Ignet

Gene Information

Gene symbol: CLU

Gene name: clusterin

HGNC ID: 2095

Synonyms: SGP-2, SP-40, TRPM-2, KUB1, CLU1, CLU2

Related Genes

#	Gene Symbol	Number of hits
1	ACE	1 hits
2	ACTB	1 hits
3	AGT	1 hits
4	ALB	1 hits
5	ALPI	1 hits
6	APBB1	1 hits
7	APOC1	1 hits
8	APOE	1 hits
9	APP	1 hits
10	BAX	1 hits
11	C1QA	1 hits
12	COL1A1	1 hits
13	CST3	1 hits
14	CTSB	1 hits
15	CYR61	1 hits
16	FN1	1 hits
17	FOS	1 hits
18	GAS6	1 hits
19	GCG	1 hits
20	GP2	1 hits
21	HAVCR1	1 hits
22	HP	1 hits
23	HPX	1 hits
24	HRAS	1 hits
25	HSF1	1 hits
26	HTATIP	1 hits
27	IGFBP6	1 hits
28	INS	1 hits
29	KCNH7	1 hits
30	KLF10	1 hits
31	LDLR	1 hits
32	LPAL2	1 hits
33	LPL	1 hits
34	LTF	1 hits
35	NES	1 hits
36	NGF	1 hits
37	NOV	1 hits
38	NRAS	1 hits
39	PARP1	1 hits
40	PDX1	1 hits
41	PDXP	1 hits
42	PON1	1 hits
43	PPA1	1 hits
44	PRDX1	1 hits
45	PRKAR2A	1 hits
46	RBP4	1 hits
47	SPP1	1 hits
48	TGFB1	1 hits
49	TNF	1 hits
50	TNFRSF10B	1 hits
51	TRPM2	1 hits
52	TRPM3	1 hits
53	TRPM4	1 hits
54	TRPM5	1 hits
55	TRPM7	1 hits
56	TRPV1	1 hits
57	TRPV2	1 hits
58	TRPV4	1 hits

Related Sentences

#	PMID	Sentence
1	6664829	The lithium clearance technique has been proposed as a non-invasive method whereby fluid delivery from the pars recta and pars convoluta of proximal tubules can be measured as CLi and CIN [0.78 CLi/CIN + 0.22], respectively [12], CLi being the clearance of lithium and CIN that of inulin.
2	7633902	Attachments of dorsal root ganglion (DRG) neurons from streptozotocin (STZ)-induced diabetic and normal C57BL mice to the following substrates were evaluated in vitro: a) poly L-lysine (PL), b) PL + type I collagen (CL-I), c) PL + type IV collagen (CL-IV), d) PL + laminin (LM) and e) PL + fibronectin (FN).
3	8171758	Utilizing cDNA probes, the gene products sulfated glycoprotein-2 (SGP-2), transforming growth factor-beta (TGF-beta), beta-actin (beta-actin), N-ras and beta nerve growth factor (beta-NGF), were quantitated in bladders of male Sprague-Dawley rats at 1, 2, 4 and 6 weeks after induction of diabetes with streptozotocin (STZ). beta-actin and SGP-2 expression were transiently increased at 1 and 4 weeks after induction, respectively.
4	8171758	N-ras was reduced at all times compared with control rat bladders.
5	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
6	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
7	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
8	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
9	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
10	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
11	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
12	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
13	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
14	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
15	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
16	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
17	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
18	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
19	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
20	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
21	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
22	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
23	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
24	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
25	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
26	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
27	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
28	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
29	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
30	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
31	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
32	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
33	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
34	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
35	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
36	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
37	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
38	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
39	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
40	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
41	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
42	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
43	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
44	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
45	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
46	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
47	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
48	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
49	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
50	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
51	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
52	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
53	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
54	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
55	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
56	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
57	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
58	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
59	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
60	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
61	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
62	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
63	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
64	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
65	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
66	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
67	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
68	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
69	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
70	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
71	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
72	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
73	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
74	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
75	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
76	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
77	9109446	Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.
78	9109446	We have examined the effects of mildly oxidized LDL and atherosclerosis on the levels of two proteins associated with HDL; apolipoprotein J (apoJ), and paraoxonase (PON).
79	9109446	On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).
80	9109446	Plasma PON activity was also significantly decreased, and apoJ levels were markedly increased in apolipoprotein E knockout mice on the chow diet, resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.
81	9109446	Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor knockout mice when they were fed a 0.15%-cholesterol-enriched diet.
82	9109446	Injection of mildly oxidized LDL (but not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ levels (P < 0.01).
83	9109446	Treatment of HepG2 cells in culture with mildly oxidized LDL (but not native LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for apoJ (2.0-fold increase).
84	9109446	In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72+/-0.2 in the controls (P < 0.009).
85	9109446	We conclude that: (a) mildly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosclerosis than the total cholesterol/HDL cholesterol ratio.
86	9428419	Tumor necrosis factor-alpha (TNF-alpha), a cytokine whose synthesis is up-regulated in the diabetic uterus, did not induce nuclear fragmentation nor clusterin expression but increased the incidence of TUNEL-positive nuclei.
87	12456808	Loss of interleukin 6 results in delayed mammary gland involution: a possible role for mitogen-activated protein kinase and not signal transducer and activator of transcription 3.
88	12456808	This study was based on the hypothesis that IL-6 is the activating cytokine for signal transducer and activator of transcription 3 (Stat), the transcription factor whose presence is required for controlled mammary gland involution.
89	12456808	We now show that expression of IL-6 is low during lactation but increases at the onset of involution in parallel with the activation of Stat3 and p44/42 MAPK.
90	12456808	Moreover, we demonstrated that injection of IL-6 into virgin and lactating mice activates Stat3 in mammary epithelium.
91	12456808	Involution of mammary tissue in IL-6-null mice was delayed similar to that seen in mammary conditional Stat3- and Bax-null mice.
92	12456808	However, Stat3 activation during involution was independent of the IL-6 status.
93	12456808	This suggests that either IL-6 does not induce Stat3 in vivo or its absence is compensated for by other cytokines, such as leukemia-inhibitory factor (LIF).
