Target intelligence / Profile preview

Inactive phospholipase C-like protein 2 (PLCL2)

Target
PLCL2
Molecular classification
Enzyme (phospholipase C-like family, though catalytically inactive), Signal transduction molecule, C2 domain containing protein
01

Overview

Inactive phospholipase C-like protein 2 (PLCL2) is a member of the phospholipase C (PLC) protein family that, while structurally related to active PLC enzymes, lacks enzymatic activity. Unlike classical PLCs, which hydrolyze phosphatidylinositol 4,5-bisphosphate (PIP2) to generate second messengers and control calcium signaling[1][3], PLCL2 lacks the essential catalytic residues and instead participates in regulatory roles within signaling pathways. It is specifically involved in GABA receptor binding, modulation of immune cell functions (particularly B cells), and plays a part in regulating the GABAergic synaptic transmission and responses to cold-induced thermogenesis[2][4]. Genome-wide association studies implicate PLCL2 in cardiovascular diseases (including myocardial infarction and atherosclerosis) and as a tumor suppressor whose loss can contribute to colon cancer[2][4]. PLCL2’s primary biological importance is regulatory, modulating diverse processes through protein-protein interactions and signaling scaffolding, especially in hematopoietic cells and neuronal tissues[2][4]. There are currently no drugs in clinical use that directly target PLCL2.

Other names
PLCE2KIAA1092PLC-L2PLC-epsilon-2Phospholipase C-L2phospholipase C-epsilon-2PLC-L(2)
02

Biological functions

Gamma-aminobutyric acid (GABA) receptor bindingNegative regulation of cold-induced thermogenesisRegulation of GABAergic synaptic transmissionB cell proliferation involved in immune responseB-1a B cell differentiationNegative regulation of B cell receptor signaling pathway
03

Disease associations

Cardiovascular disease (myocardial infarction, atherosclerosis)Stroke (large artery atherosclerotic stroke)Cancer (tumor suppressor role in colon cancer)Other immune-related conditions (based on expression in lymphocytes and role in B cell biology)
04

Safety considerations

Loss of function associated with immune dysregulation (altered B cell proliferation)Hypermethylation/deletion associated with increased tumor risk (colon cancer)Potential complex systemic effects if modulated therapeutically, given non-catalytic, regulatory roles

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