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CFTR encodes a member of the ATP-binding cassette (ABC) transporter superfamily. Additionally we are shipping CFTR Antibodies (233) and CFTR Kits (33) and many more products for this protein.
Showing 4 out of 7 products:
NDPK-A (show NME1 Proteins) exists in a functional cellular complex with AMPK (show PRKAA2 Proteins) and CFTR in airway epithelia, and NDPK-A (show NME1 Proteins) catalytic function is required for the AMPK (show PRKAA2 Proteins)-dependent regulation of CFTR
Study conclude that when both CFTR and NPT2a (show SLC34A1 Proteins) are expressed in X. laevis oocytes, CFTR confers to NPT2a (show SLC34A1 Proteins) a cAMPi-dependent trafficking to the membrane.
wild-type CFTR channel gating cycle is essentially irreversible and tightly coupled to the ATPase cycle, and that this coupling is completely destroyed by the NBD2 Walker B mutation D1370N but only partially disrupted by the NBD1 Walker A mutation K464A.
The cystic fibrosis transmembrane conductance regulator (CFTR) is a protein that belongs to the superfamily of ATP binding cassette (ABC (show ABCB6 Proteins)) transporters.
These data suggest that the Xenopus P2Y1 receptor (show P2RY1 Proteins) can increase both cyclic AMP (show TMPRSS5 Proteins)/protein kinase A and calcium/protein kinase C levels and that the PKC pathway is involved in CFTR activation via potentiation of the PKA pathway.
a new and more convenient approach, based on in vivo imaging analysis, has been set up to evaluate the inflammatory response in the lung of CFTR-deficient (CF) mice, a murine model of cystic fibrosis (show S100A8 Proteins).
results reveal that by potentiating adenosine triphosphate-sensitive K+ (KATP) channel, cystic fibrosis transmembrane conductance regulator CFTR acts as a glucose-sensing negative regulator of glucagon (show GCG Proteins) secretion in alpha cells
This study demonstrates that CFTR plays an important role in tenogenic differentiation and tendon regeneration by inhibiting the beta-catinin/pERK1/2 signaling pathway.
CFTR is a tumor suppressor gene in murine and human colorectal cancer
Insulin (show INS Proteins) stimulation of Akt1 (show AKT1 Proteins) and Akt2 (show AKT2 Proteins) signaling in Cystic fibrosis (show S100A8 Proteins) airway cells was diminished compared with that observed in airway cells expressing wild-type CFTR.
Biotinylation and streptavidin pull-down assays confirmed that CAL (show S100A11 Proteins) dramatically reduces the expression level of total and cell surface Mrp2 (show ABCC2 Proteins) in Huh-7 cells. Our findings suggest that CAL (show S100A11 Proteins) interacts with Mrp2 (show ABCC2 Proteins) and is a negative regulator of Mrp2 (show ABCC2 Proteins) expression.
Myelinosomes secreted from testis somatic TM4 (show TPM4 Proteins) Sertoli cells provide the release of aggregate-prone mutant, but not normal Huntingtin (Htt (show HTT Proteins)) exon1. Myelinosomes also support the release of other aggregate-prone mutant protein responsible for cystic fibrosis (show S100A8 Proteins) (CF), F508delCFTR.
ATP8B1 (show ATP8B1 Proteins) is important for proper CFTR expression and function.
Loss of cystic fibrosis (show S100A8 Proteins) transmembrane regulator impairs intestinal oxalate secretion
CFTR plays a role in suppressing MAPK (show MAPK1 Proteins)/NF-kappaB (show NFKB1 Proteins) to relieve inflammation, reduce proliferation and promote differentiation of keratinocytes, and thus promotes cutaneous wound healing.
CFTR correctors are strong candidates for the treatment of Sjogren's syndrome and pancreatitis, since correcting ductal function is sufficient to rescue acinar cell function in salivary glands and pancreas.
results suggest that cystic fibrosis transmembrane conductance regulator (CFTR) affects beta-cell function via a paracrine mechanism involving proinflammatory factors secreted from islet-associated exocrine-derived cell types
Molecular dynamics of the cryo-EM CFTR structure
report the interaction between CFTR and HDAC2 (show HDAC2 Proteins), and its involvement in the development of Ph+ leukemia
Vmax for wild-type CFTR was 240+/-60nmol/min/mg.
Data suggest that the stability of the second nucleotide-binding domain (NBD2) of CFTR (which exhibits a catalytically active ATPase active site and ATP binding site) can be affected by specific point mutations or deletion mutations; point mutations and deletion mutations observed in patients with cystic fibrosis (show S100A8 Proteins) were used in this study.
