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Report ABCB4 mutations in severe intrahepatic cholestasis of pregnancy.
Results indicate that ABCB4 is overexpressed in breast cancer cells with acquired doxorubicin resistance, which could be attributed, at least partially, to the epigenetic modifications of ABCB4 gene.
some synonymous SNPs in the ABCB4 gene, considered up to now as neutral, may be involved in the MDR3 deficiency
Mutations in the genes responsible for PFIC may be involved in both young and adults with cryptogenic cholestasis in a considerable number of cases, including in heterozygous status.
High mRNA expression of MDR3 in preterm infants may be associated with the development of parenteral nutrition-associated cholestasis
ABCB4 is down-regulated in the 5-Fu resistant cells and knockdown of ABCB4 alleviated the cell apoptosis and predicts a shorter recurrence-free survival and overall survival in colorectal cancer.
The overrepresentation of mutated variants of the 1331T > C ABCB11 polymorphism in the ICP group suggests its contribution to the etiology of the intrahepatic cholestasis of pregnancy. Analysis of genotypes' co-existence pointed to the possibility of the mutated variants of polymorphism 1954A > G ABCB4 and 1331T > C ABCB11 having a summation effect on the development ofintrahepatic cholestasis of pregnancy
FIC1, BSEP, and MDR3 represent hepatobiliary transport proteins essential for bile formation.
reduced ABCB4 expression predisposes to extrahepatic biliary atresia
The functional impact of ABCB4 mutations found in progressive familial intrahepatic cholestasis type 3.
Several members of a family exhibited cholestasis and were found to have a substitution of glycine 68 by arginine in ABCB4 due to a missense mutation at base 202. The 18-year-old propositus was heterozygous for this mutation and also suffered acute pancreatitis.
ABCB4 variants identified in patients with biliary diseases
results are suggestive of a potential downstream molecular effect for the described polymorphisms on the expression pattern of the ABCB4 underlining the importance of synonymous variants
the first characterisation at the protein level of six ABCB4 variants (D243A, K435T, G535D, I490T, R545C, and S978P) previously found in patients with inflammatory liver diseases or liver cancer, is reported.
Ivacaftor is a potential therapy for selected patients with cystic fibrosis with mutations of ABCB4.
Data show that patients with low multidrug resistance protein 3 (MDR3) expression were significantly associated with a better outcome than patients with high MDR3 expression.
In patients with intrahepatic cholestasis of pregnancy, ABCB4 gene mutation was not associated with response to ursodeoxycholic acid treatment.
Data suggest that MDR3 isoforms, both human and mouse isoforms, exhibit different affinities for fluorescent dyes and drugs; thus, ligands likely occupy partially overlapping but distinct binding sites.
Single-nucleotide polymorphism in ABCB4 gene is associated with gallbladder cancer.
the cholestatic potential of certain drugs may be aggravated by simultaneous inhibition of BSEP and MDR3.
These results provide evidence that zebrafish Pxr may play a role in MDR/MXR through transcriptional regulation of abcb4 and cyp3a65 gene expression.
Zebrafish Abcb4 plays crucial roles in cellular efflux of microcystin-LR and is a potential molecular marker for the monitoring of cyanobacteria contamination in the aquatic environment.
Thyroid hormone receptor beta1 stimulates ABCB4 to increase biliary phosphatidylcholine excretion
When looking at the gender-specific response to corticosterone treatment, male MDR2KO mice tended to have a more pronounced reversal of liver fibrosis than females treated with corticosterone
Findings imply a close link between Mdr2 (-/-) -associated tumorigenesis and perturbation of these biological processes and suggest potential extrahepatic functions of Mdr2.
The antifibrotic effects of rapamycin, everolimus, captopril and irbesartan seen in other models of fibrosis were not replicated in the Mdr2(-/-) model of liver fibrosis.
A new Mdr2(-/-) mouse model of sclerosing cholangitis with rapid fibrosis progression, early-onset portal hypertension, and liver cancer.
