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1. GENETIC DISEASES AND MOLECULAR GENETICS

Author

C. Legendre, D. Cohen, Y. Delmas, T. Feldkamp, D. Fouque, R. Furman, O. Gaber, L. Greenbaum, T. Goodship, H. Haller, M. Herthelius, M. Hourmant, C. Licht, B. Moulin, N. Sheerin, A. Trivelli, C. L. Bedrosian, C. Loirat, S. Babu, T. Jungraithmayr, Y. Lebranchu, M. Riedl, A. O. Gaber, C. Bedrosian, P. Muus, K. Douglas, G. Remuzzi, A. Kourouklaris, K. Ioannou, I. Athanasiou, K. Demetriou, A. Panagidou, M. Zavros, N. Y. Rodriguez C, M. Blasco, C. Arcal, L. F. Quintana, S. Rodriguez de Cordoba, J. M. Campistol, N. Bachmann, T. Eisenberger, C. Decker, H. J. Bolz, C. Bergmann, F. Pesce, S. N. Cox, G. Serino, G. De Palma, F. P. Sallustio, F. Schena, M. Falchi, M. Pieri, C. Stefanou, A. Zaravinos, K. Erguler, G. Lapathitis, H. Dweep, C. Sticht, N. Anastasiadou, I. Zouvani, K. Voskarides, N. Gretz, C. C. Deltas, A. Ruiz, O. Bonny, F. Sallustio, C. Curci, S. Cox, E. Kemter, S. Sklenak, B. Aigner, R. Wanke, T. M. Kitzler, J. L. Moskowitz, S. E. Piret, K. Lhotta, A. Tashman, E. Velez, R. V. Thakker, P. Kotanko, J. Leierer, M. Rudnicki, P. Perco, C. Koppelstaetter, G. Mayer, M. J. N. Sa, S. Alves, H. Storey, F. Flinter, P. J. Willems, F. Carvalho, J. Oliveira, M. Arsali, L. Papazachariou, P. Demosthenous, A. Lazarou, M. Hadjigavriel, C. Stavrou, L. Yioukkas, C. Deltas, A. Pierides, M. Kkolou, H. R. Toka, S. Dibartolo, B. Lanske, E. M. Brown, M. R. Pollak, A. Familiari, B. Zavan, S. Sanna Cherchi, A. Fabris, R. Cristofaro, G. Gambaro, A. D'Angelo, F. Anglani, H. Toka, D. Mount, M. Pollak, G. Curhan, G. Sengoge, T. Bajari, A. Kupczok, A. von Haeseler, M. Schuster, W. Pfaller, P. Jennings, A. Weltermann, S. Blake, G. Sunder-Plassmann, A. Kerti, R. Csohany, L. Wagner, E. Javorszky, E. Maka, T. Tulassay, K. Tory, J. Kingswood, N. Nikolskaya, J. Mbundi, S. Jozwiak, E. Belousova, M. Frost, R. Kuperman, M. Bebin, B. Korf, R. Flamini, M. Kohrman, S. Sparagana, J. Wu, T. Brechenmacher, K. Stein, J. Bissler, D. Franz, B. Zonnenberg, W. Cheung, J. Wang, D. Lam, K. Budde, L. Ivanitskiy, E. Sowershaewa, T. Krasnova, L. Samokhodskaya, M. Safarikova, R. Jana, S. Jitka, L. Obeidova, M. Kohoutova, V. Tesar, H. Evrengul, P. Ertan, E. Serdaroglu, S. Yuksel, S. Mir, E. Yang n Ergon, A. Berdeli, A. Zawada, K. Rogacev, B. Rotter, P. Winter, D. Fliser, G. Heine, S. Bataille, V. Moal, Y. Berland, L. Daniel, C. Rosado, E. Bueno, P. Fraile, C. Lucas, P. Garcoa-Cosmes, J. M. Tabernero, R. Gonzalez, P. Garcia-Cosmes, M. Silska-Dittmar, K. Zaorska, A. Malke, A. Musielak, D. Ostalska-Nowicka, J. Zachwieja, V. K d r, E. Uz, A. Yigit, A. Altuntas, B. Yigit, S. Inal, M. Sezer, R. Yilmaz, B. Visciano, C. Porto, E. Acampora, R. Russo, E. Riccio, I. Capuano, G. Parenti, A. Pisani, S. Feriozzi, A. Perrin, M. West, K. Nicholls, J. Torras, M. Cybulla, M. Conti, A. Angioi, M. Floris, P. Melis, A. M. Asunis, D. Piras, A. Pani, D. Warnock, A. Guasch, C. Thomas, C. Wanner, R. Campbell, B. Vujkovac, I. Okur, G. Biberoglu, F. Ezgu, L. Tumer, A. Hasanoglu, Z. Bicik, Y. Akin, M. Mumcuoglu, T. Ecder, C. Paliouras, G. Mattas, N. Papagiannis, G. Ntetskas, F. Lamprianou, N. Karvouniaris, and P. Alivanis

Subjects
Genetics, Transplantation, medicine.medical_specialty, Nephrology, business.industry, Molecular genetics, medicine, business
Published
2014

2. An inosine 5'-monophosphate dehydrogenase 2 single-nucleotide polymorphism impairs the effect of mycophenolic acid

Author

Wolfgang Winnicki, Günter Weigel, T Bajari, B Winter, Harald Herkner, Gere Sunder-Plassmann, and G. Sengoelge

Subjects
Guanine, Lymphocyte, Single-nucleotide polymorphism, Isozyme, Polymorphism, Single Nucleotide, Mycophenolic acid, chemistry.chemical_compound, Exon, IMP Dehydrogenase, Genetics, medicine, Humans, Lymphocytes, Inosine-5′-monophosphate dehydrogenase, Inosine, Cell Proliferation, Pharmacology, biology, Mycophenolic Acid, Molecular biology, medicine.anatomical_structure, chemistry, biology.protein, Molecular Medicine, Immunosuppressive Agents, medicine.drug
Abstract

