Disease relevance of BANF1P1

• Murine breast cancer resistance protein 1 (Bcrp1) is expressed in the brush-border membrane of proximal tubule cells of the kidney [1].

High impact information on BANF1P1

• Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro [2].
• The breast cancer resistance protein (Bcrp1/Abcg2) restricts exposure to the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine [3].
• The stem cell marker Bcrp/ABCG2 enhances hypoxic cell survival through interactions with heme [4].
• The functional importance of MRP4 and BCRP in the urinary excretion of HCT and furosemide was investigated using gene knockout mice [5].
• Using Spodoptera frugiperda-BCRP membrane vesicles, we showed that the ATP-dependent vesicular transport of 1 muM methotrexate by BCRP is 5-fold higher at pH 5.5 than at physiological pH [6].

Biological context of BANF1P1

• We conclude that Bcrp1 is one of the determinants for the bioavailability of fluoroquinolones and their secretion into the milk [7].
• Breast cancer resistance protein (BCRP/ABCG2) transports fluoroquinolone antibiotics and affects their oral availability, pharmacokinetics, and milk secretion [7].
• Furthermore, with MDCKII-BCRP monolayers, we found that resveratrol, which is a neutral compound at pH </= 7.4, is efficiently transported by BCRP at pH 6.0, whereas we did not detect active transport at pH 7 [6].
• Functional analysis of SNPs variants of BCRP/ABCG2 [8].
• Disruption of the membrane fluidity was carried out to appraise changes in membrane adsorption of MTX and drug uptake in sensitive (HCT-116 S) and resistant BCRP/MXR (HCT-116 R) cells [9].

Anatomical context of BANF1P1

• The breast cancer resistance protein (BCRP/ABCG2) is an ATP-binding cassette drug efflux transporter that extrudes xenotoxins from cells in intestine, liver, mammary gland, and other organs, affecting the pharmacological and toxicological behavior of many compounds, including their secretion into the milk [7].
• The phenotypic characters of the stem cells in hepatocytes during liver regeneration: the expression of the Bcrp1/Abcg2 membrane transporter and the Hoechst 33342 export [10].

Associations of BANF1P1 with chemical compounds

• The purpose of the present study is to investigate whether Bcrp1 could be involved in the urinary excretion of the human BCRP substrates, 6-hydroxy-5,7-dimethyl-2-methylamino-4-(3-pyridylmethyl) benzothiazole sulfate (E3040S) and 4-methylumbelliferone sulfate (4MUS), using Bcrp1(-/-) mice [1].
• Knockout of Bcrp1 did not affect the creatinine clearance [7.17 +/- 1.00 and 8.66 +/- 2.02 ml/min/kg for Bcrp1(-/-) and wild-type mice, respectively] [1].
• Impaired renal excretion of 6-hydroxy-5,7-dimethyl-2-methylamino-4-(3-pyridylmethyl) benzothiazole (E3040) sulfate in breast cancer resistance protein (BCRP1/ABCG2) knockout mice [1].
• The milk concentration and milk/plasma ratio of ciprofloxacin were 2-fold higher in wild-type than in Bcrp1(-/-) lactating mice [7].
• The purpose of this study was to determine whether three widely used fluoroquinolone antibiotics (ciprofloxacin, ofloxacin, and norfloxacin) are substrates of Bcrp1/BCRP and to investigate the possible role of this transporter in the in vivo pharmacokinetic profile of these compounds and their secretion into the milk [7].

Other interactions of BANF1P1

• Two of these were novel cDNAs (D14S1460E and D14S1461E) [11].

Analytical, diagnostic and therapeutic context of BANF1P1

• In vivo pharmacokinetic studies showed that the ciprofloxacin plasma concentration was more than 2-fold increased in Bcrp1(-/-) compared with wild-type mice (1.77 +/- 0.73 versus 0.85 +/- 0.39 microg/ml, p < 0.01) after oral administration of ciprofloxacin (10 mg/kg) [7].
• BCRP/MXR expression was determined by Western blot and immunohistochemistry [12].

References