The Experts below are selected from a list of 312 Experts worldwide ranked by ideXlab platform

T Murali G Dhar - One of the best experts on this subject based on the ideXlab platform.

Joel C Barrish - One of the best experts on this subject based on the ideXlab platform.

Scott H Watterson - One of the best experts on this subject based on the ideXlab platform.

Beverly S Mitchell - One of the best experts on this subject based on the ideXlab platform.

  • regulation of the interaction of Inosine Monophosphate dehydrogenase with mycophenolic acid by gtp
    Journal of Biological Chemistry, 2006
    Co-Authors: Yan Shan Ji, Jing Jin Gu, Alexander M Makhov, Jack D Griffith, Beverly S Mitchell
    Abstract:

    Abstract Inosine Monophosphate dehydrogenase (IMPDH), a rate-limiting enzyme in the de novo synthesis of guanine nucleotides, is a major therapeutic target. A prototypic uncompetitive inhibitor of IMPDH, mycophenolic acid (MPA), is the active form of mycophenolate mofeteil (CellCept®), a widely used immunosuppressive drug. We have found that MPA interacts with intracellular IMPDH in vivo to alter its mobility on SDS-polyacrylamide gels. MPA also induces a striking conformational change in IMPDH protein in intact cells, resulting in the formation of annular aggregates of protein with concomitant inhibition of IMPDH activity. These aggregates are not associated with any known intracellular organelles and are reversible by incubating cells with guanosine, which repletes intracellular GTP, or with GTPγS. GTP also restores IMPDH activity. Treatment of highly purified IMPDH with MPA also results in the formation of large aggregates of protein, a process that is both prevented and reversed by the addition of GTP. Finally, GTP binds to IMPDH at physiologic concentrations, induces the formation of linear arrays of tetrameric protein, and prevents the aggregation of protein induced by MPA. We conclude that intracellular GTP acts as an antagonist to MPA by directly binding to IMPDH and reversing the conformational changes in the protein.

  • regulation of the human Inosine Monophosphate dehydrogenase type i gene utilization of alternative promoters
    Journal of Biological Chemistry, 1997
    Co-Authors: Jing Jin Gu, Jozef Spychala, Beverly S Mitchell
    Abstract:

    Abstract Catalysis of guanine nucleotide formation from IMP in the de novo purine synthetic pathway is carried out by two isoforms of the enzyme Inosine Monophosphate dehydrogenase (IMPDH) that are catalytically indistinguishable but are encoded by separate genes. In order to assess the potential for cell type-specific expression of IMPDH activity, we have characterized the IMPDH type I gene and identified three major RNA transcripts that are differentially expressed from three different promoters. A 4.0-kilobase pair (kb) mRNA containing 1.3 kb of 5′-untranslated region is expressed in activated peripheral blood lymphocytes and to a far lesser extent in cultured tumor cell lines. The P1 promoter that regulates the transcription of this mRNA has a high degree of sequence identity to an Alu repetitive sequence. A transcript of 2.7 kb is found in a subset of the tumor cell lines examined, whereas a 2.5-kb mRNA species is universally expressed and is the prevalent mRNA in most cell lines and tissues. The relative strengths of the three promoter regions and the effects of variable extents of 5′-flanking sequence on the P3 promoter differ in Jurkat T, as compared with Raji B lymphoid cell lines, demonstrating a complex cell type-specific transcriptional regulation of IMPDH type I gene expression.

  • effects of human t lymphocyte activation on Inosine Monophosphate dehydrogenase expression
    Journal of Immunology, 1994
    Co-Authors: Jennifer S Dayton, T Lindsten, Craig B Thompson, Beverly S Mitchell
    Abstract:

    Inosine Monophosphate dehydrogenase (IMPDH) catalyzes the first step in the formation of guanine ribonucleotides from Inosine Monophosphate and the activity of this enzyme appears to be essential for cell proliferation. Inhibitors of IMPDH have been demonstrated to be effective immunosuppressive agents and to inhibit T cell activation in vitro. IMPDH activity results from the expression of two different genes (types I and II) that encode protein subunits of identical size with 84% amino acid identity. To determine the relative contribution of the expression of these two genes to T cell activation, we have examined the effects of T cell stimulation on IMPDH activity, mRNA levels, and protein. The stimulation of isolated peripheral blood CD28+ T cells with PMA and ionomycin causes a 15-fold increase in IMPDH activity over a 72-h period. This is associated with a 10-fold increase in type II mRNA levels at 48 h. Type I mRNA is expressed at very low levels in resting T cells, but increases 10-fold by 24 h after stimulation. The type I cDNA probe also detects a second larger mRNA species of 4.0 kb that is not detectable in a variety of normal tissues or in a panel of leukemic cell lines. RNase protection assays using RNA probes corresponding to the entire coding region of the type I enzyme reveal a single protected fragment, demonstrating that the 4.0-kb message is the result of alternate splicing in the 59 or 39 untranslated regions or the use of an alternative polyadenylation site. Western blot analysis demonstrates a concomitant increase in total IMPDH protein on T cell activation, although posttranslational modifications do not allow the distinction between type I and type II on isoelectric focusing gels. We conclude that the induction of both type I and type II IMPDH contribute significantly to the T cell proliferative response. Both enzymes therefore should be considered important targets for immunosuppressive therapy.