94	12456808	In contrast, the increase of p44/42 MAPK (ERK1/2) phosphorylation at the onset of involution was dependent on the presence of IL-6.
95	12456808	Delayed involution corresponded with a decrease of epithelial cell death, and a delayed induction of Bax and sulfated glycoprotein 2 (SGP2, or clusterin) expression.
96	12456808	Our experiments demonstrate on a genetic level that IL-6 contributes to the induction of the controlled remodeling of mammary tissue during involution, possibly through the MAPK pathway and by mediating the expression of the cell death protein Bax.
97	15952035	TRPM2: a calcium influx pathway regulated by oxidative stress and the novel second messenger ADP-ribose.
98	15952035	A unique functional property within the transient receptor potential (TRP) family of cation channels is the gating of TRP (melastatin) 2 (TRPM2) channels by ADP-ribose (ADPR).
99	15952035	ADPR binds to the intracellular C-terminal tail of TRPM2, a domain that shows homology to enzymes with pyrophosphatase activity.
100	15952035	Cytosolic Ca(2+) enhances TRPM2 gating by ADPR; ADPR and Ca(2+) in concert may be an important messenger system mediating Ca(2+) influx.
101	15952035	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.
102	15952035	In this review, we summarize the gating properties of TRPM2 and the proposed pathways of channel activation in vivo.
103	15952035	TRPM2 is likely to be a key player in several signalling pathways, mediating cell death in response to oxidative stress or in reperfusion injury.
104	15952035	TRPM2: a calcium influx pathway regulated by oxidative stress and the novel second messenger ADP-ribose.
105	15952035	A unique functional property within the transient receptor potential (TRP) family of cation channels is the gating of TRP (melastatin) 2 (TRPM2) channels by ADP-ribose (ADPR).
106	15952035	ADPR binds to the intracellular C-terminal tail of TRPM2, a domain that shows homology to enzymes with pyrophosphatase activity.
107	15952035	Cytosolic Ca(2+) enhances TRPM2 gating by ADPR; ADPR and Ca(2+) in concert may be an important messenger system mediating Ca(2+) influx.
108	15952035	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.
109	15952035	In this review, we summarize the gating properties of TRPM2 and the proposed pathways of channel activation in vivo.
110	15952035	TRPM2 is likely to be a key player in several signalling pathways, mediating cell death in response to oxidative stress or in reperfusion injury.
111	15952035	TRPM2: a calcium influx pathway regulated by oxidative stress and the novel second messenger ADP-ribose.
112	15952035	A unique functional property within the transient receptor potential (TRP) family of cation channels is the gating of TRP (melastatin) 2 (TRPM2) channels by ADP-ribose (ADPR).
113	15952035	ADPR binds to the intracellular C-terminal tail of TRPM2, a domain that shows homology to enzymes with pyrophosphatase activity.
114	15952035	Cytosolic Ca(2+) enhances TRPM2 gating by ADPR; ADPR and Ca(2+) in concert may be an important messenger system mediating Ca(2+) influx.
115	15952035	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.
116	15952035	In this review, we summarize the gating properties of TRPM2 and the proposed pathways of channel activation in vivo.
117	15952035	TRPM2 is likely to be a key player in several signalling pathways, mediating cell death in response to oxidative stress or in reperfusion injury.
118	15952035	TRPM2: a calcium influx pathway regulated by oxidative stress and the novel second messenger ADP-ribose.
119	15952035	A unique functional property within the transient receptor potential (TRP) family of cation channels is the gating of TRP (melastatin) 2 (TRPM2) channels by ADP-ribose (ADPR).
120	15952035	ADPR binds to the intracellular C-terminal tail of TRPM2, a domain that shows homology to enzymes with pyrophosphatase activity.
121	15952035	Cytosolic Ca(2+) enhances TRPM2 gating by ADPR; ADPR and Ca(2+) in concert may be an important messenger system mediating Ca(2+) influx.
122	15952035	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.
123	15952035	In this review, we summarize the gating properties of TRPM2 and the proposed pathways of channel activation in vivo.
124	15952035	TRPM2 is likely to be a key player in several signalling pathways, mediating cell death in response to oxidative stress or in reperfusion injury.
125	15952035	TRPM2: a calcium influx pathway regulated by oxidative stress and the novel second messenger ADP-ribose.
126	15952035	A unique functional property within the transient receptor potential (TRP) family of cation channels is the gating of TRP (melastatin) 2 (TRPM2) channels by ADP-ribose (ADPR).
127	15952035	ADPR binds to the intracellular C-terminal tail of TRPM2, a domain that shows homology to enzymes with pyrophosphatase activity.
128	15952035	Cytosolic Ca(2+) enhances TRPM2 gating by ADPR; ADPR and Ca(2+) in concert may be an important messenger system mediating Ca(2+) influx.
129	15952035	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.
130	15952035	In this review, we summarize the gating properties of TRPM2 and the proposed pathways of channel activation in vivo.
131	15952035	TRPM2 is likely to be a key player in several signalling pathways, mediating cell death in response to oxidative stress or in reperfusion injury.
132	15952035	TRPM2: a calcium influx pathway regulated by oxidative stress and the novel second messenger ADP-ribose.
133	15952035	A unique functional property within the transient receptor potential (TRP) family of cation channels is the gating of TRP (melastatin) 2 (TRPM2) channels by ADP-ribose (ADPR).
134	15952035	ADPR binds to the intracellular C-terminal tail of TRPM2, a domain that shows homology to enzymes with pyrophosphatase activity.
135	15952035	Cytosolic Ca(2+) enhances TRPM2 gating by ADPR; ADPR and Ca(2+) in concert may be an important messenger system mediating Ca(2+) influx.
136	15952035	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.
137	15952035	In this review, we summarize the gating properties of TRPM2 and the proposed pathways of channel activation in vivo.
138	15952035	TRPM2 is likely to be a key player in several signalling pathways, mediating cell death in response to oxidative stress or in reperfusion injury.
139	15952035	TRPM2: a calcium influx pathway regulated by oxidative stress and the novel second messenger ADP-ribose.
140	15952035	A unique functional property within the transient receptor potential (TRP) family of cation channels is the gating of TRP (melastatin) 2 (TRPM2) channels by ADP-ribose (ADPR).
