| First Author | Ohba T | Year | 2006 |
| Journal | Biochem Biophys Res Commun | Volume | 351 |
| Issue | 3 | Pages | 764-70 |
| PubMed ID | 17084381 | Mgi Jnum | J:115579 |
| Mgi Id | MGI:3691959 | Doi | 10.1016/j.bbrc.2006.10.107 |
| Citation | Ohba T, et al. (2006) Regulatory role of neuron-restrictive silencing factor in expression of TRPC1. Biochem Biophys Res Commun 351(3):764-70 |
| abstractText | 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(2+) channel (SOCC)-mediated Ca(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. |
