Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00492 (hypoxanthine-guanine phosphoribosyltransferase)
 2,385 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fusion of interferon-gamma activated peripheral blood monocytes to a mutagenized hypoxanthine-guanine phosphoribosyltransferase (HGPRT)-deficient U937 parent line was performed resulting in the generation of a series of unique cloned monocyte hybridomas. These cell lines were proven to be true hybrids by the acquisition of donor class I antigens as well as other donor derived chromosomes. In addition, novel functional characteristics were observed including secretion of specific monokines and the acquisition of phagocytic capabilities. The ability to generate immortalized human monocyte hybridomas will allow for more in depth analysis of monocyte subpopulations and dissection of specific monocyte functions.
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PMID:The generation and characterization of human monocyte hybridomas. 206 13

This report describes T cell lines derived from a patient with subacute cutaneous lupus after treatment with intravenous pulse cyclophosphamide. We selected for mitotically active, hypoxanthine-guanine phosphoribosyltransferase-deficient (HPRT-) T cells, by culture in a selective medium containing 6-thioguanine. When HPRT- cell lines were derived 6 days after pulse cyclophosphamide (CYC) treatment, they were predominantly CD8+ and T cell receptor (TCR) gamma/delta+, producing interferon-gamma (IFN gamma). Cell lines derived 21 days after CYC treatment were CD4+, TCR alpha/beta+ and produced both IFN gamma and interleukin-4. These results support a possible role for gamma/delta+ T cells in subacute cutaneous lupus and suggest a mechanism for the therapeutic effect of CYC.
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PMID:Characteristics of HPRT-mutant T cell lines in a lupus patient treated with cyclophosphamide. 794 81

To better understand the mechanisms through which persistent infections/inflammation increase cancer risks, we assessed the potential genotoxic properties of NO produced by macrophages. We recently showed that mouse macrophage RAW264.7 cells were capable of resuming exponential growth after stimulation for NO production by interferon-gamma (IFN-gamma) and/or lipopolysaccharide. Here, we report that increases in mutant fraction (MF) in the endogenous, X-linked, hprt gene of the cells are associated with NO exposure. Cells stimulated with 100 units/ml IFN-gamma continuously for 14 and 23 days produced a total of 9.8 and 14 micromol of NO per 10(7) cells, respectively. MFs in the hprt gene of NO-producing cells were 16.6 and 31.3 x 10(-5), respectively, compared with 2.2 and 2.5 x 10(-5) in untreated cells. Addition of an NO synthase inhibitor, N-monomethyl-L-arginine, to the culture medium decreased NO production and MF by 90% and 85%, respectively. Reverse transcription-PCR and DNA sequencing revealed that NO-associated hprt mutations did not differ significantly from those arising spontaneously, with the exception that certain small deletions/insertions and multiple exon deletions were observed only in the former. MF also increased significantly in cells stimulated for only 4 days with lipopolysaccharide plus IFN-gamma for higher rates of NO production. The types and proportion of hprt mutations induced under these conditions were strikingly similar to those associated with long-term NO exposure. These results indicate that NO exposure results in gene mutations in RAW264.7 cells through mechanisms yet to be identified and may also contribute to spontaneous mutagenesis.
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PMID:Mutagenesis associated with nitric oxide production in macrophages. 965 79