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CFTR encodes a member of the ATP-binding cassette (ABC) transporter superfamily. Zusätzlich bieten wir Ihnen CFTR Kits (33) und CFTR Proteine (7) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 234 products:
Chicken Monoclonal CFTR Primary Antibody für BP, FACS - ABIN152670
Walker, Watson, Holmes, Edelman, Banting et al.: Production and characterisation of monoclonal and polyclonal antibodies to different regions of the cystic fibrosis transmembrane conductance regulator (CFTR): detection of immunologically related ... in Journal of cell science 1995
Zeige alle 9 Referenzen für 152670
Human Monoclonal CFTR Primary Antibody für IHC (p) - ABIN115197
Sealock, Butler, Kramarcy, Gao, Murnane, Douville, Froehner: Localization of dystrophin relative to acetylcholine receptor domains in electric tissue and adult and cultured skeletal muscle. in The Journal of cell biology 1991
Human Monoclonal CFTR Primary Antibody für IF, IP - ABIN180604
Kartner, Augustinas, Jensen, Naismith, Riordan: Mislocalization of delta F508 CFTR in cystic fibrosis sweat gland. in Nature genetics 1993
NDPK-A (zeige NME1 Antikörper) exists in a functional cellular complex with AMPK (zeige PRKAA2 Antikörper) and CFTR in airway epithelia, and NDPK-A (zeige NME1 Antikörper) catalytic function is required for the AMPK (zeige PRKAA2 Antikörper)-dependent regulation of CFTR
Study conclude that when both CFTR and NPT2a (zeige SLC34A1 Antikörper) are expressed in X. laevis oocytes, CFTR confers to NPT2a (zeige SLC34A1 Antikörper) a cAMPi-dependent trafficking to the membrane.
wild-type CFTR channel gating cycle is essentially irreversible and tightly coupled to the ATPase (zeige DNAH8 Antikörper) 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 (zeige ABCB6 Antikörper)) transporters.
These data suggest that the Xenopus P2Y1 receptor (zeige P2RY1 Antikörper) can increase both cyclic AMP (zeige TMPRSS5 Antikörper)/protein kinase A and calcium/protein kinase C (zeige PKC Antikörper) levels and that the PKC (zeige PKC Antikörper) pathway is involved in CFTR activation via potentiation of the PKA pathway.
CFTR is a tumor suppressor gene in murine and human colorectal cancer
Insulin (zeige INS Antikörper) stimulation of Akt1 (zeige AKT1 Antikörper) and Akt2 (zeige AKT2 Antikörper) signaling in Cystic fibrosis (zeige S100A8 Antikörper) airway cells was diminished compared with that observed in airway cells expressing wild-type CFTR.
Biotinylation and streptavidin pull-down assays confirmed that CAL (zeige S100A11 Antikörper) dramatically reduces the expression level of total and cell surface Mrp2 (zeige ABCC2 Antikörper) in Huh-7 cells. Our findings suggest that CAL (zeige S100A11 Antikörper) interacts with Mrp2 (zeige ABCC2 Antikörper) and is a negative regulator of Mrp2 (zeige ABCC2 Antikörper) expression.
Myelinosomes secreted from testis somatic TM4 (zeige TPM4 Antikörper) Sertoli cells provide the release of aggregate-prone mutant, but not normal Huntingtin (Htt (zeige HTT Antikörper)) exon1. Myelinosomes also support the release of other aggregate-prone mutant protein responsible for cystic fibrosis (zeige S100A8 Antikörper) (CF), F508delCFTR.
ATP8B1 (zeige ATP8B1 Antikörper) is important for proper CFTR expression and function.
Loss of cystic fibrosis (zeige S100A8 Antikörper) transmembrane regulator impairs intestinal oxalate secretion
CFTR plays a role in suppressing MAPK (zeige MAPK1 Antikörper)/NF-kappaB (zeige NFKB1 Antikörper) to relieve inflammation, reduce proliferation and promote differentiation of keratinocytes, and thus promotes cutaneous wound healing.
physiological fetal hypercalcemia, acting on the CaSR (zeige CASR Antikörper), promotes human fetal lung development via cAMP-dependent opening of CFTR.
CFTR expressed by alveolar or peritoneal macrophages regulates acute proinflammatory responses.
CFTR silencing in pancreatic beta-cells significantly reduced insulin (zeige INS Antikörper) output in response to glucose, and made the cells more sensitive to oxidative stress.
Data suggest that the stability of the second nucleotide-binding domain (NBD2) of CFTR (which exhibits a catalytically active ATPase (zeige DNAH8 Antikörper) 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 (zeige S100A8 Antikörper) 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 (zeige S100A8 Antikörper) (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]
CFTR gating is regulated in complex manner as phosphorylation is mandatory for channel activity and gating is directly regulated by binding of ATP to specific intracellular sites on the CFTR protein. This review covers our current understanding on the gating mechanism in CFTR and illustrates the relevance of alteration of these mechanisms in the onset of cystic fibrosis (zeige S100A8 Antikörper). [review]
This review will discuss the effects of PKA phosphorylation on wild-type CFTR, the consequences of cystic fibrosis (zeige S100A8 Antikörper) mutations on PKA phosphorylation, and the development of therapies that target PKA-mediated signaling. [review]
As an ion channel, CFTR must form a continuous pathway across the cell membrane-referred to as the channel pore-for the rapid electrodiffusional movement of ions. This review summarizes our current understanding of the architecture of the channel pore, as defined by electrophysiological analysis and molecular modeling studies. [review]
This review covers old and recent knowledge on CFTR folding and trafficking from its synthesis to the regulation of its stability at the plasma membrane and highlights how several of these steps can be modulated to promote the rescue of mutant CFTR. [review]
This review explores the link between stability and structure/function relationships of membrane proteins and CFTR in particular and how approaches to study CFTR structure depend on its stability. [review]
CFTR regulates many mechanisms in epithelial physiology, such as maintaining epithelial surface hydration and regulating luminal pH. This chapter illustrates the different operational roles of CFTR in epithelial function by describing its characteristics in three different tissues: the airways, the pancreas, and the sweat gland. [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 (zeige TGFB1 Antikörper), via TGF-beta1 (zeige TGFB1 Antikörper) receptor I and p38 MAPK (zeige MAPK14 Antikörper) 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 (zeige SNRPG Antikörper)) 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 (zeige S100A8 Antikörper) 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 (zeige S100A8 Antikörper) pigs, reveal some spared function in the DeltaF508 vs. null piglets.
causal link between CFTR mutations and partial or total vas (zeige AVP Antikörper) 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 (zeige DNASE1 Antikörper) hypersensitive sites showed high homology in cow and pig.
Results demonstrate functional coupling between Cftr and Slc26a6 (zeige SLC26A6 Antikörper)-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