Protein VAV1 map

Identifiers
HUGO:VAV1
vav 1 guanine nucleotide exchange factor
HUGO:VAV1, HGNC:12657, ENTREZ:7409, GENECARDS:GC19P006772, UNIPROT:P15498

Maps_Modules
HMC:AVOIDING_IMMUNE_DESTRUCTION
 Adaptive Immune Response  map  / TCR_SIGNALING  map
HMC:ACTIVATING_INVASION_AND_METASTASIS
 EMT Senescence  map  / EMT_REGULATORS  map
 EMT Senescence  map  / CYTOSKELETON_POLARITY  map
 Innate Immunity  map  / IMMUNOSTIMULATORY_CORE_PATHWAYS  map

References
PMID:10714681 PMID:25539813 PMID:12186560 PMID:11754814 PMID:10849438 PMID:10077632 PMID:9438848 PMID:10898494 PMID:14764585 PMID:11994416 PMID:10646608 PMID:11526404 PMID:12616499 PMID:26552706
VAV1,2 are GEFs for Rac1.
PMID:11080163
VAV2 is recruited by the CD19 co-receptor of the B cells and participates in the B cell receptor signaling.
PMID:12165654
in the T cell, VAV1 forms complex with LCP2.
This complex is involved in the T cell receptor and CD28 signaling cascades.
 NATURAL_KILLER  map
 MACROPHAGE  map
 MAST_CELL  map
CASCADE:KIR2DL1
CASCADE:SLAMF7
CASCADE:2B4
CASCADE:NKG2D
CASCADE:LFA1
CASCADE:Fc_gamma_RI
CASCADE:Fc_gamma_RII
CASCADE:Fc_gamma_RIII
CASCADE:INTEGRIN_A4B1
CASCADE:INTEGRIN_A5B1
PMID:12740575, PMID:16887996
VAV1 activates RHOA and RAC1 downstream of NKG2D.
PMID:11698448
RHOA signaling in NK cells provides development of natural cytotoxicity against tumor cells.
PMID:16887996
Vav1 is required for actin accumulation at the NK-target contact site in response to NKG2D-DAP10 signals,
probably via RHOA pathway.
Vav1 induces MTOC polarization at the NK-target contact site in response to NKG2D-DAP10 signals.
PMID:20189481, PMID:22786724
NKG2D, DNAM1, 2B4 signalings induce PLCG2 phosphorylation and Ca2+ release via LCP2/VAV1 pathway.
CBL inhibited Vav1-dependent activation signals in NK.
Vav-deficient NK cells exhibited nearly abolished conjugate formation and cytotoxicity toward target cells.
PMID:15169881
2B4 signaling induces phosphorylation of SHIP1,VAV1 (probably via LCP2),CBL.
This phosphorylation is dependent on SAP adn FYN.
PMID:25355530, PMID:12917349, PMID:22952938, PMID:22513334
SHP-1-mediated inhibitory signals promote responsiveness and anti-tumour functions of natural killer cells.
Gene silencing of the SHP-1 in primary NK cells abrogated the ability of ITIM-containing NK inhibitory receptors to suppress the activation signals induced by NK1.1 activating receptors.
Vav1 dephosphorylation by the tyrosine phosphatase PTPN-6 (SHP-1) as a mechanism for inhibition.
of cellular cytotoxicity downstream of KIR-receptor (KIR2DL1).
PMID:10679059, PMID:12626562
PTK2B, PYK2. Binding of NK cells to sensitive target cells or ligation of ??2 integrins results in a rapid induction of Pyk2 phosphorylation and activation.
y contrast, no detectable Pyk2 tyrosine phosphorylation is found upon CD16 stimulation.
Pyk2 activation is a crucial event for natural but not Ab-dependent cytotoxicity.
Ligation of Beta2 integrins on NK cells resulted in Pyk2-dependent Erk activation, provavli via VAV1/RAC1 pathway.
Pyk-2-mediated control of integrin-triggered Rac-1 activation involves the regulation of Vav tyrosine phosphorylation.
PMID:12885870, PMID:22786724
LFA1 signaling induces tyrosine phosphorylation of Vav1 via
Src-family kinases but not Syk or ZAP70. Probably it acts via DNAM1 which
can induce selective phosphorylation of SLP-76.
Vav1 phosphorylation is induced by beta2 integrin (CD18)engagement on natural killer cells upstream of actin cytoskeleton and lipid raft reorganization.
PMID:8189062
Stimulation of macrophage Fc gamma RIIIA activates the receptor-associated protein tyrosine kinase Syk and induces phosphorylation of multiple proteins including p95Vav and p62/GAP-associated protein.
PMID:8226994
Stimulation of the human monocytic cell line THP-1 by cross-linking either Fc gamma receptor I (Fc gamma RI) or Fc gamma receptor II (Fc gamma RII) gave rise to the rapid phosphorylation of multiple intracellular proteins. The pattern of proteins that were phosphorylated appeared to be identical. Analysis of these proteins by specific immunoprecipitation indicated that stimulation through either receptor did indeed give rise to phosphorylation of the same set of proteins. These included: Fc gamma RII, phospholipase C (PLC) gamma 1, PLC gamma 2, Vav, GAP
PMID:19909365
LAT1 binds to multiple signaling proteins
including GEFs such as Vav1 and SOS, which regulate the activity of small GTPases
in Mast cells

