Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary tissue injury and repair processes involve complex and coordinated cellular events such as necrosis, inflammation, cell growth/differentiation, apoptosis, and remodeling of extracellular matrix. These processes are regulated by expression of multiple mediator genes. Commercially available microarray blots and slides allow screening of hundreds to thousands of genes in a given tissue or cell preparation. However, often these blots do not contain cDNAs of one's interest and are difficult to interpret. In order to analyze the tissue expression profile of a large number of genes involved in pulmonary injury and pathology, we developed a rat gene array filter using array technology. This array consisted of 27 genes representing inflammatory and anti-inflammatory cytokines, growth factors, adhesion molecules, stress proteins, transcription factors and antioxidant enzymes; 3 negative controls, and 2 blank spots. Using rat gene-specific polymerase chain reaction (PCR) primer pairs, cDNAs for these genes were amplified and cloned into a TA vector. Plasmids with recombinant cDNA inserts were purified and blotted onto a nylon membrane. Lung total RNA was isolated at 3 or 24 h following intratracheal (IT) exposure of male Sprague Dawley rats to either saline (control), residual oil fly ash (ROFA; 3.3 mg/kg) or metals found in one instillate of ROFA: nickel (NiSO(4); 1. 3 micromol/kg) or vanadium (VSO(4); 2.2 micromol/kg). (32)P-Labeled cDNA was generated from RNA samples in a reverse transcriptase reaction and subsequently hybridized to array blots. Densitometric scans of array blots revealed a twofold induction of interleukin (IL)-6 and TIMP-1 at 24 h post ROFA or Ni exposure. The pulmonary expressions of cellular fibronectin (cFn-EIIIA), ICAM-1, IL-1beta, and iNOS genes were also increased 24 h post ROFA-, V-, or Ni-exposure. Consistent hybridization of beta-actin in all array blots and absence of hybridization signals in negative controls indicated gene specific hybridization. ROFA or metal-induced increase in the expression of IL-6 observed in array blot was validated by Northern blot hybridization. Developing a pulmonary rat gene array may provide a tool for screening the expression profile of tissue specific markers following exposure to toxic air contaminants.
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PMID:A pulmonary rat gene array for screening altered expression profiles in air pollutant-induced lung injury. 1111 90

Incinerator workers are exposed to polycyclic aromatic hydrocarbons (PAHs) and dioxins in workplace. Previous studies indicated that aryl hydrocarbon receptor activation, following by increased cytochrome P4501A1 (CYP1A1) and 1B1 (CYP1B1) activity and expressions, was required for PAHs and dioxin induced toxicities. This study investigated whether municipal waste incinerator workers with frequent exposure to PAHs/dioxins in fly/bottom ash had increased CYP1A1 and CYP1B1 expressions in peripheral leukocytes and assessed whether CYP1B1*3 polymorphism modified the association between PAHs/dioxins exposure and CYP1B1 expressions. Based on job contents and time-activity profiles, 112 workers were classified into high exposure, medium exposure and control groups. CYP1A1 and CYP1B1 gene expressions in workers' leukocytes were determined with the real-time reverse transcriptase polymerase chain reaction method. After taking into account age, gender and smoking in the multiple regression analyses, CYP1B1, but not CYP1A1, levels were significantly higher in the high and medium exposure groups than in the control group, and there was a statistically significant interaction between exposure group and CYP1B1 genotype. These results suggested that CYP1B1 gene expression could be a potential biomarker of biologically effective dose for occupational exposure to PAHs/dioxins and CYP1B1*3 polymorphism modified effects of occupational exposures on CYP1B1 expression.
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PMID:Increased cytochrome P4501B1 gene expression in peripheral leukocytes of municipal waste incinerator workers. 1609 93

Royal jelly (RJ) has diverse physiological and pharmacological functions. We observed its weak estrogenic activity in the previous study. RJ stimulated the proliferation of mouse osteoblast-like MC3T3-E1 cells at 0.1 mg/ml, and the effect was blocked by the specific estrogen receptor antagonist ICI 182,780. The addition of 0.1-1.0 mg/ml RJ enhanced collagen production in culture medium. Oral administration of RJ to normal female mice for 9 weeks increased the ash content of their tibiae. DNA microarray analysis revealed significant changes in gene expression related to extracellular matrix formation when the femurs of mice fed RJ were analyzed. Quantitative reverse transcriptase-PCR (RT-PCR) confirmed up-regulation of procollagen I alpha1 gene expression. These data suggest that RJ as a whole or some of its individual components stimulates production of type I collagen and other activities for bone formation through action on osteoblasts.
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PMID:Royal jelly stimulates bone formation: physiologic and nutrigenomic studies with mice and cell lines. 1703 Oct 45