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Phospholipase C, gamma 2

PLCgamma2, phospholipase Cgamma2
The protein encoded by this gene is a transmembrane signaling enzyme that catalyzes the conversion of 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate to 1D-myo-inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG), using calcium as a cofactor. IP3 and DAG are second messenger molecules important for transmitting signals from growth factor receptors and immune system receptors across the cell membrane. [provided by RefSeq, Sep 2011] (from NCBI)
Top mentioned proteins: PLC, Syk, Src, PLCgamma, V1a
Papers on PLCgamma2
Phospholipase Cγ2 plays a role in TCR signal transduction and T cell selection.
Wen et al., Milwaukee, United States. In J Immunol, 2012
PLCgamma2 participates in T cell receptor (TCR) signal transduction and plays a role in T cell selection in a transgenic mouse model.
Phospholipase Cγ-2 and intracellular calcium are required for lipopolysaccharide-induced Toll-like receptor 4 (TLR4) endocytosis and interferon regulatory factor 3 (IRF3) activation.
David et al., San Diego, United States. In J Biol Chem, 2012
a novel role of the PLCgamma2-IP(3)-Ca(2+) cascade in the LPS-induced innate immune response pathway where release of intracellular Ca(2+) mediates TLR4 trafficking and subsequent activation of IRF3.
VapB as a regulator of osteoclastogenesis via modulation of PLCγ2-Ca(2+)-NFAT signaling.
Lee et al., Iksan, South Korea. In Febs Lett, 2012
VapB positively regulates RANKL-mediated osteoclastogenesis via PLCgamma2-Ca(2+)-NFAT signaling
Cold urticaria, immunodeficiency, and autoimmunity related to PLCG2 deletions.
Milner et al., Bethesda, United States. In N Engl J Med, 2012
Genomic deletions in PLCG2 cause gain of PLCgamma(2) function, leading to signaling abnormalities in multiple leukocyte subsets and a phenotype encompassing both excessive and deficient immune function.
Phospholipase Cγ2 (PLCγ2) is key component in Dectin-2 signaling pathway, mediating anti-fungal innate immune responses.
Lin et al., Houston, United States. In J Biol Chem, 2012
PLCgamma2 deficiency impairs Dectin-2-induced NF-kappaB and MAPK activation in response to fungal infection
Syk mediates BCR- and CD40-signaling integration during B cell activation.
Zhang et al., Chicago, United States. In Immunobiology, 2011
CD40 stimulation alone also activates B cell linker (BLNK), Bruton tyrosine kinase (Btk), and Vav-2 downstream of Syk, and significantly enhances BCR-induced formation of complex consisting of, Vav-2, Btk, BLNK, and phospholipase C-gamma2 (PLC-γ2) leading to activation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase, Akt, and NF-κB required for optimal B cell activation.
A novel interaction between FlnA and Syk regulates platelet ITAM-mediated receptor signaling and function.
Hartwig et al., Boston, United States. In J Exp Med, 2010
FlnA-null platelets fail to spread and have decreased alpha-granule secretion, integrin alphaIIbbeta3 activation, and protein tyrosine phosphorylation, particularly that of the protein tyrosine kinase Syk and phospholipase C-gamma2, in response to stimulation through the collagen receptor GPVI and the C-type lectin-like receptor 2. This signaling defect was traced to the loss of a novel FlnA-Syk interaction, as Syk binds to FlnA at immunoglobulin-like repeat 5. Our findings reveal that the interaction between FlnA and Syk regulates ITAM- and ITAM-like-containing receptor signaling and platelet function.
Reducing glycosphingolipid biosynthesis in airway cells partially ameliorates disease manifestations in a mouse model of asthma.
Cheng et al., Framingham, United States. In Int Immunol, 2010
Lowering GSL levels in mast cells through inhibition of glucosylceramide synthase (GCS) reduced phosphorylation of Syk tyrosine kinase and phospholipase C gamma 2 (PLC-gamma2) as well as cytoplasmic Ca(2+) levels.
GPVI and CLEC-2 in hemostasis and vascular integrity.
Pollitt et al., Birmingham, United Kingdom. In J Thromb Haemost, 2010
Cross-linking of the Ig GPVI leads to phosphorylation of two conserved tyrosines in the FcR gamma-chain ITAM by Src family tyrosine kinases, followed by binding and activation of the tandem SH2 domain-containing Syk tyrosine kinase and stimulation of a downstream signaling cascade that culminates in activation of phospholipase Cgamma2 (PLCgamma2).
B cell receptor-mediated calcium signaling is impaired in B lymphocytes of type Ia patients with common variable immunodeficiency.
