X-RAY CRYSTALLOGRAPHY (2.6 ANGSTROMS) OF 35-359 IN COMPLEX WITH GNAQ, FUNCTION, CATALYTIC ACTIVITY, ACTIVITY REGULATION, MUTAGENESIS OF ARG-258; ASN-260; TYR-855; LEU-859; ASN-861; PRO-862 AND ILE-863
This study reveals detailed mechanistic insight into the role of ORP4L in PLCbeta3 redistribution from storage within the nucleus to the plasma membrane via RAN activation and interaction with VAPA in Jurkat T-cells.
These results besides identifying S845L as a loss-of-function variant strengthen the importance of targeting PLCB3 to mitigate the cystic fibrosis inflammatory response in bronchial epithelial cells without blunting the immune response.
Data suggest that 300-residue C-terminal domain of PLCB3 promotes adsorption to phospholipid monolayer/membrane bilayer and is required for spatial organization/adsorption of PLCB3 on membrane surface; defects in phosphatidylinositol 4 5-bisphosphate (PIP2) hydrolysis alter monolayer adsorption thus suggesting role of active site in this process; PLCB3 is preferentially adsorbed to region of bilayer enriched with PIP2.
These results indicate that the mechanism by which Galphaq and PLC-beta3 mutually regulate each other is far more complex than a simple two-state allosteric model and instead is probably kinetically determined.
Stromal cell-derived factor-1 signaling via the CXCR4-TCR heterodimer uses PLC-beta3 to activate the Ras-ERK pathway and increase intracellular calcium ion concentrations
Data demonstrate that PLCB3 by regulating intracellular calcium transients plays a relevant role in amplifying the expression and release of IL-8 the major chemokine recruiting neutrophils in CF airway lungs.
Activation of hPLCbeta3 by U73122 required covalent modification of cysteines as evidenced by the observation that enzyme activation was attenuated by thiol-containing nucleophiles l-cysteine and glutathione.
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