  • Type I Inosine Monophosphate Dehydrogenase: Evidence for a Single Functional Gene in Mammalian Species
    Biochemical and Biophysical Research Communications, 1993
    Co-Authors: Jennifer S Dayton, Beverly S Mitchell
    Abstract:

    Abstract Human Inosine Monophosphate dehydrogenase activity is the result of the expression of two independent but closely related genes, termed IMPDH type I and type II. We have documented the presence of multiple, processed pseudogenes of type I IMPDH in human and Rhesus monkey genomic DNA, as well as a single functional gene encoding low levels of type I mRNA in human brain, heart, kidney and placenta. Single copy genes for each IMPDH isoenzyme were also found in rat, mouse, dog, cow, and chicken DNA and distinct mRNA species for type I and type II were identified by Northern blots in mouse and hamster RNA. Northern blot analysis of chicken RNA revealed a single mRNA species that hybridized to human IMPDH type I and II probes. These data document the high degree of evolutionary conservation of these two genes among mammals.

Brenda M Sandmaier - One of the best experts on this subject based on the ideXlab platform.

  • Inosine Monophosphate dehydrogenase pharmacogenetics in hematopoietic cell transplantation patients
    Biology of Blood and Marrow Transplantation, 2018
    Co-Authors: Jeannine S Mccune, Barry E Storer, Sushma S Thomas, Jožefa S Mckiernan, Rohan Gupta, Brenda M Sandmaier
    Abstract:

    Abstract We evaluated Inosine Monophosphate dehydrogenase ( IMPDH) 1 and IMPDH2 pharmacogenetics in 247 recipient–donor pairs after nonmyeloablative hematopoietic cell transplant (HCT). Patients were conditioned with total body irradiation + fludarabine and received grafts from related or unrelated donors (10% HLA mismatch), with postgraft immunosuppression of mycophenolate mofetil (MMF) with a calcineurin inhibitor. Recipient and donor IMPDH genotypes (rs11706052, rs2278294, rs2278293) were not associated with day 28 T cell chimerism, acute graft-versus-host disease (GVHD), disease relapse, cytomegalovirus reactivation, nonrelapse mortality, or overall survival. Recipient IMPDH1 rs2278293 genotype was associated with a lower incidence of chronic GVHD (hazard ratio, .72; P  = .008) in nonmyeloablative HCT recipients. Additional studies are needed to confirm these results with the goal of identifying predictive biomarkers to MMF that lower GVHD.

  • recipient pretransplant Inosine Monophosphate dehydrogenase activity in nonmyeloablative hematopoietic cell transplantation
    Biology of Blood and Marrow Transplantation, 2014
    Co-Authors: Barry E Storer, Brenda M Sandmaier, Meagan J Bemer, Linda J Risler, Brian Phillips, Joanne Wang
    Abstract:

    Abstract Mycophenolic acid, the active metabolite of mycophenolate mofetil (MMF), inhibits Inosine Monophosphate dehydrogenase (IMPDH) activity. IMPDH is the rate-limiting enzyme involved in de novo synthesis of guanosine nucleotides and catalyzes the oxidation of Inosine 5′-Monophosphate to xanthosine 5′-Monophosphate (XMP). We developed a highly sensitive liquid chromatography–mass spectrometry method to quantitate XMP concentrations in peripheral blood mononuclear cells (PMNCs) isolated from the recipient pretransplant and used this method to determine IMPDH activity in 86 nonmyeloablative allogeneic hematopoietic cell transplantation (HCT) patients. The incubation procedure and analytical method yielded acceptable within-sample and within-individual variability. Considerable between-individual variability was observed (12.2-fold). Low recipient pretransplant IMPDH activity was associated with increased day +28 donor T cell chimerism, more acute graft-versus-host disease (GVHD), lower neutrophil nadirs, and more cytomegalovirus reactivation but not with chronic GVHD, relapse, nonrelapse mortality, or overall mortality. We conclude that quantitation of the recipient's pretransplant IMPDH activity in PMNC lysate could provide a useful biomarker to evaluate a recipient's sensitivity to MMF. Further trials should be conducted to confirm our findings and to optimize postgrafting immunosuppression in nonmyeloablative HCT recipients.