Vav3 Mediates Receptor Protein Tyrosine Kinase Signaling, Regulates GTPase Activity, Modulates Cell Morphology, and Induces Cell Transformation

Zeng, Liyu; Sachdev, Pallavi; Yan, LunBiao; Chan, Joseph L.-K.; Trenkle, Thomas; McClelland, Michael; Welsh, John; Wang, Lu‐Hai

doi:10.1128/mcb.20.24.9212-9224.2000

Cited by 129 publications

(146 citation statements)

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“…The overexpression of these C-terminal domains leads to a dominant negative e ect in T-cells, mast cells, and ®broblasts, probably by blocking the interaction of the autophosphorylated kinases with the endogenous Vav proteins (Arudchandran et al, 2000;Wu et al, 1996;unpublished observations Figure 1a). Interestingly, the expression of these proteins does not overlap with the full length proteins (Okumura et al, 1997;Zeng et al, 2000). These results suggest these other versions of Vav proteins have functional roles of their own, probably by working as adaptor proteins in some speci®c pathways.…”

Section: Vav Proteins: Catalytic and Adaptor Functions?mentioning

confidence: 68%

“…There are two possible, although not mutually exclusive, mechanisms for such regulation. Since Vav proteins can bind to the regulatory subunit (p85) of phosphatidylinositol-3-OH kinase (PI3-K) (Weng et al, 1994;Zeng et al, 2000), one possibility is that Vav could induce the translocation of PLC-g1 to the plasma membrane via the generation of PI3-K products. In this respect, it has been shown that phosphatidylinositol 3,4,5-trisphosphate (PIP 3 ) can trigger such translocation by interacting with the PH (Falasca et al, 1998).…”

Section: Vav Proteins: Catalytic and Adaptor Functions?mentioning

confidence: 99%

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Vav proteins, adaptors and cell signaling

2001

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The Vav family is a group of signal transduction molecules with oncogenic potential that play important roles in development and cell signaling. Members of this family are distributed in all animal metazoans but not in unicellular organisms. Recent genomic studies suggest that the function of Vav proteins co-evolved with tyrosine kinase pathways, probably to assure the optimal conversion of extracellular signals into biological responses coupled to the cytoskeleton and gene transcription. To date, the best-known function of Vav proteins is their role as GDP/GTP exchange factors for Rho/Rac molecules, a function strictly controlled by tyrosine phosphorylation. Recent publications indicate that this function is highly dependent on the interaction of adaptor proteins that aid in the proper phosphorylation of Vav proteins, their interaction with other signaling molecules, and in modulating the strength of their signal outputs. In addition to the function of Vav proteins as exchange factors, there is increasing evidence suggesting that Vav proteins can mediate other cellular functions independently of their exchange activities, probably by working themselves as adaptor molecules. In this review, we will give a summary of the recent advances in this ®eld, placing special emphasis on the non-catalytic roles of Vav and its interaction with other adaptor molecules. Oncogene (2001) 20, 6372 ± 6381.

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Section: Vav Proteins: Catalytic and Adaptor Functions?mentioning

confidence: 68%

Section: Vav Proteins: Catalytic and Adaptor Functions?mentioning

confidence: 99%

Vav proteins, adaptors and cell signaling

2001

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“…The normal and BE clusters were clearly defined, with only 1 ADC sample clustering with the BE, interestingly next to the ADC sample from the same patient (42). The BE and ADC samples for another patient (60), also clustered next to each other on the ADC branch.…”

Section: Analysis Of Tissue Typesmentioning

confidence: 80%

“…Vav3 has been implicated in control of cytokinesis, its deregulation leads to cytoskeletal changes. 41,42 Vav3 clusters with desmoplakin (DSP), a constituent of the cytoskeleton, as well as genes involved with lipid and protein binding. A calcium-ion binding and cell junction subcluster was also identified within E, which includes DSG1 and GJB2.…”

Section: Cluster Analysis Of Genesmentioning

confidence: 99%

Gene expression profiling of esophageal cancer: Comparative analysis of Barrett's esophagus, adenocarcinoma, and squamous cell carcinoma

Greenawalt¹,

Duong²,

Smyth³

et al. 2007

Intl Journal of Cancer

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Esophageal cancer is a particularly aggressive tumor with poor prognosis, however, our current knowledge of the genes and pathways involved in tumorigenesis of the esophagus are limited. To obtain insight into the molecular processes underlying tumorigenesis of the esophagus, we have used cDNA microarrays to compare the gene expression profiles of 128 tissue samples representing the major histological subtypes of esophageal cancer (squamous cell carcinoma and adenocarcinoma (ADC)) as well as Barrett's esophagus (BE), the precursor lesion to ADC, and normal esophageal epithelium. Linear discriminant analysis and unsupervised hierarchical clustering show the separation of samples into 4 distinct groups consistent with their histological subtype. Differentially expressed genes were identified between each of the tissue types. Comparison of gene ontologies and gene expression profiles identified gene profiles specific to esophageal cancer, as well as BE. “Esophageal cancer clusters,” representing proliferation, immune response, and extracellular matrix genes were identified, as well as digestion, hydrolase, and transcription factor clusters specific to the columnar phenotype observed during BE and esophageal ADC. These clusters provide valuable insight into the molecular and functional differences between normal esophageal epithelium, BE, and the 2 histologically distinct forms of esophageal cancers. Our thorough, unbiased analysis provides a rich source of data for further studies into the molecular basis of tumorigenesis of the esophagus, as well as identification of potential biomarkers for early detection of progression. © 2007 Wiley‐Liss, Inc.

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“…CXCL12 activation of PI3Ks has also been shown to mediate similar effects in human peripheral blood leukocytes [99]. PI3Ks mediate chemotaxis and cell polarization by activating the small GTPase Rho and Rac possibly providing a link for interaction with the GTP exchange factor, Vav [100,101]. Vav, however, has not been shown to be activated by chemokines.…”

Section: Phosphoinositide 3-kinase (Pi3k) and Other Signaling Eventsmentioning

confidence: 99%