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TRPC1 encodes a melanosomal enzyme that belongs to the tyrosinase family and plays an important role in the melanin biosynthetic pathway. Additionally we are shipping Transient Receptor Potential Cation Channel, Subfamily C, Member 1 Antibodies (85) and Transient Receptor Potential Cation Channel, Subfamily C, Member 1 Kits (3) and many more products for this protein.
Showing 3 out of 6 products:
these results suggest that dopaminergic neurotoxins initially decreased Ca(2 (show CA2 Proteins)+) entry, which inhibited the binding of NF-kappaB (show NFKB1 Proteins) to the TRPC1 promoter, thereby inhibiting TRPC1 expression and resulting in cell death by preventing autophagy.
TRPC1 regulated HIF1alpha (show HIF1A Proteins) levels in PTEN-deficient MDA-MB-468 and HCC1569 breast cancer cell lines. This regulation arises from effects on the constitutive translation of HIF1alpha (show HIF1A Proteins) under normoxic conditions via an Akt (show AKT1 Proteins)-dependent pathway.
Store-operated calcium entry (SOCE), a unique plasma membrane Ca(2 (show CA2 Proteins)+) entry mechanism, is activated when ER-[Ca(2 (show CA2 Proteins)+)] is decreased. SOCE is mediated via the primary channel, Orai1, as well as others such as TRPC1.
the role of TRPC1 in the development of podocyte injury and disorders of the podocyte cytoskeleton, which may contribute to the development of novel therapeutics for podocyte injury-associated kidney diseases.
TRPC1 is a primary candidate in forming SOCC that stimulates CaSRinduced SOCE and NO production in HUVECs
TRPC1-STIM1 activation modulates transforming growth factor beta-induced epithelial-to-mesenchymal transition and cell migration.
Data show that RNAi-mediated knockdown of KCa3.1 (show KCNN4 Proteins) and/or TRPC1 leads to a significant decrease in cell proliferation due to cell cycle arrest in the G1 phase
Data indicate that the inhibition of the Store Operated Calcium Entry (SOCE)-dependent colon cancer cell migration through SK3 (show KCNN3 Proteins)/TRPC1/Orai1 channel complex by the alkyl-lipid Ohmline may be a strategy to modulate Anti-EGFR (show EGFR Proteins) mAb action in metastatic colorectal cancer (mCRC).
This study provided direct evidence that increasing extracellular Ca(2 (show CA2 Proteins)+) enhanced TNF-alpha (show TNF Proteins)-induced VCAM-1 (show VCAM1 Proteins) activation and monocytes adhesion. Moreover, we identified a novel TRPC1/ERK1/2/NFkappaB (show NFKB1 Proteins) signaling pathway mediating VCAM-1 (show VCAM1 Proteins) activation and monocyte adhesion in this pathological process.
These observations suggest that mechanical stretch may induce an influx of Ca(2 (show CA2 Proteins)+) and up-regulation of IL-13 (show IL13 Proteins) and MMP-9 (show MMP9 Proteins) expression in 16HBE cells via activation of TRPC1
Endogenous as well as overexpressed xTRPV6 interacts with xTRPC1.
our results suggest that calcium influx through mechanosensitive TRPC1 channels on filopodia activates calpain to control growth cone turning during development.
This study suggested that BDNF (show BDNF Proteins)-induced synaptic potentiation involves coordinated presynaptic and postsynaptic responses and identifies TRPC1 as a molecular mediator for postsynaptic Ca2 (show CA2 Proteins)+ elevation required for BDNF (show BDNF Proteins)-induced synaptic plasticity.
