The Rac1 guanine nucleotide exchange factor, Vav, is activated in hematopoietic cells in response to a large variety of stimuli. The downstream signaling events derived from Vav have been primarily characterized as leading to transcription or ...

May 7, 1998 · Background: Vav is a guanine-nucleotide exchange factor for the Rho-like small GTPases RhoA, Rac1 and Cdc42, which regulate cytoskeletal reorganization and activation of stress-activated protein kinases (SAPK/JNKs).

Vav-L213A suppressed TCR-induced c-Jun phosphorylation, and N17Rac1 inhibited the effect of Vav, indicating that Vav stimulates c-Jun phosphorylation via a Rac1-dependent pathway. This activation of the JNK/c-Jun cascade correlated with the transcriptional activation of …

Vav1 is one of three members of the Vav family (the others being Vav2 and Vav3) of guanine nucleotide exchange factors (GEFs) for Rho-family GTPases. Vav1 is regarded primarily as a Rac GEF, but it can also activate RhoA, RhoG, and perhaps Cdc42 (Cdc42 is controversial).

Jul 2, 2015 · Vav1, a Rac/Rho guanine nucleotide exchange factor and a critical component of the T-cell receptor (TCR) signaling cascade is tyrosine phosphorylated rapidly in response to T-cell activation.

Vav also associated with Rac1 or Cdc42 in T cells, and anti-CD3 antibody stimulation enhanced this association. These findings indicate that a Rac1-dependent JNK/c-Jun/AP-1 pathway, rather than the Ca (2+)/NFAT pathway, plays the predominant role in NFAT-IL-2 activation by Vav.

Oct 17, 2001 · Using the Rac1 pathway, Vav impacts on the NF-AT route by inducing changes in the cytoskeleton that are subsequently translated into the activation of NF-AT by an as yet unknown mechanism .

Aug 3, 1998 · The Rac1 guanine nucleotide exchange factor, Vav, is activated in hematopoietic cells in response to a large variety of stimuli. The downstream signaling events derived from Vav have been primarily characterized as leading to transcription or transformation.

Jul 1, 2002 · These studies, together with experiments that used dominant-negative forms of Rac1 and RhoA 46,72, indicate that the GEF function of Vav is important for the induction of killing.

Aug 8, 1998 · In this study, we have provided both biochemical and genetic evidence that the Vav–Rac1 pathway regulates cell-mediated killing by CTLs.