).",

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

note = "Funding Information: We thank Eva Meunier and Sharon Smoot for assistance in preparation of this manuscript. This work is supported by NIH R01 DK48605 (D. A. W.) and NIH R01 HL-45635 (M. C. D.). We thank Dr. Stan Korsmeyer for useful discussions.",

year = "2000",

doi = "10.1016/S1074-7613(00)80207-1",

language = "English",

volume = "12",

pages = "557--568",

journal = "Immunity",

issn = "1074-7613",

number = "5",

}

TY - JOUR

T1 - Rac2 stimulates Akt activation affecting BAD/Bcl-XL expression while mediating survival and actin function in primary mast cells

AU - Yang, Feng Chun

AU - Kapur, Reuben

AU - King, Alastair J.

AU - Tao, Wen

AU - Kim, Chaekyun

AU - Borneo, Jovencio

AU - Breese, Robert

AU - Marshall, Mark

AU - Dinauer, Mary C.

AU - Williams, David A.

N1 - Funding Information: We thank Eva Meunier and Sharon Smoot for assistance in preparation of this manuscript. This work is supported by NIH R01 DK48605 (D. A. W.) and NIH R01 HL-45635 (M. C. D.). We thank Dr. Stan Korsmeyer for useful discussions.

PY - 2000

Y1 - 2000

N2 - 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).

AB - 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).

UR - http://www.scopus.com/inward/record.url?scp=0033678937&partnerID=8YFLogxK

U2 - 10.1016/S1074-7613(00)80207-1

DO - 10.1016/S1074-7613(00)80207-1

M3 - Article

C2 - 10843388

AN - SCOPUS:0033678937

SN - 1074-7613

VL - 12

SP - 557

EP - 568

JO - Immunity

JF - Immunity

IS - 5

ER -

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

Abstract

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