TRPC4
- Known as:
- TRPC4
- Catalog number:
- Y214131
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- TRPC4
Related genes to: TRPC4
- Gene:
- TRPC4 NIH gene
- Name:
- transient receptor potential cation channel subfamily C member 4
- Previous symbol:
- -
- Synonyms:
- HTRP4, TRP4
- Chromosome:
- 13q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2016-01-28
- Gene:
- TRPV4 NIH gene
- Name:
- transient receptor potential cation channel subfamily V member 4
- Previous symbol:
- -
- Synonyms:
- OTRPC4, TRP12, VROAC, VRL-2, VR-OAC, CMT2C
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-29
- Date modifiied:
- 2019-04-23
Related products to: TRPC4
alpha, beta, beta_2 TRPC4anti-TRPC4 (C-Terminus)anti-TRPC4 (S77-15)anti-TRPC4 (S77-15)anti-TRPC4 (S77-15) type: Primary antibodies host: MouseAnti-TRPC4 (S77-15), Mouse Monoclonal to TRPC4, Isotype IgG1, Host MouseAnti-TRPC4 (Transient Receptor Potential-Like Channel 4) produced in rabbit AntibodyAnti-TRPC4 AntibodyAnti-TRPC4 antibodyAnti-TRPC4 AntibodyAnti-TrpC4 Ca+ ChannelAnti-TRPC4, Goat Polyclonal to TRPC4, Isotype , Host GoatAntibodies: TRPC4 HOST: Goat Clonality: pAbBos taurus,Bovine,Capacitative calcium entry channel 1,CCE1,Short transient receptor potential channel 4,TrpC4,TRPC4Bovine Short transient receptor potential channel 4(TRPC4) ELISA kit Related articles to: TRPC4
- is the primary etiological agent of community-acquired pneumonia (CAP). Pneumococci promote severe lung injury through the release of virulence factors, including pneumolysin (PLY). Obesity/diabetes increases pneumonia-associated mortality, but the mechanisms remain elusive. We found that obese db/db mice have increased pulmonary barrier disruption to PLY. Previously we showed that upregulation of NOX1 in endothelial cells (EC) of db/db mice drives endothelial dysfunction, but a role for NOX1 in PLY-induced lung injury, especially in diabetic conditions, has not yet been described. Increased NOX1 in lung ECs dose-dependently increased superoxide and EC barrier disruption ( < 0.05). Even at low activity levels, NOX1 greatly potentiated PLY-induced EC barrier disruption, whereas loss of NOX1 activity, either pharmacological or genetic, reduced barrier disruption ( < 0.05). Blockade of calcium entry protected the EC barrier from combined PLY and NOX1, indicating a key role for calcium. Hyperglycemia amplified PLY-enduced EC barrier disruption and intracellular calcium and these effects were mitigated by NOX1 inhibition and silencing ( < 0.05). NOX1-enhanced calcium entry was reduced by knockout of calcium sensor STIM1, and PLY-induced barrier disruption was reduced by STIM1 inhibition. Levels of STIM1, Orai1, TRPV4, or TRPC4 were unchanged by HG, but TRPC1 significantly increased ( < 0.05). NOX1 and HG promoted increased STIM1 and TRPC1 binding, and silencing TRPC1 ameliorated PLY-induced barrier disruption ( < 0.05). Increased calcium promoted mitochondrial permeability transition pore (MPTP) opening and PPIF inhibition protected EC barrier function ( < 0.05). These results suggest that elevated glucose levels in obesity primes EC barrier disruption by amplifying PLY-induced calcium influx via a novel NOX1, STIM1, TRPC1 and MPTP signaling axis. - Source: PubMed
Publication date: 2026/02/24
Haigh StephenChen FengYu YanfangBordan ZsuzsannaLi XueyiSridhar SupriyaRomero Maritza JChakraborty TrinadCsanyi GaborJoshua Austin TPatel Tej VBrown Zachary LShivers Mitchel ASellers Hunter GAnanna FarhanaFukai TohruUshio-Fukai MasukoBelin de Chantemele Eric JVerin AlexanderStepp David WLucas RudolfFulton David J R - Disruption of Ca homeostasis after calcium electroporation (CaEP) in tumors has been shown to elicit an enhanced antitumor effect with varying impacts on healthy tissue, such as endothelium. Therefore, our study aimed to determine differences in Ca kinetics and gene expression involved in the regulation of Casignaling and homeostasis, as well as effects of CaEP on cytoskeleton and adherens junctions of the established endothelial cell lines EA.hy926 and HMEC-1. - Source: PubMed
Publication date: 2024/02/12
