Disease relevance of ABCC1

• CONCLUSIONS: HIV-1 protease inhibitors potently interact with both P-gp and MRP-related transporters in BBMEC [1].

High impact information on ABCC1

• Similarly, ABCC1 transcript levels were induced in granulosa cells 12-39 h after hCG [2].
• The objective of this study was to investigate the regulation of EST and ABCC1 during human chorionic gonadotropin (hCG)-induced ovulation/luteinization [2].
• In contrast, no significant changes in either EST or ABCC1 were detected in theca interna samples after hCG [2].
• The transcripts for EST and ABCC1 were cloned by RT-PCR, and the regulation of their mRNAs was studied in preovulatory follicles obtained during estrus at 0, 12, 24, 30, 33, 36, and 39 h after hCG [2].
• The present study demonstrates that follicular luteinization is accompanied not only by a decrease in 17 beta-estradiol biosynthesis but also by an increase in expression of genes responsible for estrogen inactivation and elimination from granulosa cells, such as EST and ABCC1, respectively [2].

Biological context of ABCC1

• Drugs demonstrating a significant effect were further quantitated using an expanded concentration range and a nonlinear regression curve fit to determine the potency (IC50) and efficacy (Imax) of the drug for P-gp and/or MRP [3].
• These results likely reflect an interaction of the ester form with P-gp and BCRP during the initial accumulation process, and an interaction of the free acid form with MRP after hydrolysis in the cell [4].

Anatomical context of ABCC1

• These studies provide the first demonstration of the localization of MRP1, MRP4, and MRP5 homologs in brain microvessel endothelial cells [5].
• Plasma membrane localization of multidrug resistance-associated protein homologs in brain capillary endothelial cells [5].
• Several multidrug resistance-associated protein (MRP) homologs are expressed in brain microvessel endothelial cells forming the blood-brain barrier (BBB) [5].
• These results indicate that chlorpheniramine and chlorcyclizine are effluxed from the olfactory mucosa by efflux transporters such as P-gp and MRP1 [6].

Associations of ABCC1 with chemical compounds

• In the presence of inhibitors such as 2,4-dinitrophenol (1 mM) and quinidine (1 mM), etoposide showed an increase in Jm-s and a decrease in Js-m. The etoposide efflux was unaffected in the presence of a specific multiresistance associated protein 1 (MRP1) inhibitor (MK571) and methotrexate, a substrate for BCRP and MRP1-4 [7].
• In the presence of metabolic inhibitors (ouabain and 2,4-dinitrophenol) and P-glycoprotein (P-gp)/multidrug resistance protein 1 (MRP1) inhibitors (quinidine and verapamil), the J(m-s) increased and J(s-m) decreased significantly [6].

Analytical, diagnostic and therapeutic context of ABCC1

• Results obtained from RT-PCR/Southern blot analyses showed significant changes in steady-state levels of both EST and ABCC1 mRNA after hCG treatment (P < 0.05) [2].

References