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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2.2

ISSN Print: 0893-9675
ISSN Online: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v8.i4.30
pages 329-342

Role of Crk Oncogene Product in Physiologic Signaling

Etsuko Kiyokawa
Department of Pathology, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8655, Japan
Naoki Mochizuki
Department of Pathology, Research Institute, International Medical Center of Japan, Shinjuku-ku, Tokyo 162-8655, Japan
Takeshi Kurata
Department of Pathology, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8655, Japan
Michiyuki Matsuda
Department of Pathology, National Institute of Infectious Diseases, and department of Pathology, Research Institute, International Medical Center of Japan, Shinjuku-ku, Tokyo 162-8655, Japan

ABSTRACT

v-Crk is a member of the family of adaptor-type signaling molecules that consist mostly of SH2 and SH3 domains. The cellular homologs of v-Crk includes CrkI, Crkll, and CrkL; these have been isolated from species ranging from lower vertebrates to man. Crk-family proteins are involved in a variety of signaling cascades such as those of growth factor receptor, integrin, T-cell receptor, B-cell antigen receptor, and cytokines. It has been postulated that the primary function of Crk is to recruit cytoplasmic proteins in the vicinity of tyrosine kinases through SH2-phosphotyrosine interaction. Thus, the output from Crk depends on the SH3-binding proteins, which include the C3G guanine nucleotide exchange protein for Rapl, Abl tyrosine kinase, DOCK 180, and the Sos guanine nucleotide exchange protein for Ras. The variety of the Crk-binding proteins indicate the pleiotropic function of Crk.

KEY WORDS: v-Crk, c-Crk, Crkll, CrkI, CrkL, oncogene, SH2, SH3

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