Ignet

Gene Information

Gene symbol: TRPC6

Gene name: transient receptor potential cation channel, subfamily C, member 6

HGNC ID: 12338

Synonyms: TRP6

Related Genes

#	Gene Symbol	Number of hits
1	ACTN4	1 hits
2	AGT	1 hits
3	CASP3	1 hits
4	CAT	1 hits
5	NOX4	1 hits
6	NOX5	1 hits
7	PRKCA	1 hits
8	SOD1	1 hits
9	TRPC1	1 hits
10	TRPC3	1 hits
11	TRPC5	1 hits
12	TRPM6	1 hits
13	TRPM7	1 hits
14	TRPV1	1 hits

Related Sentences

#	PMID	Sentence
1	17346947	TRPC6, TRPM6, and TRPP2 have been implicated in hereditary focal segmental glomerulosclerosis (FSGS), hypomagnesemia with secondary hypocalcemia (HSH), and polycystic kidney disease (PKD), respectively.
2	17699555	In cultured human MCs, high glucose significantly reduced expression of TRPC6 protein, but there was no effect on either TRPC1 or TRPC3.
3	17699555	In glomeruli isolated from streptozotocin-induced diabetic rats, TRPC6, but not TRPC1, was markedly reduced compared with the glomeruli of control rats.
4	17699555	Patch-clamp experiments showed that ANG II-stimulated membrane currents in MCs were significantly attenuated or enhanced by knockdown or overexpression of TRPC6, respectively.
5	17699555	Fura-2 fluorescence measurements revealed that the ANG II-induced Ca(2+) influxes were markedly inhibited in MCs with TRPC6 knockdown, reminiscent of the impaired Ca(2+) entry in response to ANG II in high glucose-treated MCs.
6	17699555	In cultured human MCs, high glucose significantly reduced expression of TRPC6 protein, but there was no effect on either TRPC1 or TRPC3.
7	17699555	In glomeruli isolated from streptozotocin-induced diabetic rats, TRPC6, but not TRPC1, was markedly reduced compared with the glomeruli of control rats.
8	17699555	Patch-clamp experiments showed that ANG II-stimulated membrane currents in MCs were significantly attenuated or enhanced by knockdown or overexpression of TRPC6, respectively.
9	17699555	Fura-2 fluorescence measurements revealed that the ANG II-induced Ca(2+) influxes were markedly inhibited in MCs with TRPC6 knockdown, reminiscent of the impaired Ca(2+) entry in response to ANG II in high glucose-treated MCs.
10	17699555	In cultured human MCs, high glucose significantly reduced expression of TRPC6 protein, but there was no effect on either TRPC1 or TRPC3.
11	17699555	In glomeruli isolated from streptozotocin-induced diabetic rats, TRPC6, but not TRPC1, was markedly reduced compared with the glomeruli of control rats.
12	17699555	Patch-clamp experiments showed that ANG II-stimulated membrane currents in MCs were significantly attenuated or enhanced by knockdown or overexpression of TRPC6, respectively.
13	17699555	Fura-2 fluorescence measurements revealed that the ANG II-induced Ca(2+) influxes were markedly inhibited in MCs with TRPC6 knockdown, reminiscent of the impaired Ca(2+) entry in response to ANG II in high glucose-treated MCs.
14	17699555	In cultured human MCs, high glucose significantly reduced expression of TRPC6 protein, but there was no effect on either TRPC1 or TRPC3.
15	17699555	In glomeruli isolated from streptozotocin-induced diabetic rats, TRPC6, but not TRPC1, was markedly reduced compared with the glomeruli of control rats.
16	17699555	Patch-clamp experiments showed that ANG II-stimulated membrane currents in MCs were significantly attenuated or enhanced by knockdown or overexpression of TRPC6, respectively.
17	17699555	Fura-2 fluorescence measurements revealed that the ANG II-induced Ca(2+) influxes were markedly inhibited in MCs with TRPC6 knockdown, reminiscent of the impaired Ca(2+) entry in response to ANG II in high glucose-treated MCs.
18	19098369	TRPV1 regulates adipogenesis and inflammation in adipose tissues, whereas TRPC3, TRPC5, TRPC6, TRPV1, and TRPM7 are involved in vasoconstriction and regulation of blood pressure.
19	19393642	However, the protein expression of TRPC1 and TRPC6 was downregulated in the diabetic group by 50%.
20	20337661	Expression of TRPC1, TRPC3 and TRPC6 mRNA and protein was found in Wistar rats.
21	20337661	The expression of TRPC1 and TRPC6, but not TRPC3, was increased approximately twofold in GK rats compared with Wistar rats. 5.
22	20337661	Expression of TRPC1, TRPC3 and TRPC6 mRNA and protein was found in Wistar rats.
23	20337661	The expression of TRPC1 and TRPC6, but not TRPC3, was increased approximately twofold in GK rats compared with Wistar rats. 5.
24	21525431	The present study was performed to investigate the underlying mechanism, particularly the roles of reactive oxygen species (ROS) and protein kinase C (PKC), in the diabetes-induced canonical transient receptor potential 6 (TRPC6) downregulation.