141	15952035	ADPR binds to the intracellular C-terminal tail of TRPM2, a domain that shows homology to enzymes with pyrophosphatase activity.
142	15952035	Cytosolic Ca(2+) enhances TRPM2 gating by ADPR; ADPR and Ca(2+) in concert may be an important messenger system mediating Ca(2+) influx.
143	15952035	Other stimuli of TRPM2 include NAD and H(2)O(2) and cyclic ADPR, which may act synergistically with ADPR.
144	15952035	In this review, we summarize the gating properties of TRPM2 and the proposed pathways of channel activation in vivo.
145	15952035	TRPM2 is likely to be a key player in several signalling pathways, mediating cell death in response to oxidative stress or in reperfusion injury.
146	16025303	To date, two TRPM family members, TRPM2 and TRPM7, have been implicated directly as central components of cell death pathways.
147	16025303	TRPM2, a Ca(2+)-permeant, non-selective cation channel, senses and responds to oxidative stress levels in the cell.
148	16025303	To date, two TRPM family members, TRPM2 and TRPM7, have been implicated directly as central components of cell death pathways.
149	16025303	TRPM2, a Ca(2+)-permeant, non-selective cation channel, senses and responds to oxidative stress levels in the cell.
150	17090421	Moreover, the presence of both a heat shock transcription factor-1 and an activator protein-1 element in the CLU gene promoter indicate that CLU gene can be an extremely sensitive biosensor to reactive oxygen species.
151	17192696	Apolipoprotein (apo) J, clusterin, is ubiquitously expressed in many tissues, and is a component of high-density lipoproteins (HDLs).
152	17217061	TRPM2 is a cation channel enabling influx of Na+ and Ca2+, leading to depolarization and increases in the cytosolic Ca2+ concentration ([Ca2+]i).
153	17217061	Endogenous ADPR concentrations in leucocytes are sufficiently high to activate TRPM2 in the presence of an increased [Ca2+]i but probably not at resting [Ca2+]i.
154	17217061	H2O2-stimulated TRPM2 channels essentially contribute to insulin secretion in pancreatic beta-cells and alloxan-induced diabetes mellitus.
155	17217061	Inhibition of TRPM2 channels may be achieved by channel blockers such as flufenamic acid or the anti-fungal agents clotrimazole or econazole.
156	17217061	Selective blockers of TRPM2 are not yet available; those would be valuable for a characterization of biological roles of TRPM2 in various tissues and as potential drugs directed against oxidative cell damage, reperfusion injury or leucocyte activation.
157	17217061	Activation of TRPM2 may be prevented by anti-oxidants, PARP inhibitors and glycohydrolase inhibitors.
158	17217061	In light of the wide-spread expression and growing list of cellular functions of TRPM2, useful therapeutic applications are expected for future drugs that block TRPM2 channels or inhibit their activation.
159	17217061	TRPM2 is a cation channel enabling influx of Na+ and Ca2+, leading to depolarization and increases in the cytosolic Ca2+ concentration ([Ca2+]i).
160	17217061	Endogenous ADPR concentrations in leucocytes are sufficiently high to activate TRPM2 in the presence of an increased [Ca2+]i but probably not at resting [Ca2+]i.
161	17217061	H2O2-stimulated TRPM2 channels essentially contribute to insulin secretion in pancreatic beta-cells and alloxan-induced diabetes mellitus.
162	17217061	Inhibition of TRPM2 channels may be achieved by channel blockers such as flufenamic acid or the anti-fungal agents clotrimazole or econazole.
163	17217061	Selective blockers of TRPM2 are not yet available; those would be valuable for a characterization of biological roles of TRPM2 in various tissues and as potential drugs directed against oxidative cell damage, reperfusion injury or leucocyte activation.
164	17217061	Activation of TRPM2 may be prevented by anti-oxidants, PARP inhibitors and glycohydrolase inhibitors.
165	17217061	In light of the wide-spread expression and growing list of cellular functions of TRPM2, useful therapeutic applications are expected for future drugs that block TRPM2 channels or inhibit their activation.
166	17217061	TRPM2 is a cation channel enabling influx of Na+ and Ca2+, leading to depolarization and increases in the cytosolic Ca2+ concentration ([Ca2+]i).
167	17217061	Endogenous ADPR concentrations in leucocytes are sufficiently high to activate TRPM2 in the presence of an increased [Ca2+]i but probably not at resting [Ca2+]i.
168	17217061	H2O2-stimulated TRPM2 channels essentially contribute to insulin secretion in pancreatic beta-cells and alloxan-induced diabetes mellitus.
169	17217061	Inhibition of TRPM2 channels may be achieved by channel blockers such as flufenamic acid or the anti-fungal agents clotrimazole or econazole.
170	17217061	Selective blockers of TRPM2 are not yet available; those would be valuable for a characterization of biological roles of TRPM2 in various tissues and as potential drugs directed against oxidative cell damage, reperfusion injury or leucocyte activation.
171	17217061	Activation of TRPM2 may be prevented by anti-oxidants, PARP inhibitors and glycohydrolase inhibitors.
172	17217061	In light of the wide-spread expression and growing list of cellular functions of TRPM2, useful therapeutic applications are expected for future drugs that block TRPM2 channels or inhibit their activation.
173	17217061	TRPM2 is a cation channel enabling influx of Na+ and Ca2+, leading to depolarization and increases in the cytosolic Ca2+ concentration ([Ca2+]i).
174	17217061	Endogenous ADPR concentrations in leucocytes are sufficiently high to activate TRPM2 in the presence of an increased [Ca2+]i but probably not at resting [Ca2+]i.
175	17217061	H2O2-stimulated TRPM2 channels essentially contribute to insulin secretion in pancreatic beta-cells and alloxan-induced diabetes mellitus.
176	17217061	Inhibition of TRPM2 channels may be achieved by channel blockers such as flufenamic acid or the anti-fungal agents clotrimazole or econazole.
177	17217061	Selective blockers of TRPM2 are not yet available; those would be valuable for a characterization of biological roles of TRPM2 in various tissues and as potential drugs directed against oxidative cell damage, reperfusion injury or leucocyte activation.
178	17217061	Activation of TRPM2 may be prevented by anti-oxidants, PARP inhibitors and glycohydrolase inhibitors.