VAV1|​pho|​active@INNATE_IMMUNE_CELL_Cytosol

References
in_re167( Innate Immunity  map ):
PMID:??12094222??
VAV proteins activate RAC1 via induction of GDP/GTP exchange.

Modifications:
In compartment: INNATE_IMMUNE_CELL_Cytosol
  1. VAV1@INNATE_IMMUNE_CELL_Cytosol map
  2. VAV1|​ubi@INNATE_IMMUNE_CELL_Cytosol map
  3. VAV1|​pho|​active@INNATE_IMMUNE_CELL_Cytosol map
Participates in complexes:
    Participates in reactions:
    As Reactant or Product:
    1. VAV1@INNATE_IMMUNE_CELL_Cytosol map → map VAV1|​pho|​active@INNATE_IMMUNE_CELL_Cytosol map
    2. VAV1|​ubi@INNATE_IMMUNE_CELL_Cytosol map → map degraded
    3. VAV1@INNATE_IMMUNE_CELL_Cytosol map → map VAV1|​ubi@INNATE_IMMUNE_CELL_Cytosol map
    4. VAV1|​pho|​active@INNATE_IMMUNE_CELL_Cytosol map → map VAV1@INNATE_IMMUNE_CELL_Cytosol map
    5. VAV1|​pho|​active@INNATE_IMMUNE_CELL_Cytosol map → map Conjugate_formation@INNATE_IMMUNE_CELL_Membrane map
    As Catalyser:
    1. GDP:​RAC1_2*@INNATE_IMMUNE_CELL_Cytosol map + GTP@INNATE_IMMUNE_CELL_Cytosol map → map (GTP:​RAC1_2*)|​active@INNATE_IMMUNE_CELL_Cytosol map + GDP@INNATE_IMMUNE_CELL_Cytosol map
    2. PLCG2@INNATE_IMMUNE_CELL_Cytosol map → map PLCG2|​pho@INNATE_IMMUNE_CELL_Cytosol map
    3. GDP:​RHOA@INNATE_IMMUNE_CELL_Cytosol map + GTP@INNATE_IMMUNE_CELL_Cytosol map → map (GTP:​RHOA)|​active@INNATE_IMMUNE_CELL_Cytosol map + GDP@INNATE_IMMUNE_CELL_Cytosol map
    4. CDC42:​GDP@INNATE_IMMUNE_CELL_Cytosol map + GTP@INNATE_IMMUNE_CELL_Cytosol map → map (CDC42:​GTP)|​active@INNATE_IMMUNE_CELL_Cytosol map + GDP@INNATE_IMMUNE_CELL_Cytosol map