Disease relevance of Plcb1

• The data also showed that only a PLC beta1 linked to a Pertussis toxin-insensitive G-protein and a PLC beta2 coupled to a Pertussis toxin-sensitive G-protein are involved in the effects of calcitriol and 17beta estradiol on the mobilization of Ca2+ from intracellular Ca2+ stores [1].
• Antisense constructs, consisting of the cytomegalovirus promoter driving antisense cRNA corresponding to the 3'-untranslated regions of PLC-beta1 and PLC-beta4, were injected into the nucleus of dissociated SCG neurons [2].
• Cross-talk between receptor-mediated phospholipase C-beta and D via protein kinase C as intracellular signal possibly leading to hypertrophy in serum-free cultured cardiomyocytes [3].
• Expression of Gq alpha and PLC-beta in scar and border tissue in heart failure due to myocardial infarction [4].
• Gq alpha and PLC-beta may play important roles in scar remodeling as well as cardiac hypertrophy and fibrosis of the surviving tissue in post-MI rat heart [4].

High impact information on Plcb1

• Those of PLC-I and III were short and appeared to be unrelated to these tyrosine kinases [5].
• Here, phospholipase C-related cDNA clones corresponding to PLC-I and PLC-III were isolated from a rat brain lambda gt11 expression cDNA library using specific monoclonal antibodies and sequenced [5].
• Cytosolic phosphatidylinositol transfer protein (PITP) is necessary for guanosine triphosphate (GTP)-dependent hydrolysis of PIP2 by phospholipase C-beta (PLC-beta), but the role of PITP is unclear [6].
• M(1) muscarinic (M(1)AChRs) and B(2) bradykinin (B(2)Rs) receptors are two PLCbeta-coupled receptors that mobilize Ca(2+) in nonexcitable cells [7].
• In contrast, NE also increased PLC beta 1 but did not affect PLC gamma 1 protein expression in membranes [8].

Chemical compound and disease context of Plcb1

• The association of PLC-beta1 and Gi/o-type G proteins was studied by pertussis toxin-catalyzed [32P]adenosine diphosphate ribosylation of PLC-beta1 immunoprecipitates [9].
• Applied as a model substance for the stimulation of the phosphoinositide-phospholipase C pathway, angiotensin II has been used to simulate the bronchospasm of smooth muscle in asthma [10].
• These receptors are coupled to phospholipase C beta and to dihydropyridine-sensitive calcium channels via heterotrimeric G proteins differing by their sensitivities to pertussis toxin [11].

Biological context of Plcb1

• However, recent studies showed that rat aortic VSMC do not express PLC beta-1 and that stimulation with angiotensin-II induces tyrosine kinase dependent increases in [Ca2+]i and tyrosine phosphorylation of PLC gamma-1 [12].
• A functional involvement of this PLC beta subtype in taste signal transduction emerged from biochemical analysis monitoring the second messenger response in circumvallate preparations induced by denatonium benzoate [13].
• BK inhibition of I(K(M)) was significantly reduced 48 hr after injection of the PLC-beta4, but not the PLC-beta1, antisense-encoding plasmid [2].
• Two forms of phospholipase C-beta 1 generated by alternative splicing [14].
• The presence of the 118-nucleotide insert in the cumulative 7.2-kb sequence gives rise to an open reading frame that is capable of coding a 1173-amino acid polypeptide (PLC-beta 1b), the carboxyl-terminal sequence of which differs from that of the 1216-amino acid polypeptide (PLC-beta 1a) derived from the 5.4-kb transcript [14].

