Disease relevance of IDH2

• The recombinant mNADP-IDH expressed in Escherichia coli had active enzymatic function, as well as an expected molecular weight [1].
• The Indiana Chronic Disease Management Program (ICDMP) is intended to improve the quality and cost-effectiveness of care for Medicaid members with congestive heart failure (chronic heart failure), diabetes, asthma, and other conditions [2].
• RESULTS: About 46 percent (99/215) of the hydrophobia cases admitted to the IDH in 1998 belonged to Delhi [3].
• The prevalence of discoid lateral meniscus, including ICDM and CDM, in the female cadavers was significantly higher than that in the male cadavers, but there was no significant gender difference in the prevalence of CDM [4].

High impact information on IDH2

• SDH and IDH-1, but not IDH-2, were also associated with increased all-cause mortality risk [5].
• Assignment of a gene for human mitochondrial isocitrate dehydrogenase (ICD-M, EC 1.1.1.41) to chromosome 15 [6].
• Segregation analysis of human biochemical markers and chromosomes in human-mouse somatic cell hybrids allowed to demonstrate synteny of ICDM with the genes for phosphomannose isomerase and pyruvate kinase and to assign the linkage group to human chromosome 15 [6].
• In the process of identifying genes involved in optimization of lymphocyte activation, we have cloned the human mitochondrial NADP-dependent isocitrate dehydrogenase (mNADP-IDH) cDNA [7].
• There was no cell cycle-dependent fluctuation of mNADP-IDH expression in synchronized Jurkat cells [7].

Biological context of IDH2

• Evidence from hybrid clones carrying a human X/15 translocation chromosome indicates that the human IDH-2 gene can be localized to the q11-qter region of chromosome 15 [8].
• A correlation was found between the expression of human IDH-2 and the presence of human chromosome 15 in a "panel" of eight independent hybrid clones [8].
• Electrophoretic patterns in F1 hybrid heterozygotes confirmed the dimeric structures of GPI and IDH, and indicated a multimeric structure for pyruvate kinase [9].

Anatomical context of IDH2

• The method allows one to distinguish human IDH-2 from its mouse counterpart in extracts from human-mouse somatic cell hybrids [8].
• In T and B cells, rapamycin (RAPA) could repress the mitogen-stimulated mNADP-IDH expression, although most of the early or late phase activation-related genes including a G-protein beta subunit-related gene H12.3 were not affected by the drug [7].
• Altogether, 577 lateral menisci were classified into the following three types: normal type (NM); incomplete discoid type (ICDM); and complete discoid type (CDM) [4].
• Basic MSAs for IDH and SCS patients that were introduced from a common peroneal nerve were found to be statistically higher than those of the control subjects [10].

Associations of IDH2 with chemical compounds

• A double-immunodiffusion method has been developed to detect human mitochondrial NADP-linked isocitrate dehydrogenase (EC 1.1.1.42; designated as IDH-2) using rabbit antiserum against the relevant enzyme [8].

Other interactions of IDH2

• IDH-2 and human cytoplasmic IDH (IDH-1) were found to be asyntenic [8].
• Assignment of cytoplasmic alpha-mannosidase (MANA) and confirmation of mitochondrial isocitrate dehydrogenase (IDHM) to the q11 leads to qter region of chromosome 15 in man [11].
• Mendelian inheritance of codominant autosomal alleles was established for IDH-2, LDH-1, LDH-2, ME-2, PGM-1, and PGI-2 [12].

Analytical, diagnostic and therapeutic context of IDH2

• The comparative painting results agreed completely with the limited gene mapping data available in horses, and also enabled us provisionally to assign one linkage group (U2) and one syntenic group (NP, MPI, IDH2) to specific equine chromosomes [13].
• The current report documents the molecular cloning of the mouse mitochondrial NADP-dependent isocitrate dehydrogenase (mNADP-IDH) cDNA [1].

References