Mycophenolic acid (MPA) is a selective inhibitor of inosine 5'-monophosphate dehydrogenase (IMPDH), the rate-limiting enzyme of de novo synthesis of guanine nucleotides. The isoenzyme IMPDH2 predominates in activated lymphocytes, and its inhibition by MPA is part of standard immunosuppressive regimens. Yet, there are significant unexplained differences in efficacy and tolerability among patients. The objective of this study was to analyze whether frequent variants in the IMPDH2 gene lead to changes in IMPDH activity and to differences in responsiveness to MPA therapy. All 14 exons and intron-exon boundary regions of IMPDH2 were sequenced from genomic DNA probes from 100 healthy individuals. Two novel exonic single-nucleotide polymorphisms were identified in 1% and one intronic polymorphism (rs11706052) in 19% of the study population. Lymphocyte IMPDH activity and proliferation under three MPA concentrations (2.5, 10 and 25 micromol l(-1)) were compared in rs11706052 carriers and wild-type individuals. The presence of rs11706052 polymorphism reduced the antiproliferative effect of MPA on lymphocytes by approximately 50% compared with the IMPDH2 wild-type form at therapeutic relevant concentrations of 10 micromol l(-1) and 25 micromol l(-1). We conclude that a poorer response to MPA therapy can be explained in some individuals by the presence of the rs11706052 polymorphism.

Published
2009

3. An inosine 5'-monophosphate dehydrogenase 2 single-nucleotide polymorphism impairs the effect of mycophenolic acid.

Author

Winnicki W, Weigel G, Sunder-Plassmann G, Bajari T, Winter B, Herkner H, and Sengoelge G

Subjects
Cell Proliferation drug effects, Humans, Immunosuppressive Agents therapeutic use, Lymphocytes drug effects, Lymphocytes enzymology, Mycophenolic Acid therapeutic use, Polymorphism, Single Nucleotide, IMP Dehydrogenase genetics, Immunosuppressive Agents antagonists & inhibitors, Mycophenolic Acid antagonists & inhibitors
Abstract

Mycophenolic acid (MPA) is a selective inhibitor of inosine 5'-monophosphate dehydrogenase (IMPDH), the rate-limiting enzyme of de novo synthesis of guanine nucleotides. The isoenzyme IMPDH2 predominates in activated lymphocytes, and its inhibition by MPA is part of standard immunosuppressive regimens. Yet, there are significant unexplained differences in efficacy and tolerability among patients. The objective of this study was to analyze whether frequent variants in the IMPDH2 gene lead to changes in IMPDH activity and to differences in responsiveness to MPA therapy. All 14 exons and intron-exon boundary regions of IMPDH2 were sequenced from genomic DNA probes from 100 healthy individuals. Two novel exonic single-nucleotide polymorphisms were identified in 1% and one intronic polymorphism (rs11706052) in 19% of the study population. Lymphocyte IMPDH activity and proliferation under three MPA concentrations (2.5, 10 and 25 micromol l(-1)) were compared in rs11706052 carriers and wild-type individuals. The presence of rs11706052 polymorphism reduced the antiproliferative effect of MPA on lymphocytes by approximately 50% compared with the IMPDH2 wild-type form at therapeutic relevant concentrations of 10 micromol l(-1) and 25 micromol l(-1). We conclude that a poorer response to MPA therapy can be explained in some individuals by the presence of the rs11706052 polymorphism.

Published
2010
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4. A xanthomatosis-susceptibility gene may exist in a Syrian family with familial hypercholesterolemia.

Author

Vergopoulos A, Bajari T, Jouma M, Knoblauch H, Aydin A, Bähring S, Mueller-Myhsok B, Dresel A, Joubran R, Luft FC, and Schuster H

Subjects
Adolescent, Adult, Child, Cholesterol, LDL blood, Consanguinity, Female, Genes, Recessive genetics, Genetic Predisposition to Disease, Heterozygote, Homozygote, Humans, Hyperlipoproteinemia Type II blood, Hyperlipoproteinemia Type II physiopathology, Male, Pedigree, Point Mutation genetics, Syria, Genes, Dominant genetics, Hyperlipoproteinemia Type II genetics, Receptors, LDL genetics, Xanthomatosis genetics
Abstract

Familial hypercholesterolemia (FH) is an autosomal-dominant inherited disorder characterized by high serum low-density lipoprotein (LDL)-cholesterol concentrations, xanthoma formation, and premature atherosclerosis. Homozygous individuals die of vascular disease as children or young adults; heterozygous persons are at high risk for premature cardiovascular death. Mutations in the LDL-receptor gene are responsible for FH. We studied 49 members of a consanguineous Syrian kindred containing 6 homozygous individuals from the same pedigree. Half of the homozygotes had giant xanthomas, while half did not, even though their LDL-cholesterol concentrations were elevated to similar degrees (> 14 mmol/l). Heterozygous FH individuals from this family were also clearly distinguishable with respect to xanthoma size. We performed DNA analysis and were successful in identifying a hitherto not described mutation in this family's LDL receptor. DNA sequence analysis of the LDL-receptor gene revealed a T to C substitution at nucleotide 1,999 in codon 646 of exon 14. We next conducted a segregation analysis, which suggests that a susceptibility gene may explain the formation of giant xanthomas in this family. We raise the hypothesis that the appearance of giant xanthomas in this FH family is controlled by a second gene acting in an autosomal-dominant or recessive fashion. Elucidation of this 'xanthoma' gene may shed additional light on LDL-cholesterol deposition.

Published
1997

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