Regulatory role of neuron-restrictive silencing factor in expression of TRPC1

Takayoshi Ohba; Hiroyuki Watanabe; Yoichiro Takahashi; Takashi Suzuki; Ichiro Miyoshi; Shinnsuke Nakayama; Eisaku Satoh; Kenji Iino; Hironobu Sasano; Yasuo Mori; Sadao Kuromitsu; Keiichi Imagawa; Yoshihiko Saito; Toshihiko Iijima; Hiroshi Ito; Manabu Murakami

doi:10.1016/j.bbrc.2006.10.107

Regulatory role of neuron-restrictive silencing factor in expression of TRPC1

Takayoshi Ohba, Hiroyuki Watanabe, Yoichiro Takahashi, Takashi Suzuki, Ichiro Miyoshi, Shinnsuke Nakayama, Eisaku Satoh, Kenji Iino, Hironobu Sasano, Yasuo Mori, Sadao Kuromitsu, Keiichi Imagawa, Yoshihiko Saito, Toshihiko Iijima, Hiroshi Ito, Manabu Murakami

Research output: Contribution to journal › Article › peer-review

25 Citations (Scopus)

Abstract

Neuron-restrictive silencer factor (NRSF) binds its consensus element to repress the transcription of various genes. The dominant-negative form (dnNRSF) has a hypertrophic effect on cardiogenesis through an unidentified mechanism. We examined the involvement of transient receptor potential (TRP) channel proteins, using transgenic mice overexpressing dnNRSF (dnNRSF mice). Electrophoretic mobility-shift assays revealed an interaction between NRSF and a neuron-restrictive silencer element-like sequence in intron 4 of TRPC1 genomic DNA. According to RT-PCR and Western analyses, TRPC1 was up-regulated in dnNRSF mouse heart. Transient overexpression of TRPC1 in HEK 293T cells increased the activity of the nuclear factor in activated T cells (NFAT) promoter and stimulated store-operated Ca²⁺ channel (SOCC)-mediated Ca²⁺ entry. Transfection of TRPC1 into primary cardiomyocytes increased NFAT activity, indicating a major role for TRPC1 in NFAT activation. Our findings strongly suggest that NRSF regulates TRP1 gene expression and causes changes in the levels of calcium entry through SOCCs.

Original language	English
Pages (from-to)	764-770
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	351
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2006.10.107
Publication status	Published - 2006 Dec 22

Keywords

NRSF
SOC
TRPC1

Access to Document

10.1016/j.bbrc.2006.10.107

Cite this

Ohba, T., Watanabe, H., Takahashi, Y., Suzuki, T., Miyoshi, I., Nakayama, S., Satoh, E., Iino, K., Sasano, H., Mori, Y., Kuromitsu, S., Imagawa, K., Saito, Y., Iijima, T., Ito, H., & Murakami, M. (2006). Regulatory role of neuron-restrictive silencing factor in expression of TRPC1. Biochemical and Biophysical Research Communications, 351(3), 764-770. https://doi.org/10.1016/j.bbrc.2006.10.107

@article{a56c183205d64415a40f29de33d642d6,

title = "Regulatory role of neuron-restrictive silencing factor in expression of TRPC1",

abstract = "Neuron-restrictive silencer factor (NRSF) binds its consensus element to repress the transcription of various genes. The dominant-negative form (dnNRSF) has a hypertrophic effect on cardiogenesis through an unidentified mechanism. We examined the involvement of transient receptor potential (TRP) channel proteins, using transgenic mice overexpressing dnNRSF (dnNRSF mice). Electrophoretic mobility-shift assays revealed an interaction between NRSF and a neuron-restrictive silencer element-like sequence in intron 4 of TRPC1 genomic DNA. According to RT-PCR and Western analyses, TRPC1 was up-regulated in dnNRSF mouse heart. Transient overexpression of TRPC1 in HEK 293T cells increased the activity of the nuclear factor in activated T cells (NFAT) promoter and stimulated store-operated Ca2+ channel (SOCC)-mediated Ca2+ entry. Transfection of TRPC1 into primary cardiomyocytes increased NFAT activity, indicating a major role for TRPC1 in NFAT activation. Our findings strongly suggest that NRSF regulates TRP1 gene expression and causes changes in the levels of calcium entry through SOCCs.",

keywords = "NRSF, SOC, TRPC1",

author = "Takayoshi Ohba and Hiroyuki Watanabe and Yoichiro Takahashi and Takashi Suzuki and Ichiro Miyoshi and Shinnsuke Nakayama and Eisaku Satoh and Kenji Iino and Hironobu Sasano and Yasuo Mori and Sadao Kuromitsu and Keiichi Imagawa and Yoshihiko Saito and Toshihiko Iijima and Hiroshi Ito and Manabu Murakami",

