Response to ADP-ribose by activation of TRPM2 in the CRI-G1 insulinoma cell line

被引：78

作者：

Inamura, K ^{[1
]}

Sano, Y ^{[1
]}

Mochizuki, S ^{[1
]}

Yokoi, H ^{[1
]}

Miyake, A ^{[1
]}

Nozawa, K ^{[1
]}

Kitada, C ^{[1
]}

Matsushime, H ^{[1
]}

Furuichi, K ^{[1
]}

机构：

[1] Yamanouchi Pharmaceut Co Ltd, Inst Drug Discovery Res, Mol Med Labs, Tsukuba, Ibaraki 3058585, Japan

来源：

JOURNAL OF MEMBRANE BIOLOGY | 2003年 / 191卷 / 03期

关键词：

ADP-ribose; beta-NAD; TRPM2; CRI-G1; cell; calcium;

D O I：

10.1007/s00232-002-1057-x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The response to intracellular ADP-ribose in the rat CRI-G1 insulinoma cell line was studied using a patch-clamp method. Dialysis of ADP-ribose into cells induced a response in a dose-dependent manner. The reversal potentials in various solutions showed that the ADP-ribose-gated channel was a Ca2+-permeable nonselective cation channel. In inside-out recordings, ADP-ribose and beta-NAD induced responses in the same patch. The single-channel current-voltage relationships for ADP-ribose- and beta-NAD-induced responses were almost identical, indicating that ADP-ribose and beta-NAD activated the same channel. The physiological properties of the ADP-ribose-gated channel are similar to those we reported previously for the cloned transient receptor potential channel TRPM2. Moreover, RT-PCR analysis showed that TRPM2 was abundantly expressed in CRI-G1 cells, suggesting that the ADPribose-gated channel represents the native TRPM2 channel in CRI-G1 cells. These results suggest that ADP-ribose can be an endogenous modulator of Ca2+ influx through the TRPM2 channel into CRI-G1 cells.

引用

页码：201 / 207

页数：7

共 40 条

[1] CA2+ AND PANCREATIC B-CELL FUNCTION
BERGGREN, PO
LARSSON, O
[J]. BIOCHEMICAL SOCIETY TRANSACTIONS, 1994, 22 (01) : 12 - 18
[2] INOSITOL 1,4,5-TRISPHOSPHATE MOBILIZES INTRACELLULAR CA-2+ FROM PERMEABILIZED INSULIN-SECRETING CELLS
BIDEN, TJ
PRENTKI, M
IRVINE, RF
BERRIDGE, MJ
WOLLHEIM, CB
[J]. BIOCHEMICAL JOURNAL, 1984, 223 (02) : 467 - 473
[3] Duncan LM, 1998, CANCER RES, V58, P1515
[4] EFENDIC S, 1991, J INTERN MED, V229, P9
[5] IMPROVED PATCH-CLAMP TECHNIQUES FOR HIGH-RESOLUTION CURRENT RECORDING FROM CELLS AND CELL-FREE MEMBRANE PATCHES
HAMILL, OP
MARTY, A
NEHER, E
SAKMANN, B
SIGWORTH, FJ
[J]. PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1981, 391 (02): : 85 - 100
[6] LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death
Hara, Y
Wakamori, M
Ishii, M
Maeno, E
Nishida, M
Yoshida, T
Yamada, H
Shimizu, S
Mori, E
Kudoh, J
Shimizu, N
Kurose, H
Okada, Y
Imoto, K
Mori, Y
[J]. MOLECULAR CELL, 2002, 9 (01) : 163 - 173
[7] From worm to man: three subfamilies of TRP channels
Harteneck, C
Plant, TD
Schultz, G
[J]. TRENDS IN NEUROSCIENCES, 2000, 23 (04) : 159 - 166
[8] Hydrogen peroxide induces intracellular calcium overload by activation of a non-selective cation channel in an insulin-secreting cell line
Herson, PS
Lee, K
Pinnock, RD
Hughes, J
Ashford, MLJ
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (02) : 833 - 841
[9] Characterization of a nicotinamide-adenine dinucleotide-dependent cation channel in the CRI-G1 rat insulinoma cell line
Herson, PS
Dulock, KA
Ashford, MLJ
[J]. JOURNAL OF PHYSIOLOGY-LONDON, 1997, 505 (01): : 65 - 76
[10] Activation of a novel non-selective cation channel by alloxan and H2O2 in the rat insulin-secreting cell line CRI-G1
Herson, PS
Ashford, MLJ
[J]. JOURNAL OF PHYSIOLOGY-LONDON, 1997, 501 (01): : 59 - 66

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