Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.4.2.8 (
hypoxanthine-guanine phosphoribosyltransferase
)
2,527
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Excision repair deficiencies in groups A and G xeroderma pigmentosum (XP) cells are transiently complemented after microinjection of HeLa poly(A)+RNA, but those in groups D and F are not complemented (Legerski et al., 1984). We tested XP cells belonging to the seven complementation groups, A-G, and Cockayne's syndrome (CS) cells belonging to the two complementation groups, A and B, for transient correction by microinjection of total poly(A)+RNA from HeLa cells. Among the XP cells, unscheduled DNA synthesis (UDS) was increased only in XP-A cells by microinjection of total poly(A)+RNA. However, UDS was increased in XP-E and
XP-G
cells as well as in XP-A cells by microinjection of concentrated poly(A)+RNA fractionated on a 5-25% sucrose density gradient containing methylmercuric hydroxide. The sizes of XP-E and
XP-G
mRNA were estimated to be 1.5-2.7 kb and 2.0-3.8 kb, respectively, by comparison to internal marker RNAs including 18S rRNA, 28S rRNA,
HPRT
mRNA and XPAC mRNA. RNA synthesis recovery after UV exposure in CS cells was not increased by microinjection of either total poly(A)+RNA or fractionated RNA. These results provide estimates of the sizes of XP-E and
XP-G
proteins and will facilitate molecular cloning of DNA repair genes, especially of XP-E and
XP-G
genes.
...
PMID:Complementation of xeroderma pigmentosum cells by microinjection of mRNA fractionated under denaturing conditions: an estimation of sizes of XP-E and XP-G mRNA. 750 87
1-SO-adenine DNA adducts, DNA single-strand breaks (SBs), chromosomal aberrations (CAs), mutant frequency (MF) at the
HPRT
gene, and immune parameters (hematological and of humoral immunity) were studied in styrene-exposed human subjects and controls. Results were correlated with genetic polymorphisms in DNA repair genes (XPD, exon 23,
XPG
, exon 15, XPC, exon 15, XRCC1, exon 10, XRCC3, exon 7) and cell cycle gene cyclin D1. Results for biomarkers of genotoxicity after stratification for the different DNA repair genetic polymorphisms showed that the polymorphism in exon 23 of the XPD gene modulates levels of chromosomal and DNA damage,
HPRT
MF, and moderately affects DNA adduct levels. The highest levels of biomarkers were associated with the wild-type homozygous AA genotype. The exposed individuals with the wild-type GG genotype for XRCC1 gene exhibited the lowest CA frequencies, compared to those with an A allele (P < 0.05). Cyclin D1 polymorphism seems to modulate the number of leukocytes and lymphocytes in the analyzed subjects. The number of eosinophiles was positively associated with XPD variant C allele and negatively with XRCC1 variant A allele (P < 0.05) and XPC variant C allele (P < 0.05). Immunoglobulin IgA was positively associated with an XRCC3 variant T allele (P < 0.01) and negatively with XPC variant C allele (P < 0.05). Both C3- and C4-complement components were lower in individuals with XRCC3 CT (P < 0.05) and TT genotypes (P < 0.01). Adhesion molecules sL-selectin and sICAM-1 were associated with XPC genotype (P < 0.05). Individual susceptibility may be reflected in genotoxic and immunotoxic responses to environmental and occupational exposures to xenobiotics.
...
PMID:DNA repair and cyclin D1 polymorphisms and styrene-induced genotoxicity and immunotoxicity. 1599 42