Anatomical context of Plcb1

• Through interactions with PDZ domains, this motif may endow the PLC-beta isozyme with specific roles in GPCR signaling events that occur in compartmentalized regions of the plasma membrane [15].
• The data showed that phospholipase C beta was involved in the mobilization of Ca2+ from the endoplasmic reticulum of Fura-2-loaded confluent osteoblasts by calcitriol and 17beta estradiol, and PLC gamma was ineffective [1].
• Since G proteins activate IP3 production via stimulation of phospholipase C beta isoforms in many tissues, and agonist-stimulated IP3 production in smooth muscle requires G protein activation, phospholipase C beta 2 may be required for agonist-stimulated force production in vascular smooth muscle [16].
• However, the levels of PLC-beta1, PLC-beta3, and PLC-beta4 were significantly lower in the hippocampus of RHA/Verh than in RLA/Verh rats [17].
• PLC-beta isozymes (beta1, beta2, beta3, and beta4), delta1, and delta2 were detected in both acinar and islet cells, whereas PLC-gamma1 and gamma2 were observed only in acinar tissues [18].

Associations of Plcb1 with chemical compounds

• Phospholipase C beta and membrane action of calcitriol and estradiol [1].
• RATIONALE: One of the major pathways for neurotransmitter signaling involves phosphoinositide-specific and G-protein-dependent phospholipase C-beta (PLC-beta), which stimulates the formation of inositol 1,4,5-trisphosphate and diacylglycerol [17].
• Membrane signaling and progesterone in female and male osteoblasts. II. Direct involvement of G alpha q/11 coupled to PLC-beta 1 and PLC-beta 3 [19].
• An opposite order of sensitivity was found for inhibition of PLC activity by anti-PLC-beta 3 antibody (carbachol > bombesin > CCK-8) [20].
• Temporal dispersion of activation of phospholipase C-beta1 and -gamma isoforms by angiotensin II in vascular smooth muscle cells. Role of alphaq/11, alpha12, and beta gamma G protein subunits [21].

Regulatory relationships of Plcb1

• Fibroblast growth factor-2 stimulates phospholipase Cbeta in adult cardiomyocytes [22].
• Endothelin-1-induced phospholipase C-beta and D and protein kinase C isoenzyme signaling leading to hypertrophy in rat cardiomyocytes [23].
• However, following unilateral olfactory bulbectomy (OBX), PLC beta 1 was expressed in the dentrites of some olfactory receptor neurons, primarily in the endoturbinates on the unoperated side [24].
• However, regulation of PPII activity by TRH was inhibited by a phospholipase C beta inhibitor or chelation of intracellular calcium [25].
• Finally, the Ca2+ responses stimulated by PACAP38 and VIP were blocked by the phospholipase C-beta blocker U73122 (5 microM) [26].

Other interactions of Plcb1

• The C terminus of PLC-beta3, but not other PLC-beta isotypes, specifically interacts with the PDZ domain of Shank2 [15].
• PKC-epsilon, -gamma, and -lambda and PLC-beta1, -beta2, and -beta4 were not present in adult or newborn type II cells [27].
• The order of sensitivity toward inhibition by anti-PLC-beta 1 antibody was CCK-8 > bombesin > carbachol [20].
• In cultured VSMC, PLC-gamma 1 and PLC-delta 1 isozymes, but not PLC-beta 1, were identified by Western analysis [28].
• Merkel cells showed positive immunoreactions of PLC-beta1 and mGluR5 [29].

Analytical, diagnostic and therapeutic context of Plcb1

• Western blot analysis of pancreatic acinar membranes revealed the presence of PLC-beta 1, -beta 3, -gamma 1, and -delta 1, but not of PLC-beta 2, -beta 4, -gamma 2, and -delta 2 [20].
• RT-PCR and antibody staining confirmed the presence of PLC-beta1, -beta2, -beta3, and -beta4 in rat SCG [2].
• Ang II-stimulated inositol trisphosphate (IP3) formation measured at 15 s, which corresponds to the peak response, was significantly inhibited by electroporation of antibodies against PLC-beta1, but not by anti-PLC-gamma and -delta antibodies [21].
• Immunoblotting analysis revealed the expression of PLC beta 3 and -gamma 1, but not PLC beta 1, -beta 2, or -beta 4 in the rat colonic epitheliums [30].
• We, therefore, reinvestigated immunohistochemical affinities to MCs of antibodies to PLC-beta isozymes and mGluRs using frozen sections of rat sinus hair follicles that were briefly postfixed in formaldehyde [29].

References