Glyceryl trinitrate improves hepatocyte engraftment and correction of metabolic disease in mdr2 (-/-) mice.
nsulin-like growth factor 1 enhances bile-duct proliferation and fibrosis in Abcb4(-/-) mice.
Data indicate that Abcb4-knockout mice displayed significantly (P<0.001) lower plasma glucose concentrations than corresponding wild-type controls.
Mdr2(-/-)IKK2(Hep-KO) mice remarkably recapitulate chronic liver failure in humans and might be of special importance for the study of the mechanisms contributing to the pathogenesis of end-stage chronic liver disease.
Flippase ATP8B1 and the floppase ABCB4 have complementary functions in maintaining canalicular membrane integrity.
Downregulation of JunD and cyclin D1 expression in myofibroblasts may be important regarding the mechanism of action of MTA in Mdr2-/- mice
The induction of Mdr2 mRNA and Mdr2 protein levels by fibrates is mediated by PPARalpha, while the induction of Mdr1a / 1b in vivo probably reflects a secondary phenomenon related to chronic PPARalpha activation.
spontaneous gallstone formation occurs in Mdr2 (Abcb4) knockout mice that are characterized by phospholipid-deficient bile
Bile duct proliferation in Mdr2(-/-) mice enhances cholehepatic shunting of bile salts, which is associated with a disproportionally high bile flow but does not affect bile salt synthesis.
MDR2 expression is required for ABCG5- and ABCG8-mediated biliary sterol secretion. Inactivation of MDR2 markedly attenuated the reduction in fractional sterol absorption associated with ABCG5, ABCG8 overexpression
Mdr2 (+/-) mice have diminished susceptibility to MCD diet-induced NASH, which is associated with a relative decrease in PEMT activity and increased SAM:SAH ratios.
24-norUrsodeoxycholic acid ameliorates sclerosing cholangitis in Mdr2 deficient mice.
Mdr2 seems not to be involved in the protection of the fetus from teratogens.
Multiple genes regulating inflammation and fibrosis not previously linked to Abcb4 deficient cholangitis are identified as being differentially transcribed in Abcb4 deficient livers, where they contribute to the pathogenesis of liver tissue pathology.
The membrane-associated protein encoded by this gene is a member of the superfamily of ATP-binding cassette (ABC) transporters. 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 MDR/TAP subfamily. Members of the MDR/TAP subfamily are involved in multidrug resistance as well as antigen presentation. This gene encodes a full transporter and member of the p-glycoprotein family of membrane proteins with phosphatidylcholine as its substrate. The function of this protein has not yet been determined\; however, it may involve transport of phospholipids from liver hepatocytes into bile. Alternative splicing of this gene results in several products of undetermined function.
ATP-binding cassette sub-family B member 4
, P glycoprotein 3/multiple drug resistance 3
, P-glycoprotein 3
, P-glycoprotein-3/multiple drug resistance-3
, multidrug resistance protein 3
, multiple drug resistance 3
, ABC efflux transporter 4
, multidrug resistance 3
, ATP-binding cassette, subfamily B, member 4
, P glycoprotein 2
, multidrug resistance protein 2
, ATP-binding cassette sub-family B (MDR/TAP) member 4 (P-glycoprotein 3/ multidrug resistance 2
, ATP-binding cassette sub-family B (MDR/TAP) member 4 (P-glycoprotein 3/ multidrug resistance 2)
, ATP-binding cassette, sub-family B (MDR/TAP), member 4 (P-glycoprotein 3/ multidrug resistance 2)
, P-glycoprotein 2
, P-glycoprotein 3/ multidrug resistance 2
, ATP-binding cassette, sub-family B (MDR/TAP), member 4
, multidrug resistance protein 3-like
, ATP-binding cassette transporter protein
, Beta-defensin 1
, Defensin, beta 1
, p-glycoprotein isoform III
, LOW QUALITY PROTEIN: phosphatidylcholine translocator ABCB4
, RUN domain containing 3B
, RUN domain-containing protein 3B
, phosphatidylcholine translocator ABCB4
, P glycoprotein 3/ multiple drug resistance 3