Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.6 (RNA polymerase)
 34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcohol has been reported to be a risk factor in psoriasis mainly based on the observation that there is a higher prevalence of alcohol abuse in individuals with psoriasis. The mechanism by which alcohol affects this disease is still elusive. So far there are no reports describing the effects of metabolites relevant to alcohol metabolism on the growth of human keratinocytes. In the present study we examined the effects of ethanol and acetone, which exceeds its normal endogenous level in the blood of heavy drinkers, on the proliferation of HaCaT keratinocytes. HaCaT cells were incubated for 30 min in the presence of various concentrations of ethanol (2.14 m M-1.71 M) and acetone (1.7 mM-1.36 M). The numbers of viable and proliferating cells were determined at different times after ethanol and acetone treatment. The effects of ethanol and acetone on the mRNA levels of genes characteristic for proliferating keratinocytes such as alpha5 integrin, keratinocyte growth factor receptor and cyclin D1 were studied by reverse-transcriptase polymerase chain reaction. Both ethanol and acetone induced proliferation of HaCaT cells. The maximum increase in the number of viable cells and the maximum proliferative response was observed with 4.28 m M ethanol and 13.6 m M acetone. The alpha5 integrin, keratinocyte growth factor receptor and cyclin D1 mRNA levels were higher compared to the controls as early as 2 h after ethanol and 30 min after acetone treatment of the cells. The stimulatory effect of ethanol and acetone on human keratinocytes may be one of the reasons why psoriasis can be precipitated by alcohol misuse.
 ...
PMID:Ethanol and acetone stimulate the proliferation of HaCaT keratinocytes: the possible role of alcohol in exacerbating psoriasis. 1272 8

Real-time PCR is frequently used for gene expression quantification due to its methodological sensitivity and reproducibility. The gene expression is quantified by normalization to one or more reference genes, usually beta-actin (ACTB), glyceraldehyde-3-phosphate dehydrogenase (GAPD) or to ribosomal RNA (18S). However, different environmental or pathological conditions might also influence the expression of normalizing genes, which could severely skew the interpretation of quantitative results. This study evaluates whether 16 genes frequently used as endogenous controls in expression studies, can serve as such for comparison of human brain tissues of chronic alcoholics and control subjects. The prefrontal and motor cortices that are affected differently by chronic alcohol consumption were analyzed. The reference genes that have no or small differences in expression in alcoholics and control subjects, were found to be specific for each region: beta-actin (ACTB) and ribosomal large P0 (RPLP0) for the prefrontal cortex while importin 8 (IPO8) and RNA polymerase II (POLR2A) for the motor cortex. Four out of sixteen analyzed genes demonstrated significant differences in expression between alcoholics and controls: phosphoglycerate kinase (PGK1), hypoxanthine phosphoribosyl transferase (HPRT1) and peptidylprolyl isomerase A (PPIA) in the motor cortex and beta-2-microglobulin (B2M) in the prefrontal cortex. Our study demonstrates the importance of validation of endogenous control genes prior to real-time PCR analysis of human brain tissues. Prescribed and non-prescribed drugs, pathological or environmental conditions along with alcohol abuse may differentially influence expression of reference genes.
 ...
PMID:Validation of endogenous controls for quantitative gene expression analysis: application on brain cortices of human chronic alcoholics. 1718 56