Structural Requirements for PAK Activation by Rac GTPases
نویسندگان
چکیده
منابع مشابه
Pak and Rac GTPases promote oncogenic KIT-induced neoplasms.
An acquired somatic mutation at codon 816 in the KIT receptor tyrosine kinase is associated with poor prognosis in patients with systemic mastocytosis and acute myeloid leukemia (AML). Treatment of leukemic cells bearing this mutation with an allosteric inhibitor of p21-activated kinase (Pak) or its genetic inactivation results in growth repression due to enhanced apoptosis. Inhibition of the u...
متن کاملRac, PAK, and eNOS ACTion.
Rac1 is a member of the Rho family of GTPases, which includes Rho, Rac, and cdc42 subfamilies.1,2 On activation by guanine nucleotide exchange factors, the Rho family GTPases exchange a GDP molecule for a GTP and act as molecular switches to transduce signals in response to various extracellular stimuli.2 Apart from their characteristic role in the regulation of cytoskeletal rearrangement and c...
متن کاملPAK promotes morphological changes by acting upstream of Rac.
The serine/threonine kinase p21-activated kinase (PAK) has been implicated as a downstream effector of the small GTPases Rac and Cdc42. While these GTPases evidently induce a variety of morphological changes, the role(s) of PAK remains elusive. Here we report that overexpression of betaPAK in PC12 cells induces a Rac phenotype, including cell spreading/membrane ruffling, and increased lamellipo...
متن کاملRac GTPases in Human Diseases
Rho GTPases are members of the Ras superfamily of GTPases that regulate a wide variety of cellular functions. While Rho GTPase pathways have been implicated in various pathological conditions in humans, to date coding mutations in only the hematopoietic specific GTPase, RAC2, have been found to cause a human disease, a severe phagocytic immunodeficiency characterized by life-threatening infecti...
متن کاملJak3 Enables Chemokine-Dependent Actin Cytoskeleton Reorganization by Regulating Cofilin and Rac/Rhoa GTPases Activation
We have previously shown that Jak3 is involved in the signaling pathways of CCR7, CCR9 and CXCR4 in murine T lymphocytes and that Jak3⁻/⁻ lymphocytes display an intrinsic defect in homing to peripheral lymph nodes. However, the molecular mechanism underlying the defective migration observed in Jak3⁻/⁻ lymphocytes remains elusive. Here, it is demonstrated for the first time, that Jak3 is require...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Biological Chemistry
سال: 1998
ISSN: 0021-9258
DOI: 10.1074/jbc.273.34.21512