XTRPC1, a Xenopus homolog of mammalian TRPC1, is required for proper growth cone turning responses of Xenopus spinal neurons to netrin-1 (show NTN1 Proteins), brain-derived neurotrophic factor (show BDNF Proteins) and myelin-associated glycoprotein (show MAG Proteins), but not to semaphorin 3A (show SEMA3A Proteins).
downregulation of Xenopus TRP-1 (show TYRP1 Proteins) (xTRPC1) expression with a specific morpholino oligonucleotide abolished the growth-cone turning and Ca2 (show CA2 Proteins)+ elevation induced by a netrin-1 (show NTN1 Proteins) gradient
By use of electrophysiology and intracellular Ca2 (show CA2 Proteins)+ imaging, this study characterises a Ca2 (show CA2 Proteins)+ permeable channel in white adipocytes. The current shows functional characteristics resembling the Ca2 (show CA2 Proteins)+ -permeable transient receptor potential channel 1 (TRPC1).
Silencing of beta 1 integrin gene regulates the gene expression of storeoperated Ca2 (show CA2 Proteins)+ entry (SOCE)-associated genes (STIM1 (show STIM1 Proteins), ORAI1 (show TMEM132A Proteins) and TRPC1).
TRPC3-induced Ca2+ entry promotes astrocyte proliferation and migration i.e. astrocyte activity in vitro which is attenuated by the presence of TRPC1. Following brain injury, the absence of TRPC3 results in a significant reduction of astrogliosis and cortical edema in vivo, suggesting that a targeted therapy to reduce TRPC3 channel activity might be beneficial in traumatic brain injury.
Data show that transient receptor potential channel 1 (TRPC1) deficiency caused neuronal apoptosis in basal ganglia.
TRPC1 is indispensable for the enriched environment-induced hippocampal neurogenesis and cognitive enhancement.
Data (including data from studies using knockout mice) suggest that TRPC1 inhibits positive effects of exercise on insulin (show INS Proteins) resistance and type II diabetes in a high-fat diet-induced obesity environment.
TRPC1 regulated directly or indirectly the expression of multiple proteins, which may be crucial for the maintenance of memory ability.
we confirmed that the activation of OTX2 (show OTX2 Proteins), a determinant of DA neuron development and the expression of which is induced by thyroid hormone (show PTH Proteins), is dependent on TRPC1-mediated calcium signaling.
the link between HG-induced changes in TRPC1 expression, enhanced Ca(2 (show CA2 Proteins)+) entry, and endothelial dysfunction require further study
These results provide the first in vivo evidence that TRPC1 is essential for angiogenesis in zebrafish.
Demonstrate a novel role of the NO-cGMP-PKG (show PRKG1 Proteins) pathway in the inhibition of 11,12-EET-induced smooth muscle hyperpolarization and relaxation via PKG (show PRKG1 Proteins)-mediated phosphorylation of TRPC1.
Data found that the pig adrenal medulla expressed predominantly TRPC1, TRPC5 (show TRPC5 Proteins), and TRPC6 (show TRPC6 Proteins) transcripts. The expression level of these TRPCs was significantly elevated in the adrenal medulla from pigs with metabolic syndrome.
Heteromeric TRPV4 (show TRPV4 Proteins)-TRPC1 channels mediate CaSR (show CASR Proteins)-induced vasorelaxation through NO production but not IKCa channel activation in rabbit mesenteric arteries.
a novel activation mechanism for TRPC1 SOCs in VSMCs, in which store depletion induces formation of TRPC1-Galphaq-PLCbeta1 complexes that lead to PKC stimulation and channel gating.
The protein encoded by this gene is a membrane protein that can form a non-selective channel permeable to calcium and other cations. The encoded protein appears to be induced to form channels by a receptor tyrosine kinase-activated phosphatidylinositol second messenger system and also by depletion of intracellular calcium stores. Two transcript variants encoding different isoforms have been found for this gene.
, short transient receptor potential channel 1
, transient receptor potential canonical 1
, transient receptor protein 1
, transient receptor potential protein
, trp-related protein 1
, transient receptor potential channel 1
, store-operated calcium channel
, transient receptor potential channel subfamily C member 1
, transient receptor potential cation channel, subfamily C, member 1
, transient receptor potential cation channel subfamily C member 1
, short transient receptor potential channel 1-like
, calcium influx channel TRPC1A
, putative calcium influx channel TRPC1A