Trp1, a Candidate Protein for the Store-operated Ca2+Influx Mechanism in Salivary Gland Cells

Abstract

The trp gene family has been proposed to encode the store-operated Ca 2؉ influx (SOC) channel(s

Up-Regulation of Transient Receptor Potential Canonical 1 (TRPC1) following Sarco(endo)plasmic Reticulum Ca2+ATPase 2 Gene Silencing Promotes Cell Survival: A Potential Role for TRPC1 in Darier's Disease

“…Quantification of the TRPC1 band indicated an ϳ1.4-fold increase in DD patient samples ( Figure 1F), which was consistent with the confocal data described above. Although, the TRPC1 antibody used here is very specific (ϳ95% immunoreactivity toward TRPC1; Liu et al, 2000;Singh et al, 2001), similar results were also obtained using another B. Pani et al …”

“…However, the mechanism of this Ca 2ϩ -dependent regulation is not elaborately investigated. Our previous studies demonstrated that transient receptor potential canonical (TRPC)1 functions as store-operated calcium entry (SOCE) channel (Liu et al, 2000;Singh et al, 2001). Furthermore, a role of TRPC1 in the proliferation of neuronal and epithelial cells has been shown (Bollimuntha et al, 2005).…”

“…mRNA was isolated using oligo(dT) column (QIAGEN, Valencia, CA). First-strand cDNA synthesis and RT-PCR were performed as described previously (Liu et al, 2000;Bollimuntha et al, 2005). After 30 cycles of amplifications, 10 l of the RT-PCR product was analyzed on a 1% agarose gel, cloned into TA cloning vector (Invitrogen), and confirmed either by sequencing or restriction analysis.…”

Thapsigargin activates Ca2+ entry both by store-dependent, STIM1/Orai1-mediated, and store-independent, TRPC3/PLC/PKC-mediated pathways in human endothelial cells

“…Number of reports has shown a reduced SOCE activity when TRPC expression was knocked down or knocked out [8][9][10][11]. When exogenously expressed some TRPC channels displayed SOCE activity [12][13][14]. However, numerous studies also demonstrated that TRPC channels did not operate as SOCE channels, but rather are gated by second messengers like Ca 2+ or diacylglycerol (DAG; [15][16][17]).…”

TRPC3: a versatile transducer molecule that serves integration and diversification of cellular signals

“…Highly discrepant results obtained in heterologous expression studies and the inability to reproducibly reconstitute native capacitative Ca 2+ entry channels by overexpression of a TRPC species led to the hypothesis that TRPC proteins are pore-forming subunits, which may require association with unidentified endogenous proteins to form a SOCE (or CCE) channel (Sinkins et al 1998;McKay et al 2000). This concept was later on continuously supported by studies using antisense and siRNA knock-down strategies or expression of dominant negative TRP species to suppress or modify endogenous SOCE (Groschner et al 1998;Liu et al 2000;Philipp et al 2000;Wu et al 2000;Baldi et al 2003;Liu et al 2003;Wu et al 2004) and appears reasonable and sufficient to explain the phenomenon that expression of a TRPC species generates divergently regulated Ca 2+ entry pathways in different cell systems or even in one host cell type at different levels of expression . The concept implies that a given TRPC species is able to associate with other channel and auxiliary subunits to form distinct signaling complexes with a composition dependent on the availability of the complex partners.…”