179	17217061	In light of the wide-spread expression and growing list of cellular functions of TRPM2, useful therapeutic applications are expected for future drugs that block TRPM2 channels or inhibit their activation.
180	17217061	TRPM2 is a cation channel enabling influx of Na+ and Ca2+, leading to depolarization and increases in the cytosolic Ca2+ concentration ([Ca2+]i).
181	17217061	Endogenous ADPR concentrations in leucocytes are sufficiently high to activate TRPM2 in the presence of an increased [Ca2+]i but probably not at resting [Ca2+]i.
182	17217061	H2O2-stimulated TRPM2 channels essentially contribute to insulin secretion in pancreatic beta-cells and alloxan-induced diabetes mellitus.
183	17217061	Inhibition of TRPM2 channels may be achieved by channel blockers such as flufenamic acid or the anti-fungal agents clotrimazole or econazole.
184	17217061	Selective blockers of TRPM2 are not yet available; those would be valuable for a characterization of biological roles of TRPM2 in various tissues and as potential drugs directed against oxidative cell damage, reperfusion injury or leucocyte activation.
185	17217061	Activation of TRPM2 may be prevented by anti-oxidants, PARP inhibitors and glycohydrolase inhibitors.
186	17217061	In light of the wide-spread expression and growing list of cellular functions of TRPM2, useful therapeutic applications are expected for future drugs that block TRPM2 channels or inhibit their activation.
187	17217061	TRPM2 is a cation channel enabling influx of Na+ and Ca2+, leading to depolarization and increases in the cytosolic Ca2+ concentration ([Ca2+]i).
188	17217061	Endogenous ADPR concentrations in leucocytes are sufficiently high to activate TRPM2 in the presence of an increased [Ca2+]i but probably not at resting [Ca2+]i.
189	17217061	H2O2-stimulated TRPM2 channels essentially contribute to insulin secretion in pancreatic beta-cells and alloxan-induced diabetes mellitus.
190	17217061	Inhibition of TRPM2 channels may be achieved by channel blockers such as flufenamic acid or the anti-fungal agents clotrimazole or econazole.
191	17217061	Selective blockers of TRPM2 are not yet available; those would be valuable for a characterization of biological roles of TRPM2 in various tissues and as potential drugs directed against oxidative cell damage, reperfusion injury or leucocyte activation.
192	17217061	Activation of TRPM2 may be prevented by anti-oxidants, PARP inhibitors and glycohydrolase inhibitors.
193	17217061	In light of the wide-spread expression and growing list of cellular functions of TRPM2, useful therapeutic applications are expected for future drugs that block TRPM2 channels or inhibit their activation.
194	17217061	TRPM2 is a cation channel enabling influx of Na+ and Ca2+, leading to depolarization and increases in the cytosolic Ca2+ concentration ([Ca2+]i).
195	17217061	Endogenous ADPR concentrations in leucocytes are sufficiently high to activate TRPM2 in the presence of an increased [Ca2+]i but probably not at resting [Ca2+]i.
196	17217061	H2O2-stimulated TRPM2 channels essentially contribute to insulin secretion in pancreatic beta-cells and alloxan-induced diabetes mellitus.
197	17217061	Inhibition of TRPM2 channels may be achieved by channel blockers such as flufenamic acid or the anti-fungal agents clotrimazole or econazole.
198	17217061	Selective blockers of TRPM2 are not yet available; those would be valuable for a characterization of biological roles of TRPM2 in various tissues and as potential drugs directed against oxidative cell damage, reperfusion injury or leucocyte activation.
199	17217061	Activation of TRPM2 may be prevented by anti-oxidants, PARP inhibitors and glycohydrolase inhibitors.
200	17217061	In light of the wide-spread expression and growing list of cellular functions of TRPM2, useful therapeutic applications are expected for future drugs that block TRPM2 channels or inhibit their activation.
201	17512083	Besides the well-established genes including Pdx-1 and Ngn-3, we propose the nestin and clusterin as the new morphogenic factors for beta-cell neogenesis and their functional associations.
202	17512083	In in vitro culture, the nestin-rich epithelial cells of the neogenic ductules also displayed extensive self-replication leading to monolayer of epithelial cell explants and transformed into the insulin secreting beta cells as well as duct cells.
203	17512083	Insulin expression, both insulin mRNA and peptide levels, was increased and showed glucose dependent manner by ectopic expression of clusterin upon the culture of neogenic ductules when compared to the mock-transfected control, implying that the duct cells transformed functional beta cells.
204	17512083	We observed that clusterin over-expression led to up-regulation of Pdx-1 and Ngn-3, and clusterin levels were increased upon the transfection of cDNAs of Pdx-1 or Ngn-3, suggesting a close functional association of these morphogenic factors.
205	17512083	In conclusion, we suggest that adult pancreatic stem cells can be recapitulated for neogenesis of insulin secreting beta cells not only by reactivation Pdx-1 and Ngn-3, the classical differentiation factors for pancreas development, but also by the intervention of new morphogenic factors including nestin and clusterin.
206	17512083	In particular, by modulation of Pdx-1 and Ngn-3, clusterin induces remarkable differentiation of the functional beta cells secreting insulin in response to glucose stimulation.
207	17512083	Besides the well-established genes including Pdx-1 and Ngn-3, we propose the nestin and clusterin as the new morphogenic factors for beta-cell neogenesis and their functional associations.
208	17512083	In in vitro culture, the nestin-rich epithelial cells of the neogenic ductules also displayed extensive self-replication leading to monolayer of epithelial cell explants and transformed into the insulin secreting beta cells as well as duct cells.
209	17512083	Insulin expression, both insulin mRNA and peptide levels, was increased and showed glucose dependent manner by ectopic expression of clusterin upon the culture of neogenic ductules when compared to the mock-transfected control, implying that the duct cells transformed functional beta cells.
210	17512083	We observed that clusterin over-expression led to up-regulation of Pdx-1 and Ngn-3, and clusterin levels were increased upon the transfection of cDNAs of Pdx-1 or Ngn-3, suggesting a close functional association of these morphogenic factors.
211	17512083	In conclusion, we suggest that adult pancreatic stem cells can be recapitulated for neogenesis of insulin secreting beta cells not only by reactivation Pdx-1 and Ngn-3, the classical differentiation factors for pancreas development, but also by the intervention of new morphogenic factors including nestin and clusterin.
