Ignet

Gene Information

Gene symbol: PLCG1

Gene name: phospholipase C, gamma 1

HGNC ID: 9065

Synonyms: PLC148, PLC-II, PLCgamma1, NCKAP3

Related Genes

#	Gene Symbol	Number of hits
1	AGTR1	1 hits
2	BRAF	1 hits
3	CD36	1 hits
4	GHRL	1 hits
5	IPPK	1 hits
6	MAPK1	1 hits
7	PLA2G1B	1 hits
8	PLCB1	1 hits
9	PLCE1	1 hits
10	TRPC1	1 hits
11	TRPC3	1 hits
12	TRPC6	1 hits

Related Sentences

#	PMID	Sentence
1	31017709	Western blot analysis showed that ghrelin upregulated COX-2 protein expression in a time and dose-dependent manner.
2	31017709	Western blot analysis showed that ghrelin upregulated COX-2 protein expression in a time and dose-dependent manner.
3	31017709	Additionally, ghrelin activated P38 MAPK, AKT, and ERK1/2 pathways and also induced P38 MAPK phosphorylation in high glucose conditions.
4	31017709	Additionally, ghrelin activated P38 MAPK, AKT, and ERK1/2 pathways and also induced P38 MAPK phosphorylation in high glucose conditions.
5	31017709	Ghrelin mediated podocyte cell death was partially reversed by pharmacologically inhibiting P38 MAPK or phospholipase C (PLC).
6	31017709	Ghrelin mediated podocyte cell death was partially reversed by pharmacologically inhibiting P38 MAPK or phospholipase C (PLC).
7	31017709	Furthermore, PLC inhibitor (U73122) inhibited ghrelin induced P38 MAPK activation.
8	31017709	Furthermore, PLC inhibitor (U73122) inhibited ghrelin induced P38 MAPK activation.
9	31017709	While PI3K inhibitor (LY294002) was without effect on cell survival or P38 MAPK activation, it inhibited ghrelin induced ERK1/2 phosphorylation.
10	31017709	While PI3K inhibitor (LY294002) was without effect on cell survival or P38 MAPK activation, it inhibited ghrelin induced ERK1/2 phosphorylation.
11	31017709	Finally, ghrelin induced TAU phosphorylation was reversed by pharmacologic inhibitors of either P38 MAPK or PKA.
12	31017709	Finally, ghrelin induced TAU phosphorylation was reversed by pharmacologic inhibitors of either P38 MAPK or PKA.
13	31017709	In this study, we first showed that ghrelin receptor is expressed on glomerular podocytes.
14	31017709	In this study, we first showed that ghrelin receptor is expressed on glomerular podocytes.
15	31017709	Also, ghrelin showed negative impact on podocyte survival through modulating signalling pathways such as P38 MAPK and AKT known to play a key role in podocyte health.
16	31017709	Also, ghrelin showed negative impact on podocyte survival through modulating signalling pathways such as P38 MAPK and AKT known to play a key role in podocyte health.
17	26583319	Loss of the ER Ca(2+) pool induced by palmitate was reverted by the phospholipase C (PLC) inhibitor edelfosine.
18	26583319	Loss of the ER Ca(2+) pool induced by palmitate was reverted by the phospholipase C (PLC) inhibitor edelfosine.
19	26583319	These data suggest that oxidative stress caused by saturated FFA leads to mitochondrial dysfunction and ER Ca(2+) depletion through FAT/CD36 and PLC signaling, possibly contributing to podocyte injury.
20	26583319	These data suggest that oxidative stress caused by saturated FFA leads to mitochondrial dysfunction and ER Ca(2+) depletion through FAT/CD36 and PLC signaling, possibly contributing to podocyte injury.
21	25521631	Phospholipase C epsilon (PLCε) induced TRPC6 activation: a common but redundant mechanism in primary podocytes.
22	25521631	Phospholipase C epsilon (PLCε) induced TRPC6 activation: a common but redundant mechanism in primary podocytes.
23	25521631	In eukaryotic cells, activation of phospholipase C (PLC)-coupled membrane receptors by hormones leads to an increase in the intracellular Ca(2+) concentration [Ca(2+) ]i .
24	25521631	In eukaryotic cells, activation of phospholipase C (PLC)-coupled membrane receptors by hormones leads to an increase in the intracellular Ca(2+) concentration [Ca(2+) ]i .
25	25521631	Catalytic activity of PLCs results in the hydrolysis of phosphatidylinositol 4,5-bisphosphate to generate inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG) which opens DAG-sensitive classical transient receptor channels 3, 6, and 7 (TRPC3/6/7), initiating Ca(2+) influx from the extracellular space.
