Regulatory role of neuron-restrictive silencing factor in expression of TRPC1
- Second Department of Internal Medicine, Akita University School of Medicine, Akita (Japan)
- Department of Pathology, Tohoku University School of Medicine, Sendai (Japan)
- Center for Experimental Animal Science, Nagoya City University Graduate School of Medical Sciences, Nagoya (Japan)
- Department of Cell Physiology, Nagoya University Graduate School of Medicine, Tsuruma-cho, Shouwa, Nagoya (Japan)
- Department of Pharmacology, Akita University School of Medicine, 1-1-1 Hondoh, Akita 010-8543 (Japan)
- Laboratory of Molecular Biology, Department of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering, Kyoto University, Kyoto (Japan)
- Institute for Drug Discovery Research, Astellas Pharmaceutical Co. Ltd, Ibaraki (Japan)
- First Department of Internal Medicine, Nara Medical University, Nara (Japan)
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 Ca{sup 2+} channel (SOCC)-mediated Ca{sup 2+} 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.
- OSTI ID:
- 20857932
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 351, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2006.10.107; PII: S0006-291X(06)02374-6; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
Similar Records
Essential role of STIM1 in the development of cardiomyocyte hypertrophy
Annexin A7 deficiency potentiates cardiac NFAT activity promoting hypertrophic signaling