212	17512083	In particular, by modulation of Pdx-1 and Ngn-3, clusterin induces remarkable differentiation of the functional beta cells secreting insulin in response to glucose stimulation.
213	17512083	Besides the well-established genes including Pdx-1 and Ngn-3, we propose the nestin and clusterin as the new morphogenic factors for beta-cell neogenesis and their functional associations.
214	17512083	In in vitro culture, the nestin-rich epithelial cells of the neogenic ductules also displayed extensive self-replication leading to monolayer of epithelial cell explants and transformed into the insulin secreting beta cells as well as duct cells.
215	17512083	Insulin expression, both insulin mRNA and peptide levels, was increased and showed glucose dependent manner by ectopic expression of clusterin upon the culture of neogenic ductules when compared to the mock-transfected control, implying that the duct cells transformed functional beta cells.
216	17512083	We observed that clusterin over-expression led to up-regulation of Pdx-1 and Ngn-3, and clusterin levels were increased upon the transfection of cDNAs of Pdx-1 or Ngn-3, suggesting a close functional association of these morphogenic factors.
217	17512083	In conclusion, we suggest that adult pancreatic stem cells can be recapitulated for neogenesis of insulin secreting beta cells not only by reactivation Pdx-1 and Ngn-3, the classical differentiation factors for pancreas development, but also by the intervention of new morphogenic factors including nestin and clusterin.
218	17512083	In particular, by modulation of Pdx-1 and Ngn-3, clusterin induces remarkable differentiation of the functional beta cells secreting insulin in response to glucose stimulation.
219	17512083	Besides the well-established genes including Pdx-1 and Ngn-3, we propose the nestin and clusterin as the new morphogenic factors for beta-cell neogenesis and their functional associations.
220	17512083	In in vitro culture, the nestin-rich epithelial cells of the neogenic ductules also displayed extensive self-replication leading to monolayer of epithelial cell explants and transformed into the insulin secreting beta cells as well as duct cells.
221	17512083	Insulin expression, both insulin mRNA and peptide levels, was increased and showed glucose dependent manner by ectopic expression of clusterin upon the culture of neogenic ductules when compared to the mock-transfected control, implying that the duct cells transformed functional beta cells.
222	17512083	We observed that clusterin over-expression led to up-regulation of Pdx-1 and Ngn-3, and clusterin levels were increased upon the transfection of cDNAs of Pdx-1 or Ngn-3, suggesting a close functional association of these morphogenic factors.
223	17512083	In conclusion, we suggest that adult pancreatic stem cells can be recapitulated for neogenesis of insulin secreting beta cells not only by reactivation Pdx-1 and Ngn-3, the classical differentiation factors for pancreas development, but also by the intervention of new morphogenic factors including nestin and clusterin.
224	17512083	In particular, by modulation of Pdx-1 and Ngn-3, clusterin induces remarkable differentiation of the functional beta cells secreting insulin in response to glucose stimulation.
225	18619471	RT-PCR data verified significant differences in the mRNA expression levels of Igfbp6, Tieg, and Clu between euglycemic and hyperglycemic groups, whereas expression levels of these genes in control and euglycemic diabetic groups were not significantly different.
226	18619471	In ventral prostate, the mRNA expression levels of Igfbp6 and Tieg were significantly higher in the hyperglycemic STZ-induced diabetic than in the hyperglycemic spontaneously diabetic BBDP/Wor rats.
227	18676994	Proteins related to cell growth (CYR61, protein NOV, and clusterin) were increased, whereas growth arrest-specific 6 (GAS6) and growth/differentiation factor 6 were decreased by Ang II stimulation.
228	18676994	Ang II-stimulated changes of plasminogen activator inhibitor-1, GAS6, cathepsin B, and periostin were validated by Western blot.
229	18723004	Quantitative PCR confirmed altered regulation in 6 of 7 Alzheimer-related genes (Apbb1, C1qa, Clu, App, Cst3, Fn1, Htatip) in iron-deficient rats relative to iron-sufficient controls at P15.
230	18949565	The effects of ACE inhibitor and angiotensin receptor blocker on clusterin and apoptosis in the kidney tissue of streptozotocin-diabetic rats.
231	18949565	We also aimed to investigate the post-effects of angiotensin II blockage treatment on clusterin expression and to compare these with apoptosis.
232	18949565	The effects of ACE inhibitor and angiotensin receptor blocker on clusterin and apoptosis in the kidney tissue of streptozotocin-diabetic rats.
233	18949565	We also aimed to investigate the post-effects of angiotensin II blockage treatment on clusterin expression and to compare these with apoptosis.
234	19353783	We report that proteasome inhibition promotes both heat-shock factor 1 (HSF-1)-dependent CLU gene expression induction and protein accumulation due to reduced degradation.
235	19353783	Overall our findings indicate that CLU overexpression after proteasome inhibition relates to both positive gene transcriptional regulation by HSF-1 and posttranslational protein accumulation due to reduced proteasomal and lysosomal degradation.
236	19353783	We report that proteasome inhibition promotes both heat-shock factor 1 (HSF-1)-dependent CLU gene expression induction and protein accumulation due to reduced degradation.
237	19353783	Overall our findings indicate that CLU overexpression after proteasome inhibition relates to both positive gene transcriptional regulation by HSF-1 and posttranslational protein accumulation due to reduced proteasomal and lysosomal degradation.
238	19875648	Mice with streptozotocin-induced diabetes and advanced glycation end product-treated human retinal microvascular endothelial cells (HRMECs) were used to determine the effect of clusterin on vascular permeability and tight junction protein expression, through perfusion of retinal vessels with FITC-bovine serum albumin, a [(3)H]sucrose permeability assay, a cell viability assay, Western blot analysis, immunocytochemistry, immunohistochemistry, and terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling.
239	20410100	Genetic variation in APOJ, LPL, and TNFRSF10B affects plasma fatty acid distribution in Alaskan Eskimos.
240	20817608	These associations include the recognition of cholesterol transporters apolipoprotein E (APOE), APOC1 and APOJ as major genetic risk factors for common AD and observations associating risk factors for cardiovascular disease such as high midlife plasma cholesterol, diabetes, stroke, obesity and hypertension to dementia.
