Psychiatry related information on Plcd1

• It was previously demonstrated that an antibody to an isozyme of PLC, PLC-delta, produces intense staining of neurofibrillary tangles (NFT), the neurites surrounding senile plaque (SP) cores and neuropil threads in the brains of patients with Alzheimer's disease (AD) [1].

High impact information on Plcd1

• PLC-L2 is a novel PLC-like protein which lacks PLC activity, although it is very homologous with PLC delta [2].
• The phospholipase C (PLC)-beta isozymes differ from the PLC-gamma and PLC-delta isozymes in that they possess a long COOH-terminal sequence downstream of their catalytic domain, are activated by alpha subunits of the Gq class of G proteins, associate with the particulate subcellular fraction, and are present in the nucleus [3].
• Cells of the osteoblastic cell line MC3T3-E1 were shown to contain at least three phosphatidylinositol-specific phospholipase C (PI-PLC) isoenzymes (PLC-beta, PLC-gamma and PLC-delta) by Western blotting analysis with various anti-PLC antibodies [4].
• In the present study, an anti-PLC-delta antibody was used to examine the influence of glutamate on PLC-delta immunoreactivity in cultured rat cortical neurons [1].
• The glutamate-induced increase in PLC-delta immunoreactivity was also prevented by N omega-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor [1].

Biological context of Plcd1

• The map locations of seven of these genes were consistent with previously defined regions of conserved synteny; Plcd1 defines a new region of homology between human Chr 3 and mouse Chr 8 [5].

Anatomical context of Plcd1

• All the B cell lines tested expressed high levels of PLC alpha and PLC gamma 2 mRNA, whereas PLC beta and PLC delta mRNA expression were undetectable by both Northern blot and PCR analysis [6].
• Differentiating keratinocytes cultured in 1.4 mM Ca++ express two- to threefold more PLC-gamma 1 protein and PLC-delta 1, but no detectable PLC-beta 1 [7].
• The decreased PLC activity during chronic ethanol exposure may be caused by a decrease in the protein levels of the PLC-beta 1 isozyme but not of PLC-delta 1 or PLC-gamma 1 isozymes in the rat cerebral cortex [8].

Associations of Plcd1 with chemical compounds

• Both glutamate-induced neuronal degeneration and the increases in PLC-delta immunoreactivity were prevented by removal of extracellular Ca2+ or the application of an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 [1].

Other interactions of Plcd1

• These results suggest that NO formation secondary to Ca2+ influx by NMDA receptor activation leads to similar modifications of PLC-delta to those seen in AD [1].

References