anti-ATP-Binding Cassette, Sub-Family B (MDR/TAP), Member 1B (ABCB1B) Antikörper

Human ATP-Binding Cassette, Sub-Family B (MDR/TAP), Member 1B (ABCB1B) Interaktionspartner

1. miR-381 could overcome cisplatin resistance of breast cancer by directly targeting MDR1.

2. We also generated two haplotypes to determine individual SNP effects for a total of 16 studied. Compared with the ancestral haplotype, three haplotypes significantly up-regulated (107-266% increase; P<0.05), one significantly down-regulated (95.4% decrease; P<0.01), and 12 had no statistically significant effect on ABCB1 promoter activity

3. Our results suggest that female citalopram users with ABCB1 1236T-2677T-3435T are more vulnerable to adverse effects of the drugs as this haplotype was enriched in non-violent suicides of female citalopram users

4. Histone deacetylase 6 regulated expression of IL-8 is involved in the doxorubicin (Dox) resistance of osteosarcoma cells via modulating ABCB1 transcription

5. examined the association between rs1045642 and rs2032582 and blood lipids in the same group of hyperlipidemic patients and normolipidemic controls in an effort to further understanding of the apparently complex but potentially clinically significant relationship between lipid homeostasis and ABCB1

6. Minor allele frequencies (MAF) in a Puerto Rican population were 46% for PON1 (rs662), 41% for ABCB1 (rs1045642), 14% for CYP2C19*17, 13% for CYP2C19*2, 12% for P2RY12-H2 and 0.3% for CYP2C19*4. No carriers of the CYP2C19*3 variants were detected. All alleles and genotype proportions were found to be in HardyWeinberg equilibrium (HWE).

7. Data suggest that up-regulation of ABCB1 in lysosomes of neoplastic cells results in drug resistance (such as doxorubicin resistance).

8. ABCB1 is an environment susceptible gene that codes for P-glycoprotein (P-gp). P-gp is responsible for multidrug resistance during chemotherapy of breast cancer. Six different non-synonymous Single Nucleotide Polymorphism (nsSNPs) of human ABCB1 gene were found in COSMIC database. Out of the six nsSNPs, two were predicted to have deleterious effects.

9. NFV and LPV restored CFZ activity at therapeutically relevant drug levels and thus represent ready-to-use drugs to be tested in clinical trials to target ABCB1.

10. Conformational dynamics of P-glycoprotein in lipid nanodiscs and detergent micelles reveal complex motions on a wide time scale.

11. Study demonstrated that TWIST protein expression was elevated in liver cancer tissue specimens and was positively correlated with MDR1 expression. Knockdown of TWIST increased the sensitivity of RHepG2 cells to antineoplastic agents through a reduction in MDR1 expression and drug efflux ability.

12. the over-expression of SLC7A11, or supplementation with sufficiently cystine, or treatment with N-acetylcysteine significantly decreased P-gp expression and activity. It was suggested that ROS and SLC7A11/cystine were the two relevant factors responsible for the expression and function of P-gp, and that SLC7A11 might be a potential target modulating ADR resistance.

13. Data provide a mechanistic explanation for the differential effects of ABCB1 haplotypes on its promoter activity and underscore the importance of evaluating genetic variants in the context of haplotypes rather than individual SNPs when investigating their effects on gene/protein expression and disease risk.

14. CYP3A5, ABCB1 and two POR genotypes were assessed by real-time PCR.

15. ABCB1 C3435T polymorphism can affect the elimination of some antipsychotic/antidepressant drugs.

16. High BCL11A and MDR1 expression was associated with a poor response to chemotherapy.

17. The methylation/expression ratios of ABCB1 were unaffected by increasing BMI values.

18. Neither the ABCB1 C3435T nor the SLCO1B1 T521C polymorphism affected edoxaban PK.

19. Our results show that ABCB1 C3435T polymorphism may modulate serum THC levels in chronic heavy cannabis users. The exact mechanisms and roles that this may play in cannabis dependence genesis and evolution remain to be elucidated. These results should be controlled in a replication study using a larger population.

20. MDR1 is not expressed on erythrocyte membrane.

Mouse (Murine) ATP-Binding Cassette, Sub-Family B (MDR/TAP), Member 1B (ABCB1B) Interaktionspartner

1. this study shows that MDR1 deficiency impairs mitochondrial homeostasis and promotes intestinal inflammation

2. A panel of 18 P-gp substrates were administered into the airways of an isolated perfused mouse lung (IPML) model derived from Mdr1a/Mdr1b knockout mice. Parallel intestinal absorption studies were performed. Lung P-gp can affect the pulmonary kinetics of a subset of P-gp substrates.

3. Data suggest that the overexpression of P-gp in neoplastic cells may be associated with alterations in O-glycosylated cell surface proteins, including mucins, and this alteration may be responsible for the reduced cell sensitivity to the O-glycosylation inhibitor GalNAc-alpha-O-benzyl.

4. We conclude that mdr1b and bcrp are essential to ovarian protection from chemotoxicity and may have an important physiological role in the ovary.

5. Molecular Dynamics simulations and docking of drugs performed for P-gp (P-gp, multi-drug resistance protein, MDR1).Drugs with ER < 1 almost do not bind the main binding cavity (MBC) of P-gp.

6. conclusion, MDR1 and BCRP are expressed on apical membranes of the rodent placental SynT-II layer.

7. Mdr1 enforces T Cell homeostasis in the presence of intestinal bile acids.

8. Loss of ABCB1 expression is associated with neonatal hyperbilirubinemia.

9. the high-affinity site of P-glycoprotein is inaccessible because of either a conformational change or binding of detergent at the binding site in a detergent micelle environment; ligands bind to a low-affinity site, resulting in altered modulation of P-gp ATPase activity

10. Data suggest that ATP binding to Abcb1b/P-glycoprotein (Pgp) in liposomes exhibits cooperativity with verapamil (a cardiovascular/antiarrhythmia drug); cooperativity between verapamil and a nonhydrolyzable ATP analog (AMPPNP) leads to distinct global conformational changes in Abcb1b/Pgp.

11. Chrysosplenetin inhibited P-gp activity and reverse the up-regulated P-gp and MDR1 levels induced by artemisinin.

12. Tamsulosin and tolterodine with P-gp gene expression and activity in an enantiomer-specific way.

13. Pgp-coupled ATPase activity kinetics measured with a range of verapamil and digoxin concentrations fit well to a DDI model encompassing non-competitive and competitive inhibition of digoxin by verapamil.

14. Data show that human transgenic mutant huntingtin (mHtt) aggregation might be regulated by multidrug resistance protein 1 (MDR1) which suggests that MDR1 might be a potential therapeutic target for Huntington's disease.

15. In vitro and in vivo downregulation of the ATP binding cassette transporter B1 by the HMG-CoA reductase inhibitor simvastatin

16. Efficient chemoprotection of CDD and MDR1 transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara-C and anthracycline application

17. Mdr1b participates in the elimination of paraquat from the kidneys and protects against subsequent toxicity.

18. These study data have facilitated understanding of the molecular mechanisms of neurotoxicosis in ABCB1-1Delta mutant mice following exposure to various P-gp substrates.

19. Data indicate that the brain penetration of ABT-888 in both Abcb1a/1b-/- and Abcb1a/1b-/-;Abcg2-/- mice was significantly higher than in wild-type mice.

20. Directed evolution of P-glycoprotein cysteines reveals site-specific, non-conservative substitutions that preserve multidrug resistance.