241	20850846	The CLU gene was associated with diabetes, probably through an increase in insulin resistance primarily and through an impairment of insulin secretion secondarily.
242	20921208	Lack of TRPM2 impaired insulin secretion and glucose metabolisms in mice.
243	21135052	TRPM2: a multifunctional ion channel for calcium signalling.
244	21135052	The transient potential receptor melastatin-2 (TRPM2) channel has emerged as an important Ca(2+) signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death.
245	21135052	Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress-related pathologies.
246	21135052	TRPM2 is a non-selective, calcium (Ca(2+))-permeable cation channel of the melastatin-related transient receptor potential (TRPM) ion channel subfamily.
247	21135052	In addition to its role mediating Ca(2+) influx into the cells, TRPM2 can also function as a lysosomal Ca(2+) release channel, contributing to cell death.
248	21135052	The physiological and pathophysiological context of ROS-mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases.
249	21135052	TRPM2: a multifunctional ion channel for calcium signalling.
250	21135052	The transient potential receptor melastatin-2 (TRPM2) channel has emerged as an important Ca(2+) signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death.
251	21135052	Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress-related pathologies.
252	21135052	TRPM2 is a non-selective, calcium (Ca(2+))-permeable cation channel of the melastatin-related transient receptor potential (TRPM) ion channel subfamily.
253	21135052	In addition to its role mediating Ca(2+) influx into the cells, TRPM2 can also function as a lysosomal Ca(2+) release channel, contributing to cell death.
254	21135052	The physiological and pathophysiological context of ROS-mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases.
255	21135052	TRPM2: a multifunctional ion channel for calcium signalling.
256	21135052	The transient potential receptor melastatin-2 (TRPM2) channel has emerged as an important Ca(2+) signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death.
257	21135052	Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress-related pathologies.
258	21135052	TRPM2 is a non-selective, calcium (Ca(2+))-permeable cation channel of the melastatin-related transient receptor potential (TRPM) ion channel subfamily.
259	21135052	In addition to its role mediating Ca(2+) influx into the cells, TRPM2 can also function as a lysosomal Ca(2+) release channel, contributing to cell death.
260	21135052	The physiological and pathophysiological context of ROS-mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases.
261	21135052	TRPM2: a multifunctional ion channel for calcium signalling.
262	21135052	The transient potential receptor melastatin-2 (TRPM2) channel has emerged as an important Ca(2+) signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death.
263	21135052	Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress-related pathologies.
264	21135052	TRPM2 is a non-selective, calcium (Ca(2+))-permeable cation channel of the melastatin-related transient receptor potential (TRPM) ion channel subfamily.
265	21135052	In addition to its role mediating Ca(2+) influx into the cells, TRPM2 can also function as a lysosomal Ca(2+) release channel, contributing to cell death.
266	21135052	The physiological and pathophysiological context of ROS-mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases.
267	21135052	TRPM2: a multifunctional ion channel for calcium signalling.
268	21135052	The transient potential receptor melastatin-2 (TRPM2) channel has emerged as an important Ca(2+) signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death.
269	21135052	Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress-related pathologies.
270	21135052	TRPM2 is a non-selective, calcium (Ca(2+))-permeable cation channel of the melastatin-related transient receptor potential (TRPM) ion channel subfamily.
271	21135052	In addition to its role mediating Ca(2+) influx into the cells, TRPM2 can also function as a lysosomal Ca(2+) release channel, contributing to cell death.
272	21135052	The physiological and pathophysiological context of ROS-mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases.
273	21135052	TRPM2: a multifunctional ion channel for calcium signalling.
274	21135052	The transient potential receptor melastatin-2 (TRPM2) channel has emerged as an important Ca(2+) signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death.
275	21135052	Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress-related pathologies.
276	21135052	TRPM2 is a non-selective, calcium (Ca(2+))-permeable cation channel of the melastatin-related transient receptor potential (TRPM) ion channel subfamily.
277	21135052	In addition to its role mediating Ca(2+) influx into the cells, TRPM2 can also function as a lysosomal Ca(2+) release channel, contributing to cell death.
278	21135052	The physiological and pathophysiological context of ROS-mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases.
279	21290315	The TRPC members TRPC3 and TRPC4 can serve as subunits of a redox-sensitive ion channel in native aortic endothelial cells.
280	21290315	The TRPM family member TRPM2 has a number of physiologic isoforms expressed in many cell types and responds to stimuli including oxidative stress, TNFα, and β-amyloid peptide.
281	21290315	The important role of TRPM2 isoforms in cell proliferation and oxidant-induced cell death has been well established using divergent cell systems and techniques including overexpression, channel depletion or inhibition, and calcium chelation.
282	21290315	The TRPC members TRPC3 and TRPC4 can serve as subunits of a redox-sensitive ion channel in native aortic endothelial cells.
283	21290315	The TRPM family member TRPM2 has a number of physiologic isoforms expressed in many cell types and responds to stimuli including oxidative stress, TNFα, and β-amyloid peptide.
284	21290315	The important role of TRPM2 isoforms in cell proliferation and oxidant-induced cell death has been well established using divergent cell systems and techniques including overexpression, channel depletion or inhibition, and calcium chelation.
285	21468429	We developed a strategy involving comparative proteomic analysis to detect CLI associated plasma biomarkers. 2D-DIGE and subsequent MALDI-TOF MS analyses provided 50 differentially expressed plasma proteins (including alkaline phosphatase and haptoglobin), between hemodialytic diabetic patients with and without CLI.
286	21525168	Biometric evaluation of the fluorescence data followed by mass spectrometric protein identification revealed altered levels of 12, 71, and 13 protein species in the proteomes of the type-1 diabetic, type-2 diabetic, and non-diabetic obese patients, respectively, with considerably enhanced amounts of the same set of one molecular form of semenogelin-1, one form of clusterin, and two forms of lactotransferrin in each group of pathologic samples.
287	21636972	TRPM2 modulates insulin secretion in pancreatic β-cells.
288	21636972	One recent report found that TRPM2 is expressed in pancreatic β-cells and modulates insulin secretion stimulated by glucose and further potentiated by incretin hormones.
