TRPC7, affinity purified antibody, goat, 100 ug.
- Known as:
- TRPC7, antigenic enriched (anti-), caprine, 100 ug.
- Catalog number:
- GT41031-100
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- TRPC7 affinity purified antibody goat 100 .
Related genes to: TRPC7, affinity purified antibody, goat, 100 ug.
- Gene:
- TRPC7 NIH gene
- Name:
- transient receptor potential cation channel subfamily C member 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-31
- Date modifiied:
- 2016-10-25
- Gene:
- TRPM2 NIH gene
- Name:
- transient receptor potential cation channel subfamily M member 2
- Previous symbol:
- TRPC7
- Synonyms:
- KNP3, LTRPC2, NUDT9L1, NUDT9H, EREG1
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-23
- Date modifiied:
- 2016-01-28
- Gene:
- TRPM7 NIH gene
- Name:
- transient receptor potential cation channel subfamily M member 7
- Previous symbol:
- -
- Synonyms:
- CHAK1, LTRPC7, TRP-PLIK
- Chromosome:
- 15q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-11
- Date modifiied:
- 2019-04-23
Related products to: TRPC7, affinity purified antibody, goat, 100 ug.
Related articles to: TRPC7, affinity purified antibody, goat, 100 ug.
- Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and is a major cause of morbidity and mortality. The upregulation of TRP channels is believed to mediate the progression of electrical remodelling and the arrhythmogenesis of the diseased heart. However, there is limited data about the contribution of the TRP channels to development of AF. The aim of this study was to investigate leukocyte TRP channels gene expressions in non-valvular atrial fibrillation (NVAF) patients. The study included 47 NVAF patients and 47 sex and age matched controls. mRNA was extracted from blood samples, and real-time polymerase chain reaction was performed for gene expressions by using a dynamic array system. Low levels of TRP channel expressions in the controls were markedly potentiated in NVAF group. We observed marked increases in MCOLN1 (TRPML1), MCOLN2 (TRPML2), MCOLN3 (TRPML3), TRPA1, TRPM1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM6, TRPM7, TRPM8, TRPC1, TRPC2, TRPC3, TRPC4, TRPC5, TRPC6, TRPC7, TRPV1, TRPV2, TRPV3, TRPV4, TRPV5, TRPV6, and PKD2 (TRPP2) gene expressions in NVAF patients (P < 0.05). However, there was no change in PKD1 (TRPP1) gene expression. This is the first study to provide evidence that elevated gene expressions of TRP channels are associated with the pathogenesis of NVAF. - Source: PubMed
Publication date: 2017/08/24
Düzen Irfan VYavuz FethiVuruskan ErtanSaracoglu ErhanPoyraz FatihGöksülük HüseyinCandemir BasarDemiryürek Seniz - Ca2+ signaling plays a central role in microglial activation, and several studies have demonstrated a store-operated Ca2+ entry (SOCE) pathway to supply this ion. Due to the rapid pace of discovery of novel Ca2+ permeable channels, and limited electrophysiological analyses of Ca2+ currents in microglia, characterization of the SOCE channels remains incomplete. At present, the prime candidates are 'transient receptor potential' (TRP) channels and the recently cloned Orai1, which produces a Ca2+-release-activated Ca2+ (CRAC) current. We used cultured rat microglia and real-time RT-PCR to compare expression levels of Orai1, Orai2, Orai3, TRPM2, TRPM7, TRPC1, TRPC2, TRPC3, TRPC4, TRPC5, TRPC6 and TRPC7 channel genes. Next, we used Fura-2 imaging to identify a store-operated Ca2+ entry pathway that was reduced by depolarization and blocked by Gd3+, SKF-96365, diethylstilbestrol (DES), and a high concentration of 2-aminoethoxydiphenyl borate (50 microM 2-APB). The Fura-2 signal was increased by hyperpolarization, and by a low concentration of 2-APB (5 microM), and exhibited Ca(2+)-dependent potentiation. These properties are entirely consistent with Orai1/CRAC, rather than any known TRP channel and this conclusion was supported by patch-clamp electrophysiological analysis. We identified a store-operated Ca2+ current with the same properties, including high selectivity for Ca2+ over monovalent cations, pronounced inward rectification and a very positive reversal potential, Ca(2+)-dependent current potentiation, and block by SKF-96365, DES and 50 microM 2-APB. Determining the contribution of Orai1/CRAC in different cell types is crucial to future mechanistic and therapeutic studies; this comprehensive multi-strategy analysis demonstrates that Orai1/CRAC channels are responsible for SOCE in primary microglia. - Source: PubMed
Publication date: 2009/03/02
Ohana LilyNewell Evan WStanley Elise FSchlichter Lyanne C