The Ala893 variant has decreased activity compared with the 893Ser variant; therefore, the association with human IBD is consistent with the murine model of mdr1 deficiency.
The data showed that IBD patient with homozygous variant carrying MDR1 3435 T/T genotype has elevated risk for development of routine IBD clinical symptoms like Abdominal pain ( P = 0.005) and chronic Diarrhea ( P = 0.013) compared with MDR1 3435 C/C homozygotes who has reduced risk for development of IBD symptoms.
The membrane transporter multi-drug resistance 1 (MDR1, P-gp) regulates the bioavailability of endogenous and exogenous compounds and has been implicated in disorders such as Parkinson's disease, cancer, epilepsy, human immunodeficiency virus disease, and inflammatory bowel disease.
The present study aimed to determine the mRNA levels of MDR1 and COX2 in cats with IBD and LGAL, and to evaluate their correlation with clinical signs, histological severity and between genes.
These results indicate the possible involvement of Nrf2-mediated upregulation of P-gp in the therapeutic effect of berberine on colitis and highlight the potential of P-gp and/or Nrf2 as new therapeutic targets for IBD.
This article aims to review all relevant studies investigating the role of the polymorphisms of the ABCB1 gene in disease susceptibility, behavior and response to treatment in IBD.
This Editorial discusses how altered expression and function of <i>ABCB1/MDR1</i> p-gp may contribute to the development and persistence of chronic intestinal inflammation in inflammatory bowel diseases (IBD).
This research is intended to compile the frequency distribution of the drug metabolizing enzyme, thiopurine methyl transferase(TPMT) and the drug transporter, Multi drug resistance(MDR1) which are involved in metabolism of many therapeutics such as thiopurines in inflammatory bowel disease(IBD).
This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.
We aimed to investigate whether the polymorphisms of five genes including MDR1 influence the response to GC in Chinese patients and the relationship between MDR1 and IBD susceptibility.
We have utilized a gene-wide haplotype tagging approach to further define the identity of germ-line variations in the ABCB1/MDR1 gene contributing to IBD susceptibility.
We studied the association of both polymorphisms in an independent population to reveal the impact of the MDR1 gene on predisposition to inflammatory bowel disease.
We used coding and noncoding polymorphisms evenly spaced across the ABCB1/MDR1 gene to perform association analysis in Slovenian patients with inflammatory bowel diseases and to obtain haplotype structure and patterns of linkage disequilibrium (LD) in the MDR1 gene.