289	21636972	Glucose tolerance was impaired and insulin secretion was decreased in TRPM2 knockout mice.
290	21636972	Insulin secretion via TRPM2 occurs not only through control of intracellular Ca2+ concentrations but also through Ca2+ influx-independent mechanisms.
291	21636972	Although further examination is needed to clarify the mechanism of TRPM2-mediated insulin secretion, TRPM2 may be a key player in regulation of insulin secretion and could represent a new target for diabetes therapy.
292	21636972	TRPM2 modulates insulin secretion in pancreatic β-cells.
293	21636972	One recent report found that TRPM2 is expressed in pancreatic β-cells and modulates insulin secretion stimulated by glucose and further potentiated by incretin hormones.
294	21636972	Glucose tolerance was impaired and insulin secretion was decreased in TRPM2 knockout mice.
295	21636972	Insulin secretion via TRPM2 occurs not only through control of intracellular Ca2+ concentrations but also through Ca2+ influx-independent mechanisms.
296	21636972	Although further examination is needed to clarify the mechanism of TRPM2-mediated insulin secretion, TRPM2 may be a key player in regulation of insulin secretion and could represent a new target for diabetes therapy.
297	21636972	TRPM2 modulates insulin secretion in pancreatic β-cells.
298	21636972	One recent report found that TRPM2 is expressed in pancreatic β-cells and modulates insulin secretion stimulated by glucose and further potentiated by incretin hormones.
299	21636972	Glucose tolerance was impaired and insulin secretion was decreased in TRPM2 knockout mice.
300	21636972	Insulin secretion via TRPM2 occurs not only through control of intracellular Ca2+ concentrations but also through Ca2+ influx-independent mechanisms.
301	21636972	Although further examination is needed to clarify the mechanism of TRPM2-mediated insulin secretion, TRPM2 may be a key player in regulation of insulin secretion and could represent a new target for diabetes therapy.
302	21636972	TRPM2 modulates insulin secretion in pancreatic β-cells.
303	21636972	One recent report found that TRPM2 is expressed in pancreatic β-cells and modulates insulin secretion stimulated by glucose and further potentiated by incretin hormones.
304	21636972	Glucose tolerance was impaired and insulin secretion was decreased in TRPM2 knockout mice.
305	21636972	Insulin secretion via TRPM2 occurs not only through control of intracellular Ca2+ concentrations but also through Ca2+ influx-independent mechanisms.
306	21636972	Although further examination is needed to clarify the mechanism of TRPM2-mediated insulin secretion, TRPM2 may be a key player in regulation of insulin secretion and could represent a new target for diabetes therapy.
307	21636972	TRPM2 modulates insulin secretion in pancreatic β-cells.
308	21636972	One recent report found that TRPM2 is expressed in pancreatic β-cells and modulates insulin secretion stimulated by glucose and further potentiated by incretin hormones.
309	21636972	Glucose tolerance was impaired and insulin secretion was decreased in TRPM2 knockout mice.
310	21636972	Insulin secretion via TRPM2 occurs not only through control of intracellular Ca2+ concentrations but also through Ca2+ influx-independent mechanisms.
311	21636972	Although further examination is needed to clarify the mechanism of TRPM2-mediated insulin secretion, TRPM2 may be a key player in regulation of insulin secretion and could represent a new target for diabetes therapy.
312	21744203	Knock out models of TRPM2 and TRPM5, which show a pre-diabetic phenotype, will be illustrative for this purpose.
313	21744203	In addition, an unexpected role of the TRP channel TRPM3 as a gatekeeper of zinc, which is required for insulin storage, will be considered.
314	21782840	Molecular physiology of glucagon-like peptide-1 insulin secretagogue action in pancreatic β cells.
315	21782840	Insulin secretion from pancreatic β cells is stimulated by glucagon-like peptide-1 (GLP-1), a blood glucose-lowering hormone that is released from enteroendocrine L cells of the distal intestine after the ingestion of a meal.
316	21782840	GLP-1 mimetics (e.g., Byetta) and GLP-1 analogs (e.g., Victoza) activate the β cell GLP-1 receptor (GLP-1R), and these compounds stimulate insulin secretion while also lowering levels of blood glucose in patients diagnosed with type 2 diabetes mellitus (T2DM).
317	21782840	Investigational compounds that stimulate GLP-1 secretion also exist, and in this regard a noteworthy advance is the demonstration that small molecule GPR119 agonists (e.g., AR231453) stimulate L cell GLP-1 secretion while also directly stimulating β cell insulin release.
318	21782840	In this review, we summarize what is currently known concerning the signal transduction properties of the β cell GLP-1R as they relate to insulin secretion.
319	21782840	Emphasized are the cyclic AMP, protein kinase A, and Epac2-mediated actions of GLP-1 to regulate ATP-sensitive K⁺ channels, voltage-dependent K⁺ channels, TRPM2 cation channels, intracellular Ca⁺ release channels, and Ca⁺-dependent exocytosis.
320	21785227	Interestingly, six of them (TRPM2, TRPM4, TRPM5, TRPV1, TRPV2 and TRPV4) are thermosensitive TRP channels.
321	21785227	TRPM channels (TRPM2, TRPM4 and TRPM5) control insulin secretion levels by sensing intracellular Ca2+ increase, NAD metabolites, or hormone receptor activation.
322	21785227	TRPV2 is involved not only in insulin secretion but also cell proliferation, and is regulated by the autocrine effects of insulin.
323	21785227	Interestingly, six of them (TRPM2, TRPM4, TRPM5, TRPV1, TRPV2 and TRPV4) are thermosensitive TRP channels.
324	21785227	TRPM channels (TRPM2, TRPM4 and TRPM5) control insulin secretion levels by sensing intracellular Ca2+ increase, NAD metabolites, or hormone receptor activation.
325	21785227	TRPV2 is involved not only in insulin secretion but also cell proliferation, and is regulated by the autocrine effects of insulin.
326	21800835	Among the 35 proteins identified and quantified, Apo AII, clusterin, hemopexin precursor, and potassium voltage-gated channel subfamily H member 7 showed the most dramatic changes in concentration.