Warnatz et al., Freiburg, Germany. In J Immunol, 2010
Although proximal BCR signaling events are unperturbed in patients' B cells, including normal phospholipase Cgamma2 phosphorylation and Ca2+ release from intracellular stores, Ca2+ influx from the extracellular space is significantly impaired.
Killing tumor cells through their surface beta(2)-microglobulin or major histocompatibility complex class I molecules.
Yi et al., Houston, United States. In Cancer, 2010
Antibodies against beta(2)M or MHC class I induce tumor cell apoptosis by 1) recruiting MHC class I molecules to lipid rafts and activating LYN kinase and the signal-transducing enzyme phospholipase C-gamma2-dependent c-Jun N-terminal kinase signaling pathway and 2) expelling interleukin 6 and insulin-like growth factor 1 receptors out of lipid rafts and inhibiting the growth and survival factor-induced activation of the phosphatidylinositol 3-kinase/Akt and extracellular signal-related kinase pathways.
PLCgamma2: where bone and immune cells find their common ground.
Cremasco et al., Saint Louis, United States. In Ann N Y Acad Sci, 2010
PLCgamma2 is a critical regulator of the cellular and molecular mechanisms occurring in bone and immune cells during autoimmune inflammation.
Synergistic signals for natural cytotoxicity are required to overcome inhibition by c-Cbl ubiquitin ligase.
Long et al., Rockville, United States. In Immunity, 2010
Synergistic phosphorylation of phospholipase PLC-gamma2, Ca(2+) mobilization, and degranulation triggered by NKG2D and 2B4 coengagement were blocked by Vav1 siRNA knockdown, but enhanced by knockdown of c-Cbl.
Cyclic nucleotides and mitogen-activated protein kinases: regulation of simvastatin in platelet activation.
Sheu et al., Taipei, Taiwan. In J Biomed Sci, 2009
SQ22536, an inhibitor of adenylate cyclase, markedly reversed the simvastatin-mediated inhibitory effects on platelet aggregation, PLCgamma2 and p38 MAPK phosphorylation, and simvastatin-mediated stimulatory effects on VASP and eNOS phosphorylation.
CD14 regulates the dendritic cell life cycle after LPS exposure through NFAT activation.
Granucci et al., Milano, Italy. In Nature, 2009
Here we show that mouse dendritic cell stimulation with lipopolysaccharide (LPS) induces Src-family kinase and phospholipase Cgamma2 activation, influx of extracellular Ca(2+) and calcineurin-dependent nuclear NFAT translocation.
Novel interactions in platelet biology: CLEC-2/podoplanin and laminin/GPVI.
Inoue et al., Japan. In J Thromb Haemost, 2009
CLEC-2 is specifically expressed in platelets and megakaryocytes, and has an atypical ITAM, which undergoes tyrosine phosphorylation by Src kinases, resulting in downstream signaling including Syk, SLP-76 and PLCgamma2.
Control of the B cell-intrinsic tolerance programs by ubiquitin ligases Cbl and Cbl-b.
Gu et al., New York City, United States. In Immunity, 2007
Concomitantly, BCR-proximal signaling, including tyrosine phosphorylation of Syk tyrosine kinase, Phospholipase C-gamma2 (PLC-gamma2), and Rho-family GTP-GDP exchange factor Vav, and Ca2+ mobilization were enhanced, whereas tyrosine phosphorylation of adaptor protein BLNK was substantially attenuated in the mutant B cells.
Bruton's tyrosine kinase and phospholipase Cgamma2 mediate chemokine-controlled B cell migration and homing.
Spaargaren et al., Amsterdam, Netherlands. In Immunity, 2007
Furthermore, SDF-1 induced tyrosine phosphorylation of Phospholipase Cgamma2 (PLCgamma2), which, unlike activation of the migration regulatory GTPases Rac or Rap1, was mediated by Btk.
Targeting beta2-microglobulin for induction of tumor apoptosis in human hematological malignancies.
Yi et al., Houston, United States. In Cancer Cell, 2006
The mAbs induced cell death via recruiting MHC class I molecules to lipid rafts and activating Lyn and PLCgamma2, leading to activated JNK and inhibited PI3K/Akt and ERK, compromised mitochondrial integrity, and caspase-9-dependent cascade activation.
Regulation of phospholipase C-gamma2 networks in B lymphocytes.
Kurosaki et al., Yokohama, Japan. In Adv Immunol, 2004
The modulation of inositol-1,4,5-trisphosphate (IP3), a product of phospholipase C (PLC) activity, is one of a common signaling mechanism used in many biological systems.
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