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抗Human TRPV6 抗体:
抗Mouse (Murine) TRPV6 抗体:
抗Rat (Rattus) TRPV6 抗体:
This study provides both genetic and functional evidence that transcellular epithelial calcium uptake via TRPV5-6 is vital to sustain life and enable bone formation.
These results suggest that the zECaC plays a key role in Ca(2+) absorption in developing zebrafish.
TRPV6 and CaBP-9k are expressed during pregnancy in the bovine uterine endometrium and placentomes, suggesting a functional role for these proteins in Ca2+ metabolism during pregnancy.
TRPV5 and TRPV6 were upregulated with time and passage in culture suggesting that a shift in the phenotype of the cells in monolayer culture alters the expression of these channels.
TRPV6 mRNA levels were similar in the duodenum, kidney and heart of Equus caballus. Protein expression followed a similar pattern.
Transient neonatal hyperparathyroidism is an autosomal-recessive disease caused by TRPV6 mutations that affect maternal-fetal calcium transport.
this review describes the role of TRPV6 in male fertility and cancer
High TRPV6 expression is associated with development and progression of pancreatic cancer.
cryo-electron microscopy structures of human TRPV6 in the open and closed states
TRPV5 and TRPV6 lack a positively charged residue in the TM4-TM5 loop that was shown to interact with PI(4,5)P2 in TRPV1, which shows high affinity for this lipid
TRPV6 down-regulation is associated with decreased Ca(2+) response pattern and reduced NFAT activity.
TRPV6 expression is significantly decreased in chondrocytes from patients with osteoarthritis of the knees. TRPV6 could regulate certain chondrocyte functions, including ECM secretion, cell proliferation, and apoptosis.
The findings indicate that p38alpha and GADD45alpha are involved in an enhanced vitamin D signaling on TRPV6 expression.
TRPV6 is down-regulated in esophageal squamous cell carcinoma and plays a role in predicting survival of male and female patients.
These results suggest that CAT-1 is a novel CAM that directly regulates endothelial integrity and mediates the protective actions of L-Arg to endothelium via a NO-independent mechanism.
TRPV6 calcium ion channel plays a critical role in flow-induced Ca(2+) influx and microvilli formation.
our results demonstrate that hCAT-1 is a key component of efficient T-cell activation
TRPV6 and PLC-delta1 are critical actor of Ca(2+) homeostasis in CF human bronchial epithelial cells.
focus on TRPV6 gene polymorphisms, the start of TRPV6 translation at a non-AUG codon and the functions of TRPV6 in intestinal Ca(2+) uptake, sperm maturation, and male fertility.
TRPV6 channel acquires its oncogenic potential in prostate cancer due to the remodeling mechanism via the Orai1-mediated calcium/Annexin I/S100A11 pathway.
High TRPV6 expression is aassociated with adenoma of parathyroid glands.
A non-AUG start codon in used in both human and mouse, extending the N-terminus of the protein by 40 amino acids. The increased translation of the smaller TRPV6 cDNA version may overestimate the in vivo situation where translation efficiency may represent an additional mechanism to tightly control the TRPV6-mediated Ca(2+) entry to prevent deleterious Ca(2+) overload
Decreased expression of TRPV6 is associated with non-small cell lung cancer.
These results suggest that TRPV5 and TRPV6 are crucial gates controlling cadmium and zinc levels in the human body.
these data showed that TRPV5/TRPV6 in human lymphocytes are functionally active, and their activity is associated with proliferative status of blood cells.
Study suggest that amyloid beta-protein increase the expression of TRPC6 via NF-kappaB in BV-2 microglia and promotes the production of COX-2, which induces hippocampus neuron damage.
Study showed that TRPV6-expressing elements seem to be discretely organized in the brain of mouse. TRPV6-immunoreactive arcuate neurons co-express estrogen receptor alpha and the ion channel protein expression in the mediobasal hypothalamus showed correlation with estrous cycle.
TRPV6-/- mice spontaneously developed osteoarthritis at a younger age and had more severe manifestations of OA than wild-type controls. TRPV6 could regulate certain chondrocyte functions, including ECM secretion, cell proliferation, and apoptosis.
TRPV6 plays an essential role in bone metabolism and is a critical regulator in osteoclasts differentiation and bone resorption.
CAT1 overexpression prevents obesity-induced hypertension by reducing the influence of the SNS on the maintenance of arterial pressure but not by buffering pressor responses to stress.
Adra2a is expressed in the mesenchyme of the mouse stomach primordium at E11.5. Fzd5 and Trpv6 are expressed in the epithelial layer of the stomach primordium after E11.5.
these data indicate that obesity-induced down-regulation of CAT1 expression and subsequent reduced bioavailability of nitric oxide may contribute to the development of obesity-induced hypertension.
Fibroblasts from two long-lived mice mutants (Snell dwarf and PAPP-A knockout) expressed higher levels of CAT1 (a ATF4 target gene) during stress, suggesting a connection to longevity.
A non-AUG start codon is used in both human and mouse, extending the N-terminus of the protein by 40 amino acids. The increased translation of the smaller TRPV6 cDNA version may overestimate the in vivo situation where translation efficiency may represent an additional mechanism to tightly control the TRPV6-mediated Ca(2+) entry to prevent deleterious Ca(2+) overload.
Augmented endothelial l-arginine transport attenuated the prohypertensive effects of systemic and renal oxidative stress, suggesting that manipulation of endothelial CAT1 may provide a new therapeutic approach for the treatment of cardiovascular disease.
TRPV6, NCX1, and CaBP-9k in the fetal placenta and CaBP-28k in the maternal placenta may play key roles in controlling calcium transport across the placenta during pregnancy.
Trpv6 excision affects epididymal Ca(2+) handling and male fertility to the same extent as the introduction of the D541A pore mutation, arguing against residual functions of the TRPV6(D541A) pore mutant in epididymal epithelial cells
Data show that the transient receptor potential ion channel TRPV6 is expressed only at low levels in osteoblasts and plays little functional role in osteoblastic calcium uptake.
Data suggest that TRPV6 and other proteins involved in transcellular Ca(2+) transport are dynamically expressed in bone cells, while TRPV6 appears not crucial for bone metabolism and matrix mineralization.
appropriate Ca(2)+ absorption and a consequent TRPV6-mediated decrease in the extracellular Ca(2)+ concentration toward the distal segments of the epididymal duct are essential for the acquisition of basic functions and the survival of spermatozoa.
TRPV6 contributes to intestinal calcium transport when dietary calcium supply is limited and in this condition indirectly regulates bone formation and/or mineralization.
The mechanism of dietary protection by high dietary calcium in a mouse model of colonic hyperplasia is reported.
found in supporting cells of the organ of Corti, with weak labelling in outer and inner hair cells; expression patterns identical in old and young animals
to characterize ECaC2 in more detail and to compare its properties with those of ECaC1 to obtain a better understanding of transcellular Ca2+ transport in epithelia.
This gene encodes a member of the vanilloid family of transient receptor potential (TRP) calcium channel proteins. Proteins in this TRP family have an N-terminal ankyrin repeat domain, which is required for channel assembly and regulation.
epithelial calcium channel
, transient receptor potential cation channel subfamily V member 6
, transient receptor potential vanilloid 5-6
, transient receptor potential cation channel, subfamily V, member 6
, Alu-binding protein with zinc finger domain
, calcium transport protein 1
, calcium transporter-like protein
, epithelial apical membrane calcium transporter/channel CaT1
, epithelial calcium channel 2
, osmosensitive transient receptor potential channel 3
, transient receptor potential cation channel, subfamily 5, member 6