Structural changes fundamental to gating of the cystic fibrosis transmembrane conductance regulator anion channel pore have been summerized. (Review)
Resting neutrophils had pronounced CFTR expression. Neutrophil ativation with soluble or particulate agonists did not significantly increase CFTR expression, but induced its redistribution to cell surface. CFTR mobilization correlated with cell-surface recruitment of formyl-peptide receptor during secretory vesicle exocytosis. Neutrophils with DeltaF508-CF showed little cell-surface mobilization upon stimulation.
Considerable progress has been made over the last years in the understanding of the molecular basis of the CFTR functions, as well as dysfunctions causing the common genetic disease cystic fibrosis (show S100A8 Proteins) (CF). This review provides a global overview of the theoretical studies that have been performed so far, especially molecular modelling and molecular dynamics (MD) simulations. [review]
Results suggest that acetylcholine does not regulate the activity of the CFTR in tracheal epithelia of pigs which opposes observation from studies using mice airway epithelium.
Expression of CFTR-F508del interferes with smooth muscle cell calcium handling and decreases aortic responsiveness.
Pseudomonas aeruginosa and other bacteria into the lumen of intact isolated swine tracheas triggers CFTR-dependent airway surface liquid secretion by the submucosal glands.
TGF-beta1 (show TGFB1 Proteins), via TGF-beta1 (show TGFB1 Proteins) receptor I and p38 MAPK (show MAPK14 Proteins) signaling, reduces CFTR expression to impair CFTR-mediated anion secretion, which would likely compound the effects associated with mild CFTR mutations and ultimately would compromise male fertility.
The esophageal submucosal glands (SMG (show SNRPG Proteins)) secrete HCO(3)(-) and mucus into the esophageal lumen, where they contribute to acid clearance and epithelial protection. We investigated the presence of CFTR, its involvement in the secretion process, and the effect of cAMP on HCO3 secretion in this tissue. This is the first report on the presence of CFTR channels in the esophagus.
data suggest that loss of CFTR directly alters Schwann cell function and that some nervous system defects in people with cystic fibrosis (show S100A8 Proteins) are likely primary
The data suggest, that during bacterial infections and resulting release of proinflammatory cytokines, the glands are stimulated to secrete fluid, and this response is mediated by cAMP-activated CFTR.
CFTR is required for maximal liquid absorption by lung alveoli under cAMP stimulation
These findings reveal differences between nasal and tracheal glands, show defective fluid secretion in nasal glands of cystic fibrosis (show S100A8 Proteins) pigs, reveal some spared function in the DeltaF508 vs. null piglets.
causal link between CFTR mutations and partial or total vas (show AVP Proteins) deferens and/or epididymis atresia at birth
conserved CFTR sequences between species are examined for potential regulatory elements. Regions of introns 2, 3, 10, 17a, 18, and 21 and 3' flanking sequence corresponding to human CFTR DNase I (show DNASE1 Proteins) hypersensitive sites showed high homology in cow and pig.
Results demonstrate functional coupling between Cftr and Slc26a6 (show SLC26A6 Proteins)-like Cl(-)/HCO(3)(-) exchange activity in apical membrane of guinea pig pancreatic interlobular duct.
This gene encodes a member of the ATP-binding cassette (ABC) transporter superfamily. ABC proteins transport various molecules across extra- and intra-cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the MRP subfamily that is involved in multi-drug resistance. The encoded protein functions as a chloride channel and controls the regulation of other transport pathways. Mutations in this gene are associated with the autosomal recessive disorders cystic fibrosis and congenital bilateral aplasia of the vas deferens. Alternatively spliced transcript variants have been described, many of which result from mutations in this gene.
cystic fibrosis transmembrane conductance regulator
, cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7)
, cystic fibrosis transmembrane conductance regulator, ATP-binding cassette (sub-family C, member 7)
, ATP-binding cassette sub-family C member 7
, ATP-binding cassette transporter sub-family C member 7
, ATP-binding cassette, subfamily c, member 7
, cAMP-dependent chloride channel
, channel conductance-controlling ATPase
, cystic fibrosis transmembrane conductance regulator homolog
, cystic fibrosis transmembrane conductance regulator homolog; ATP-binding cassette, subfamily c, member 7
, CFTR chloride channel
, chloride channel
, CFTR cAMP-dependent chloride channel protein
, Channel conductance-controlling ATPase