25	21525431	Catalase as well as superoxide dismutase were able to prevent the inhibitory effect of HG on TRPC6.
26	21525431	Specific knockdown of Nox4, a component of NADPH oxidase, increased TRPC6 protein expression.
27	21525431	Furthermore, either knockdown of TRPC6 or HG treatment significantly decreased ANG II-stimulated MC contraction, and the HG-impaired MC contraction was rescued by overexpression of TRPC6.
28	21525431	These results suggest that hyperglycemia in diabetes downregulated TRPC6 protein expression in MCs through a NADPH oxidase Nox4-ROS-PKC pathway, proving a mechanism for impaired MC contraction in diabetes.
29	21525431	The present study was performed to investigate the underlying mechanism, particularly the roles of reactive oxygen species (ROS) and protein kinase C (PKC), in the diabetes-induced canonical transient receptor potential 6 (TRPC6) downregulation.
30	21525431	Catalase as well as superoxide dismutase were able to prevent the inhibitory effect of HG on TRPC6.
31	21525431	Specific knockdown of Nox4, a component of NADPH oxidase, increased TRPC6 protein expression.
32	21525431	Furthermore, either knockdown of TRPC6 or HG treatment significantly decreased ANG II-stimulated MC contraction, and the HG-impaired MC contraction was rescued by overexpression of TRPC6.
33	21525431	These results suggest that hyperglycemia in diabetes downregulated TRPC6 protein expression in MCs through a NADPH oxidase Nox4-ROS-PKC pathway, proving a mechanism for impaired MC contraction in diabetes.
34	21525431	The present study was performed to investigate the underlying mechanism, particularly the roles of reactive oxygen species (ROS) and protein kinase C (PKC), in the diabetes-induced canonical transient receptor potential 6 (TRPC6) downregulation.
35	21525431	Catalase as well as superoxide dismutase were able to prevent the inhibitory effect of HG on TRPC6.
36	21525431	Specific knockdown of Nox4, a component of NADPH oxidase, increased TRPC6 protein expression.
37	21525431	Furthermore, either knockdown of TRPC6 or HG treatment significantly decreased ANG II-stimulated MC contraction, and the HG-impaired MC contraction was rescued by overexpression of TRPC6.
38	21525431	These results suggest that hyperglycemia in diabetes downregulated TRPC6 protein expression in MCs through a NADPH oxidase Nox4-ROS-PKC pathway, proving a mechanism for impaired MC contraction in diabetes.
39	21525431	The present study was performed to investigate the underlying mechanism, particularly the roles of reactive oxygen species (ROS) and protein kinase C (PKC), in the diabetes-induced canonical transient receptor potential 6 (TRPC6) downregulation.
40	21525431	Catalase as well as superoxide dismutase were able to prevent the inhibitory effect of HG on TRPC6.
41	21525431	Specific knockdown of Nox4, a component of NADPH oxidase, increased TRPC6 protein expression.
42	21525431	Furthermore, either knockdown of TRPC6 or HG treatment significantly decreased ANG II-stimulated MC contraction, and the HG-impaired MC contraction was rescued by overexpression of TRPC6.
43	21525431	These results suggest that hyperglycemia in diabetes downregulated TRPC6 protein expression in MCs through a NADPH oxidase Nox4-ROS-PKC pathway, proving a mechanism for impaired MC contraction in diabetes.
44	21525431	The present study was performed to investigate the underlying mechanism, particularly the roles of reactive oxygen species (ROS) and protein kinase C (PKC), in the diabetes-induced canonical transient receptor potential 6 (TRPC6) downregulation.
45	21525431	Catalase as well as superoxide dismutase were able to prevent the inhibitory effect of HG on TRPC6.
46	21525431	Specific knockdown of Nox4, a component of NADPH oxidase, increased TRPC6 protein expression.
47	21525431	Furthermore, either knockdown of TRPC6 or HG treatment significantly decreased ANG II-stimulated MC contraction, and the HG-impaired MC contraction was rescued by overexpression of TRPC6.
48	21525431	These results suggest that hyperglycemia in diabetes downregulated TRPC6 protein expression in MCs through a NADPH oxidase Nox4-ROS-PKC pathway, proving a mechanism for impaired MC contraction in diabetes.
49	22550476	Cells subjected to either glucolipotoxicity or tunicamycin exhibited increased ROS generation, gene and protein (PERK, GRP-78, IRE1α, and CHOP) expression of ER stress markers.
50	22550476	In addition, these cells showed increased TRPC-6 channel expression and apoptosis as revealed by DNA damage and increased caspase-3 activity.
51	23689571	Screening of ACTN4 and TRPC6 mutations in a Chinese cohort of patients with adult-onset familial focal segmental glomerulosclerosis.