Lisec BarbaraBozic TimSantek IvaMarkelc BostjanVrecl MilkaFrangez RobertCemazar Maja - Human cardiac fibroblasts (HCFs) have mRNA transcripts that encode different mechanosensitive ion channels and channel regulatory proteins whose functions are not known yet. The primary goal of this work was to define the mechanosensitive ion channelome of HCFs. The most common type of cationic channel is the transient receptor potential (TRP) family, which is followed by the TWIK-related K channel (TREK), transmembrane protein 63 (TMEM63), and PIEZO channel (PIEZO) families. In the sodium-dependent NON-voltage-gated channel (SCNN) subfamily, only SCNN1D was shown to be highly expressed. Particular members of the acid-sensing ion channel (ASIC) (ASIC1 and ASIC3) subfamilies were also significantly expressed. The transcripts per kilobase million (TPMs) for Piezo 2 were almost 100 times less abundant than those for Piezo 1. The tandem of P domains in a weak inward rectifying K channel (TWIK)-2 channel, TWIK-related acid-sensitive K channel (TASK)-5, TASK-1, and the TWIK-related K1 (TREK-1) channel were the four most prevalent types in the K2P subfamily. The highest expression in the TRPP subfamily was found for PKD2 and PKD1, while in the TRPM subfamily, it was found for TRPM4, TRPM7, and TRPM3. TRPV2, TRPV4, TRPV3, and TRPV6 (all members of the TRPV subfamily) were also substantially expressed. A strong expression of the TRPC1, TRPC4, TRPC6, and TRPC2 channels and all members of the TRPML subfamily (MCOLN1, MCOLN2, and MCOLN3) was also shown. In terms of the transmembrane protein 16 (TMEM16) family, the HCFs demonstrated significant expression of the TMEM16H, TMEM16F, TMEM16J, TMEM16A, and TMEM16G channels. TMC3 is the most expressed channel in HCFs of all known members of the transmembrane channel-like protein (TMC) family. This analysis of the mechanosensitive ionic channel transcriptome in HCFs: (1) agrees with previously documented findings that all currently identified mechanosensitive channels play a significant and well recognized physiological function in elucidating the mechanosensitive characteristics of HCFs; (2) supports earlier preliminary reports that point to the most common expression of the TRP mechanosensitive family in HCFs; and (3) points to other new mechanosensitive channels (TRPC1, TRPC2, TWIK-2, TMEM16A, ASIC1, and ASIC3). - Source: PubMed
Publication date: 2023/12/30
Mitrokhin VadimBilichenko AndreiKazanski ViktorSchobik RomanShileiko StanislavRevkova VeronikaKalsin VladimirKamkina OlgaKamkin AndreMladenov Mitko - The channels from the superfamily of transient receptor potential (TRP) activated by reactive oxygen species (ROS) can be defined as redox channels. Those with the best exposure of the cysteine residues and, hence, the most sensitive to oxidative stress are TRPC4, TRPC5, TRPV1, TRPV4, and TRPA1, while others, such as TRPC3, TRPM2, and TRPM7, are indirectly activated by ROS. Furthermore, activation by ROS has different effects on the tumorigenic process: some TRP channels may, upon activation, stimulate proliferation, apoptosis, or migration of cancer cells, while others inhibit these processes, depending on the cancer type, tumoral microenvironment, and, finally, on the methods used for evaluation. Therefore, using these polymodal proteins as therapeutic targets is still an unmet need, despite their draggability and modulation by simple and mostly unharmful compounds. This review intended to create some cellular models of the interaction between oxidative stress, TRP channels, and inflammation. Although somewhat crosstalk between the three actors was rather theoretical, we intended to gather the recently published data and proposed pathways of cancer inhibition using modulators of TRP proteins, hoping that the experimental data corroborated clinical information may finally bring the results from the bench to the bedside. - Source: PubMed
Publication date: 2023/06/23
Piciu FlorentinaBalas MihaelaBadea Madalina AndreeaCucu Dana - Transient receptor potential (TRP) channels are involved in various physiological, pathological, and tumorigenesis-related processes. However, only a few studies have comprehensively analyzed TRP family members and their association with prognosis and tumor microenvironment (TME) in various cancers. Thus, in this study, we focused on TRP channels in pan-cancer and screened two typical TRP channels, TRPV4 and TRPC4, as examples. - Source: PubMed
Publication date: 2023/02/02
Chen ZhenghaoZhao YouquanTian YeCao RuiShang Donghao