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

The p190 family of GTPases consists of at least two different isoforms both containing an N-terminal GTPase and a C-terminal Rho GAP domain. Here we have isolated and characterized genomic and cDNA clones spanning the entire coding region of the mouse p190-B gene. Genomic data were obtained by sequencing plasmid subclones of two overlapping mouse genomic phage clones. Interestingly, a single 3.9 kb exon was found to contain approx. 80% of the coding region of the mouse p190-B protein (amino acid residues 1-1238) including the 5'-untranslated region, the N-terminal GTPase domain and a middle domain of unknown function. Missing from this exon, however, was the C-terminal Rho GAP domain, which was cloned from mouse brain mRNA using reverse transcriptase polymerase chain reaction. Comparison of the mouse with the human p190-B proteins revealed that approx. 97% of the amino acid residues were identical. Northern analysis of total RNA from a variety of mouse tissues detected ubiquitous expression of two p190-B transcripts of 4.0 and 6.8 kb in size. Analysis of two multilocus genetic crosses localized the mouse gene, Gfi2, to a position on chromosome 12, consistent with the mapping of the human gene to a position of conserved synteny on chromosome 14. The high level of sequence homology between the human and the mouse suggests that there is a strong selective pressure to maintain the p190-B protein structure.
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PMID:Cloning, genomic organization and chromosomal assignment of the mouse p190-B gene. 983 17

We have previously shown that miR-486-5p is one of the most downregulated micro RNAs in lung cancer. The objective of the study was to investigate the role of miR-486-5p in the progression and metastasis of non-small-cell lung cancer (NSCLC). We evaluated miR-486-5p expression status on 76 frozen and 33 formalin-fixed paraffin-embedded tissues of NSCLC by quantitative reverse transcriptase PCR to determine its clinicopathologic significance. We then performed function analysis of miR-486-5p to determine its potential roles on cancer cell migration and invasion in vitro and metastasis in vivo. We also investigated the target genes of miR-486-5p in lung tumorigenesis. miR-486-5p expression level was significantly lower in lung tumors compared with their corresponding normal tissues (P<0.0001), and associated with stage (P=0.0001) and lymph node metastasis of NSCLC (P=0.0019). Forced expression of miR-486-5p inhibited NSCLC cell migration and invasion in vitro and metastasis in mice by inhibiting cell proliferation. Furthermore, ectopic expression of miR-486-5p in cancer cells reduced ARHGAP5 expression level, whereas miR-486-5p silencing increased its expression. Luciferase assay demonstrated that miR-486-5p could directly bind to the 3'-untranslated region of ARHGAP5. The expression level of miR-486-5p was inversely correlated with that of ARHGAP5 in lung tumor tissues (P=0.0156). Reduced expression of ARHGAP5 considerably inhibited lung cancer cell migration and invasion, resembling that of miR-486-5p overexpression. miR-486-5p may act as a tumor-suppressor contributing to the progression and metastasis of NSCLC by targeting ARHGAP5. miR-486-5p would provide potential diagnostic and therapeutic targets for the disease.
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PMID:Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer. 2347 61