The Nck family of adapter proteins

Buday, László; Wunderlich, Lívius; Tamás, Péter

doi:10.1016/s0898-6568(02)00027-x

Cited by 216 publications

(72 citation statements)

References 118 publications

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“…The activation of Flk-1 induced by VEGF may result in the activation of the guanine exchange factor Sos through Nck␤ and other adaptor proteins (13). Sos has been known to stimulate Ras, which subsequently activates its downstream signaling molecules MEK1 and ERK (24).…”

Section: Discussionmentioning

confidence: 99%

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Selective adapter recruitment and differential signaling networks by VEGF vs. shear stress

Wang¹,

Chang²,

Chen³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Section: Discussionmentioning

confidence: 99%

“…The activated PAK can ultimately induce the JNK activation (12). The SH3 domains of Nck␤ have also been shown to bind a guanine exchange factor Sos (11), which could further activate Ras and ERK (13).…”

mentioning

confidence: 99%

Selective adapter recruitment and differential signaling networks by VEGF vs. shear stress

Wang¹,

Chang²,

Chen³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…In this sense, Cbp could be one of the candidate targets. Because Cbp has multiple phosphorylatable tyrosine residues other than Csk binding site, it is possible that Cbp plays some additional roles by recruiting adapter proteins having SH2 or phosphotyrosine-binding domain, such as Shc and Nck, both of which have been implicated in cell adhesion signaling (40,47). Contributions of these potential targets are now under investigation.…”

Section: Discussionmentioning

confidence: 99%

Transmembrane phosphoprotein Cbp senses cell adhesion signaling mediated by Src family kinase in lipid rafts

Shima

Nada

Okada

2003

Proc. Natl. Acad. Sci. U.S.A.

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“…The Nck family of proteins have been proposed to play a role in the regulation of the actin cytoskeleton and cell movement (Buday et al, 2002). The integrin-dependent interaction between FAK and Plcg or PI3-kinase suggests that FAK plays a role in inositol lipid metabolism and phospholipid signaling.…”

Section: Srcmentioning

confidence: 99%

The interplay between Src and integrins in normal and tumor biology

2004

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Src family nonreceptor protein tyrosine kinases transduce signals that control normal cellular processes such as cell proliferation, adhesion and motility. Normally, cellular Src is held in an inactive state, but in several cancer types, abnormal events lead to elevated kinase activity of the protein and cause pleiotropic cellular responses inducing transformation and metastasis. A prerequisite of the ability of a cancer cell to undergo metastasis into distant tissues is to penetrate surrounding extracellular matrices. These processes are facilitated by the integrin family of cell adhesion molecules. As is the case with Src, altered integrin activity or substrate affinity can contribute to the neoplastic phenotype. Therefore, understanding the interplay between Src and integrin function has been of intense interest over the past few years. This review focuses on the role of Src and integrin signaling in normal cells and how this is deregulated in human cancer. We will identify the key players in the integrin-mediated signaling pathways involved in cell motility and apoptosis, such as FAK, paxillin and p130 CAS , and discuss how Src signaling affects the formation of focal adhesions and the extracellular matrix.

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The Nck family of adapter proteins

Cited by 216 publications

References 118 publications

Selective adapter recruitment and differential signaling networks by VEGF vs. shear stress

Selective adapter recruitment and differential signaling networks by VEGF vs. shear stress

Transmembrane phosphoprotein Cbp senses cell adhesion signaling mediated by Src family kinase in lipid rafts

The interplay between Src and integrins in normal and tumor biology

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