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Phosphoinositide-specific phospholipase C C

Unless otherwise stated all data on this page refer to the human proteins. Gene information is provided for human (Hs), mouse (Mm) and rat (Rn).


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Phosphoinositide-specific phospholipase C (PLC, EC, catalyses the hydrolysis of PIP2 to IP3 and 1,2-diacylglycerol, each of which have major second messenger functions. Two domains, X and Y, essential for catalytic activity, are conserved in the different forms of PLC. Isoforms of PLC-β are activated primarily by G protein-coupled receptors through members of the Gq/11 family of G proteins. The receptor-mediated activation of PLC-γ involves their phosphorylation by receptor tyrosine kinases (RTK) in response to activation of a variety of growth factor receptors and immune system receptors. PLC-ε1 may represent a point of convergence of signalling via both G protein-coupled and catalytic receptors. Ca2+ ions are required for catalytic activity of PLC isoforms and have been suggested to be the major physiological form of regulation of PLC-δ activity. PLC has been suggested to be activated non-selectively by the small molecule m3M3FBS [2], although this mechanism of action has been questioned [12]. The aminosteroid U73122 has been described as an inhibitor of phosphoinositide-specific PLC [20], although its selectivity among the isoforms is untested and it has been reported to occupy the H1 histamine receptor [8].


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PLCβ1 C Show summary »

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PLCγ1 C Show summary » More detailed page go icon to follow link

PLCγ2 C Show summary » More detailed page go icon to follow link

PLCδ1 C Show summary »

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PLCε1 C Show summary »

PLCζ1 C Show summary »

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How to cite this family page

Database page citation:

Phosphoinositide-specific phospholipase C. Accessed on 24/07/2024. IUPHAR/BPS Guide to PHARMACOLOGY,

Concise Guide to PHARMACOLOGY citation:

Alexander SPH, Fabbro D, Kelly E, Mathie AA, Peters JA, Veale EL, Armstrong JF, Faccenda E, Harding SD, Davies JA et al. (2023) The Concise Guide to PHARMACOLOGY 2023/24: Enzymes. Br J Pharmacol. 180 Suppl 2:S289-373.