327	21969220	These new developments lead to the identification of urinary protein biomarkers, including Kim-1, clusterin, osteopontin or RPA-1, and other transcriptional biomarkers which enable the earlier detection of AKI and deliver further information about the area of nephron damage or the underlying mechanism.
328	22736507	Liquid chromatography-tandem mass spectroscopy-based analysis revealed increases in urinary proteins that are early indicators of DN (e.g., cystatin C, clusterin, cathepsin B, retinol binding protein 4, and peroxiredoxin-1) in the STZ group, which were blocked by suramin.
329	22736507	Endothelial intracellular adhesion molecule-1 (ICAM-1) activation, leukocyte infiltration, and inflammation; transforming growth factor-β1 (TGF-β1) signaling; TGF-β1/SMAD-3-activated fibrogenic markers fibronectin-1, α-smooth muscle actin, and collagen 1A2; activation of proinflammatory and profibrotic transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription factor-3 (STAT-3), respectively, were all increased in STZ rats and suramin blocked these changes.
330	22736507	In conclusion, delayed administration of suramin attenuated 1) urinary markers of DN, 2) inflammation by blocking NF-κB activation and ICAM-1-mediated leukocyte infiltration, and 3) fibrosis by blocking STAT-3 and TGF-β1/SMAD-3 signaling.
331	22750002	Divalent copper is a potent extracellular blocker for TRPM2 channel.
332	22750002	Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cationic channel in the TRP channel family.
333	22750002	However, little is known about the effect of redox-active metal ions, such as copper, on TRPM2 channels.
334	22750002	TRPM2 channel was over-expressed in HEK-293 cells and the whole-cell current was recorded by patch clamp.
335	22750002	TRPM2 current was also blocked by Hg(2+), Pb(2+), Fe(2+) and Se(2+).
336	22750002	We concluded that Cu(2+) is a potent TRPM2 channel blocker.
337	22750002	The sensitivity of TRPM2 channel to heavy metal ions could be a new mechanism for the pathogenesis of some metal ion-related diseases.
338	22750002	Divalent copper is a potent extracellular blocker for TRPM2 channel.
339	22750002	Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cationic channel in the TRP channel family.
340	22750002	However, little is known about the effect of redox-active metal ions, such as copper, on TRPM2 channels.
341	22750002	TRPM2 channel was over-expressed in HEK-293 cells and the whole-cell current was recorded by patch clamp.
342	22750002	TRPM2 current was also blocked by Hg(2+), Pb(2+), Fe(2+) and Se(2+).
343	22750002	We concluded that Cu(2+) is a potent TRPM2 channel blocker.
344	22750002	The sensitivity of TRPM2 channel to heavy metal ions could be a new mechanism for the pathogenesis of some metal ion-related diseases.
345	22750002	Divalent copper is a potent extracellular blocker for TRPM2 channel.
346	22750002	Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cationic channel in the TRP channel family.
347	22750002	However, little is known about the effect of redox-active metal ions, such as copper, on TRPM2 channels.
348	22750002	TRPM2 channel was over-expressed in HEK-293 cells and the whole-cell current was recorded by patch clamp.
349	22750002	TRPM2 current was also blocked by Hg(2+), Pb(2+), Fe(2+) and Se(2+).
350	22750002	We concluded that Cu(2+) is a potent TRPM2 channel blocker.
351	22750002	The sensitivity of TRPM2 channel to heavy metal ions could be a new mechanism for the pathogenesis of some metal ion-related diseases.
352	22750002	Divalent copper is a potent extracellular blocker for TRPM2 channel.
353	22750002	Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cationic channel in the TRP channel family.
354	22750002	However, little is known about the effect of redox-active metal ions, such as copper, on TRPM2 channels.
355	22750002	TRPM2 channel was over-expressed in HEK-293 cells and the whole-cell current was recorded by patch clamp.
356	22750002	TRPM2 current was also blocked by Hg(2+), Pb(2+), Fe(2+) and Se(2+).
357	22750002	We concluded that Cu(2+) is a potent TRPM2 channel blocker.
358	22750002	The sensitivity of TRPM2 channel to heavy metal ions could be a new mechanism for the pathogenesis of some metal ion-related diseases.
359	22750002	Divalent copper is a potent extracellular blocker for TRPM2 channel.
360	22750002	Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cationic channel in the TRP channel family.
361	22750002	However, little is known about the effect of redox-active metal ions, such as copper, on TRPM2 channels.
362	22750002	TRPM2 channel was over-expressed in HEK-293 cells and the whole-cell current was recorded by patch clamp.
363	22750002	TRPM2 current was also blocked by Hg(2+), Pb(2+), Fe(2+) and Se(2+).
364	22750002	We concluded that Cu(2+) is a potent TRPM2 channel blocker.
365	22750002	The sensitivity of TRPM2 channel to heavy metal ions could be a new mechanism for the pathogenesis of some metal ion-related diseases.
366	22750002	Divalent copper is a potent extracellular blocker for TRPM2 channel.
367	22750002	Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cationic channel in the TRP channel family.
368	22750002	However, little is known about the effect of redox-active metal ions, such as copper, on TRPM2 channels.
369	22750002	TRPM2 channel was over-expressed in HEK-293 cells and the whole-cell current was recorded by patch clamp.
370	22750002	TRPM2 current was also blocked by Hg(2+), Pb(2+), Fe(2+) and Se(2+).
371	22750002	We concluded that Cu(2+) is a potent TRPM2 channel blocker.
372	22750002	The sensitivity of TRPM2 channel to heavy metal ions could be a new mechanism for the pathogenesis of some metal ion-related diseases.
373	22750002	Divalent copper is a potent extracellular blocker for TRPM2 channel.
374	22750002	Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cationic channel in the TRP channel family.
375	22750002	However, little is known about the effect of redox-active metal ions, such as copper, on TRPM2 channels.
376	22750002	TRPM2 channel was over-expressed in HEK-293 cells and the whole-cell current was recorded by patch clamp.
377	22750002	TRPM2 current was also blocked by Hg(2+), Pb(2+), Fe(2+) and Se(2+).
378	22750002	We concluded that Cu(2+) is a potent TRPM2 channel blocker.
379	22750002	The sensitivity of TRPM2 channel to heavy metal ions could be a new mechanism for the pathogenesis of some metal ion-related diseases.