note = "Funding Information: This research was sponsored by Grants-in-Aid for Scientific Research from JSPS, KAKENHI, and a Japan Heart Foundation/Pfizer Grant for Research on Hypertension, Hyperlipidemia, and Vascular Metabolism (H.W.). We thank Misato Sugawara and Dr. Milena D. Radovanovic. ",

year = "2006",

month = dec,

day = "22",

doi = "10.1016/j.bbrc.2006.10.107",

language = "English",

volume = "351",

pages = "764--770",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Academic Press Inc.",

number = "3",

}

Ohba, T, Watanabe, H, Takahashi, Y, Suzuki, T , Miyoshi, I, Nakayama, S, Satoh, E, Iino, K, Sasano, H, Mori, Y, Kuromitsu, S, Imagawa, K, Saito, Y, Iijima, T, Ito, H & Murakami, M 2006, 'Regulatory role of neuron-restrictive silencing factor in expression of TRPC1', Biochemical and Biophysical Research Communications, vol. 351, no. 3, pp. 764-770. https://doi.org/10.1016/j.bbrc.2006.10.107

TY - JOUR

T1 - Regulatory role of neuron-restrictive silencing factor in expression of TRPC1

AU - Ohba, Takayoshi

AU - Watanabe, Hiroyuki

AU - Takahashi, Yoichiro

AU - Suzuki, Takashi

AU - Miyoshi, Ichiro

AU - Nakayama, Shinnsuke

AU - Satoh, Eisaku

AU - Iino, Kenji

AU - Sasano, Hironobu

AU - Mori, Yasuo

AU - Kuromitsu, Sadao

AU - Imagawa, Keiichi

AU - Saito, Yoshihiko

AU - Iijima, Toshihiko

AU - Ito, Hiroshi

AU - Murakami, Manabu

N1 - Funding Information: This research was sponsored by Grants-in-Aid for Scientific Research from JSPS, KAKENHI, and a Japan Heart Foundation/Pfizer Grant for Research on Hypertension, Hyperlipidemia, and Vascular Metabolism (H.W.). We thank Misato Sugawara and Dr. Milena D. Radovanovic.

PY - 2006/12/22

Y1 - 2006/12/22

N2 - Neuron-restrictive silencer factor (NRSF) binds its consensus element to repress the transcription of various genes. The dominant-negative form (dnNRSF) has a hypertrophic effect on cardiogenesis through an unidentified mechanism. We examined the involvement of transient receptor potential (TRP) channel proteins, using transgenic mice overexpressing dnNRSF (dnNRSF mice). Electrophoretic mobility-shift assays revealed an interaction between NRSF and a neuron-restrictive silencer element-like sequence in intron 4 of TRPC1 genomic DNA. According to RT-PCR and Western analyses, TRPC1 was up-regulated in dnNRSF mouse heart. Transient overexpression of TRPC1 in HEK 293T cells increased the activity of the nuclear factor in activated T cells (NFAT) promoter and stimulated store-operated Ca2+ channel (SOCC)-mediated Ca2+ entry. Transfection of TRPC1 into primary cardiomyocytes increased NFAT activity, indicating a major role for TRPC1 in NFAT activation. Our findings strongly suggest that NRSF regulates TRP1 gene expression and causes changes in the levels of calcium entry through SOCCs.

AB - Neuron-restrictive silencer factor (NRSF) binds its consensus element to repress the transcription of various genes. The dominant-negative form (dnNRSF) has a hypertrophic effect on cardiogenesis through an unidentified mechanism. We examined the involvement of transient receptor potential (TRP) channel proteins, using transgenic mice overexpressing dnNRSF (dnNRSF mice). Electrophoretic mobility-shift assays revealed an interaction between NRSF and a neuron-restrictive silencer element-like sequence in intron 4 of TRPC1 genomic DNA. According to RT-PCR and Western analyses, TRPC1 was up-regulated in dnNRSF mouse heart. Transient overexpression of TRPC1 in HEK 293T cells increased the activity of the nuclear factor in activated T cells (NFAT) promoter and stimulated store-operated Ca2+ channel (SOCC)-mediated Ca2+ entry. Transfection of TRPC1 into primary cardiomyocytes increased NFAT activity, indicating a major role for TRPC1 in NFAT activation. Our findings strongly suggest that NRSF regulates TRP1 gene expression and causes changes in the levels of calcium entry through SOCCs.

KW - NRSF

KW - SOC

KW - TRPC1

UR - http://www.scopus.com/inward/record.url?scp=33750731643&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750731643&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2006.10.107

DO - 10.1016/j.bbrc.2006.10.107

M3 - Article

C2 - 17084381

AN - SCOPUS:33750731643

SN - 0006-291X

VL - 351

SP - 764

EP - 770

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 3

ER -

Regulatory role of neuron-restrictive silencing factor in expression of TRPC1

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this