Chromosomal Localization of the Human Heme Oxygenase Genes: Heme Oxygenase-1 (HMOX1) Maps to Chromosome 22q12 and Heme Oxygenase-2 (HMOX2) Maps to Chromosome 16p13.3

Kutty, R. Krishnan; Kutty, Geetha; Rodríguez, Ignacio R.; Chader, Gerald J.; Wiggert, Barbara

doi:10.1006/geno.1994.1213

Cited by 101 publications

(65 citation statements)

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“…Sequences 5Ј to Ϫ194 in MCF TX400 matched the 5Ј UTR of CDP alternately spliced product (CASP), an alternately spliced variant of CCAAT displacement protein (CDP), a gene previously localized to 7q22 (17,18). Sequences 5Ј of Ϫ194 in S48-3s ACT 0.1 cells were homologous to the 5Ј UTR of heme-oxygenase 2 (HO-2), which is on chromosome 16 (19). As shown in Fig.…”

Section: Resultsmentioning

confidence: 80%

Gene rearrangement: a novel mechanism for MDR-1 gene activation.

Mickley¹,

Spengler²,

Knutsen³

et al. 1997

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 80%

Gene rearrangement: a novel mechanism for MDR-1 gene activation.

Mickley¹,

Spengler²,

Knutsen³

et al. 1997

J. Clin. Invest.

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“…HO-2 has been cloned from rat, mouse, and human and they share more than 90% protein homology. Human HO-2 is mapped to chromosome 16q13.3 (Kutty et al, 1994a;Abraham et al, 1996).…”

Section: A Primary Structure Of Different Heme Oxygenase Isoformsmentioning

confidence: 99%

Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications

Wang²

2005

Pharmacol Rev

843

741

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“…The human HO-1 gene has been mapped to chromosome 22q12 (6), and the number of guanosine thymidine dinucleotide repeats [(GT) n ] in the HO-1 gene microsatellite promoter is inversely associated with HO-1 mRNA levels and enzyme activity (7). An increased susceptibility to CV events and increased mortality of longer (GT) n in the HO-1 gene promoter have been reported in high-risk patients with coronary heart disease (CHD), hypercholesterolemia, diabetes mellitus, history of smoking, peripheral artery disease, or arsenic exposure (7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Length Polymorphism in Heme Oxygenase-1 and Cardiovascular Events and Mortality in Hemodialysis Patients

Chen

Hung

Tarng

2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Persistent inflammation and oxidative stress play a pathogenic role in the high cardiovascular morbidity and mortality of hemodialysis patients. Heme oxygenase-1 is considered to have antiinflammatory and antioxidant properties. This study assessed the association between the length of guanosine thymidine dinucleotide repeats in the heme oxygenase-1 gene microsatellite promoter and cardiovascular events and mortality among hemodialysis patients.Design, setting, participants, & measurements Study participants were recruited from October 1, 2006 to December 31, 2006. The allelic frequencies of the length of guanosine thymidine dinucleotide repeats (the S allele represents shorter [,27] repeats, and the L allele represents longer [$27] repeats) in the heme oxygenase-1 gene promoter were analyzed in 1080 unrelated chronic hemodialysis patients and 365 healthy controls for distribution comparison. Cardiovascular events and mortality were the study outcomes, and the hemodialysis patients were followed until June 30, 2011.Results The genotype proportions were 20.6%, 48.8%, and 30.6% for S/S, S/L, and L/L, respectively, in the hemodialysis patients and comparable with those proportions in healthy controls. The patients with the L/L genotype had significantly higher baseline serum high-sensitivity C-reactive protein and malondialdehyde levels than the patients with the S/S or S/L genotypes. During a median follow-up of 50 months, 307 patients died. A Kaplan-Meier survival analysis showed the highest cardiovascular events and all-cause mortality in patients with the L/L genotype. The adjusted hazard ratios (95% confidence intervals) for each L allele in additive model were 1.42 (1.20 to 1.67 [P,0.001]) for cardiovascular events and 1.19 (1.01 to 1.40 [P=0.03]) for all-cause mortality.Conclusions Chronic hemodialysis patients with longer lengths of guanosine thymidine dinucleotide repeats in the heme oxygenase-1 gene promoter exhibit higher inflammation and oxidative stress. These patients have higher risk of long-term cardiovascular events and mortality.

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Chromosomal Localization of the Human Heme Oxygenase Genes: Heme Oxygenase-1 (HMOX1) Maps to Chromosome 22q12 and Heme Oxygenase-2 (HMOX2) Maps to Chromosome 16p13.3

Cited by 101 publications

References 0 publications

Gene rearrangement: a novel mechanism for MDR-1 gene activation.

Gene rearrangement: a novel mechanism for MDR-1 gene activation.

Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications

Length Polymorphism in Heme Oxygenase-1 and Cardiovascular Events and Mortality in Hemodialysis Patients

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