26	25521631	Catalytic activity of PLCs results in the hydrolysis of phosphatidylinositol 4,5-bisphosphate to generate inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG) which opens DAG-sensitive classical transient receptor channels 3, 6, and 7 (TRPC3/6/7), initiating Ca(2+) influx from the extracellular space.
27	25521631	PLCε-/- podocytes however, were undistinguishable from WT podocytes in their angiotensin II-induced formation of actin stress fibers and their GTPγS-induced TRPC6 activation, pointing to a redundant role of PLCε-mediated TRPC6 activation at least in podocytes.
28	25521631	PLCε-/- podocytes however, were undistinguishable from WT podocytes in their angiotensin II-induced formation of actin stress fibers and their GTPγS-induced TRPC6 activation, pointing to a redundant role of PLCε-mediated TRPC6 activation at least in podocytes.
29	24553432	ATP effects were also abolished by inhibiting G protein signaling and by the PLC/PLA2 inhibitor D-609.
30	24037962	Angiotensin II activation of TRPC6 channels in rat podocytes requires generation of reactive oxygen species.
31	24037962	This effect was completely blocked by SKF-96365, by micromolar La(3+) , and by siRNA knockdown of TRPC6, indicating that TRPC6 is the primary source of Ca(2+) influx mobilized by endogenously expressed angiotensin II receptors in these cells.
32	24037962	These responses were also blocked by the AT1R antagonist losartan, the phospholipase C inhibitor D-609, and by inhibition of G protein signaling.
33	24037962	Significant reductions of AII effects on podocyte TRPC6 were also observed after pretreatment with NADPH oxidase inhibitors apocynin or diphenylene iodonium (DPI).
34	24037962	These data suggest that ROS production permits activation of TRPC6 channels by G protein and PLC-dependent cascades initiated by AII acting on AT1Rs in podocytes.
35	23948707	NOX2 interacts with podocyte TRPC6 channels and contributes to their activation by diacylglycerol: essential role of podocin in formation of this complex.
36	23948707	TRPC6 channels are typically activated by diacylglycerol (DAG) during PLC-dependent transduction cascades.
37	23948707	We previously showed that podocin is required for DAG analogs to produce robust activation of TRPC6 channels in podocytes.
38	23948707	Here we show that endogenous TRPC6 channels in immortalized podocytes reciprocally coimmunoprecipitate with the catalytic subunit of the NADPH oxidase NOX2 (gp91(phox)).
39	23948707	The NOX2-TRPC6 interaction was not detected in cells stably expressing a short hairpin RNA targeting podocin, although NOX2 and TRPC6 were present at normal levels.
40	23948707	OAG also increased steady-state surface expression of the NOX2 regulatory subunit p47(phox).
41	23948707	In whole cell recordings, TRPC6 activation by OAG was reduced in podocytes pretreated with the NOX2 inhibitor apocynin, by the pan-NOX inhibitor diphenylene iodonium, and by tempol, a ROS quencher.
42	23948707	These data suggest that active NOX2 assembles with TRPC6 at podocin-organized sterol-rich raft domains and becomes catalytically active in response to DAG.
43	17942568	Recently, we identified recessive mutations in the phospholipase C epsilon 1 gene (PLCE1) as a new cause of early-onset nephrotic syndrome and demonstrated interaction of PLCepsilon1 with IQGAP1.
44	17942568	It relates the PLCE1 ortholog (plc-1) to the C. elegans ortholog (lin-45) of human BRAF (v-raf murine sarcoma viral oncogene homolog B1).
45	16303855	TRPC1 colocalized with aquaporin-1, a marker for proximal tubule and thin descending limb, but not with aquaporin-2, a marker for connecting tubule and collecting duct cells.
46	16303855	TRPC3 and -C6 colocalized with aquaporin-2, but not with the Na(+)/Ca(2+) exchanger or peanut lectin.
47	16303855	In polarized cultures of M1 and IMCD-3 collecting duct cells, TRPC3 was localized exclusively to the apical domain, whereas TRPC6 was found in both the basolateral and apical membranes.
48	16303855	TRPC3 and TRPC6 were also detected in primary podocyte cultures, whereas TRPC1 was exclusively expressed in mesangial cell cultures.
49	16303855	These results suggest that TRPC1, -C3, and -C6 may play a functional role in PLC-dependent signaling in specific regions of the nephron.