Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polymerase chain reaction (PCR) primers designed to amplify bovine specific sequences of the arginine-vasopressin (ARVP), glycoprotein hormone alpha (CGA), cytochrome oxidase c subunit IV pseudogene (COXP), prochymosin (CYM), coagulation factor X (F10), inhibin beta A (INHBA), low density lipoprotein receptor (LDLR) and oxytocin (OXT) genes in hybrid cells were used in a search for single strand conformation polymorphisms. DNA from 75 animals comprising crossbred and 7 purebred breeds were analysed. ARVP, COXP, CYM, LDLR and OXT were found to be polymorphic while CGA, F10 and INHBA were not. Polymorphic regions were identified within 206 bp of exon 1 of ARVP, 582 bp of the pseudogene COXP, 253 bp of exon 9 of CYM, 519 bp of LDLR cDNA and 160 bp of the upstream regulatory region of OXT. This is the first report of bovine polymorphisms for these genes and an important step in our goal to incorporate type I comparative anchor loci into the bovine linkage map. Polymorphic loci were subsequently analysed in pedigreed full-sib families and shown to be inherited in a Mendelian fashion.
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PMID:Single-strand conformation polymorphisms (SSCPs) detected in five bovine genes. 768 2

Inflammation is critical to the pathogenesis of cardiovascular diseases (CVDs). We have uncovered intrauterine inflammation induced by lipopolysaccharide (LPS) increases CVDs in adult offspring rats. The present study aimed to explore the role of prenatal exposure to LPS on the lipid profiles in male offspring rats and to further assess their susceptibility to high fat diet (HFD). Maternal LPS (0.79 mg/kg) exposure produced a significant increase in serum and hepatic levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, aspartate amino transferase as well as liver morphological abnormalities in 8-week-old offspring rats. Meanwhile, disturbed gene expressions involved in hepatic lipid metabolism and related signaling pathways were found, especially the up-regulated very-low density lipoprotein receptor (VLDLR) and down-regulated transmembrane 7 superfamily member 2 (TM7SF2). Following HFD treatment, however, the lipid profile shifts and liver dysfunction were exacerbated compared to the offsprings treated with prenatal LPS exposure alone. Compared with that in control offsprings, the hepatic mitochondria (Mt) in offspring rats solely treated with HFD exhibited remarkably higher ATP level, enforced Complex IV expression and a sharp reduction of its activity, whereas the offsprings from LPS-treated dams showed the loss of ATP content, diminished membrane potential, decline in protein expression and activity of mitochondrial respiratory complex IV, increased level of MtDNA deletion as well. Furthermore, treatment with HFD deteriorated these mitochondrial disorders in the prenatally LPS-exposed offspring rats. Taken together, maternal LPS exposure reinforces dyslipidemia in response to a HFD in adult offsprings, which should be associated with mitochondrial abnormalities and disturbed gene expressions of cholesterol metabolism.
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PMID:Prenatal Lipopolysaccharide Exposure Promotes Dyslipidemia in the Male Offspring Rats. 2986 79