|  Help  |  About  |  Contact Us

Publication : Involvement of TRPV3 and TRPM8 ion channel proteins in induction of mammalian cold-inducible proteins.

First Author  Fujita T Year  2018
Journal  Biochem Biophys Res Commun Volume  495
Issue  1 Pages  935-940
PubMed ID  29175331 Mgi Jnum  J:271439
Mgi Id  MGI:6280806 Doi  10.1016/j.bbrc.2017.11.136
Citation  Fujita T, et al. (2018) Involvement of TRPV3 and TRPM8 ion channel proteins in induction of mammalian cold-inducible proteins. Biochem Biophys Res Commun 495(1):935-940
abstractText  Cold-inducible RNA-binding protein (CIRP), RNA-binding motif protein 3 (RBM3) and serine and arginine rich splicing factor 5 (SRSF5) are RNA-binding proteins that are transcriptionally upregulated in response to moderately low temperatures and a variety of cellular stresses in mammalian cells. Induction of these cold-inducible proteins (CIPs) is dependent on transient receptor potential (TRP) V4 channel protein, but seems independent of its ion channel activity. We herein report that in addition to TRPV4, TRPV3 and TRPM8 are necessary for the induction of CIPs. We established cell lines from the lung of TRPV4-knockout (KO) mouse, and observed induction of CIPs in them by western blot analysis. A TRPV4 antagonist RN1734 suppressed the induction in wild-type mouse cells, but not in TRPV4-KO cells. A TRPV3 channel blocker S408271 and a TRPM8 channel blocker AMTB as well as siRNAs against TRPV3 and TRPM8 suppressed the CIP induction in mouse TRPV4-KO cells and human U-2 OS cells. A TRPV3 channel agonist 2-APB induced CIP expression, but camphor did not. Neither did a TRPM8 channel agonist WS-12. These results suggest that TRPV4, TRPV3 and TRPM8 proteins, but not their ion channel activities are necessary for the induction of CIPs at 32 degrees C. Identification of proteins that differentially interact with these TRP channels at 37 degrees C and 32 degrees C would help elucidate the underlying mechanisms of CIP induction by hypothermia.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

5 Bio Entities

Trail: Publication

0 Expression