Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Visceral fat accumulation has an important role in increasing the morbidity and mortality rates, by increasing the risk of developing several metabolic disorders, such as type 2 diabetes, dyslipidemia and hypertension. New genetic loci that are associated with increased systolic and diastolic blood pressures have been identified by genome-wide association studies in Caucasian populations. This study investigates whether single nucleotide polymorphisms (SNPs) that confer susceptibility to high blood pressure are also associated with visceral fat obesity. We genotyped 1279 Japanese subjects (556 men and 723 women) who underwent computed tomography for measuring the visceral fat area (VFA) and subcutaneous fat area (SFA) at the following SNPs: FGF5 rs16998073, CACNB2 rs11014166, C10orf107 rs1530440, CYP17A1 rs1004467, NT5C2 rs11191548, PLEKHA7 rs381815, ATP2B1 rs2681472 and rs2681492, ARID3B rs6495112, CSK rs1378942, PLCD3 rs12946454, and ZNF652 rs16948048. In an additive model, risk alleles of the CYP17A1 rs1004467 and NT5C2 rs11191548 were found to be significantly associated with reduced SFA (P=0.00011 and 0.0016, respectively). When the analysis was performed separately in men and women, significant associations of rs1004467 (additive model) and rs11191548 (recessive model) with reduced VFA (P=0.0018 and 0.0022, respectively) and SFA (P=0.00039 and 0.00059, respectively) were observed in women, but not in men. Our results suggest that polymorphisms in the CYP17A1 and NT5C2 genes influence a reduction in both visceral and subcutaneous fat mass in Japanese women.
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PMID:Genetic variations in the CYP17A1 and NT5C2 genes are associated with a reduction in visceral and subcutaneous fat areas in Japanese women. 2207 13

Recently, the functions of circular RNAs (circRNAs) on cancer initiation and development arouse wide concern. Herein, we tested the influences of circ-ZNF652 on renal carcinoma cell growth and metastasis. Firstly, clinical renal carcinoma tissues and corresponding normal tissues were collected. The circ-ZNF652 expressions were tested. Then, the influences of silencing circ-ZNF652 on renal carcinoma A498 and ACHN cell proliferation, apoptosis and epithelial-mesenchymal transition (EMT) process, as well as Ras/Raf/MEK/ERK and JAK1/STAT3 pathways, were probed. Finally, whether miR-205 engaged in the influences of silencing circ-ZNF652 on A498 and ACHN cell were investigated. circ-ZNF652 had high expression level in clinical renal carcinoma tissues. Silencing circ-ZNF652 repressed A498 and ACHN cell proliferation and EMT process, but promoted cell apoptosis. Moreover, silencing circ-ZNF652 suppressed Ras/Raf/MEK/ERK and JAK1/STAT3 pathways in A498 and ACHN cells. Besides, the miR-205 expressions in A498 and ACHN cells were raised by silencing circ-ZNF652. Knockdown of miR-205 weakened the influences of silencing circ-ZNF652 on A498 and ACHN cell proliferation, apoptosis and EMT process. Silencing circ-ZNF652 repressed proliferation and EMT process of renal carcinoma A498 and ACHN cells via suppressing Ras/Raf/MEK/ERK and JAK1/STAT3 pathways, as well as raising miR-205 expression.
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PMID:Silencing circular RNA-ZNF652 represses proliferation and EMT process of renal carcinoma cells via raising miR-205. 3308 30

The pathogenesis of diabetic nephropathy is not completely understood, and the effects of existing treatments are not satisfactory. Various public platforms already contain extensive data for deeper bioinformatics analysis. From the GSE30529 dataset based on diabetic nephropathy tubular samples, we identified 345 genes through differential expression analysis and weighted gene coexpression correlation network analysis. GO annotations mainly included neutrophil activation, regulation of immune effector process, positive regulation of cytokine production and neutrophil-mediated immunity. KEGG pathways mostly included phagosome, complement and coagulation cascades, cell adhesion molecules and the AGE-RAGE signalling pathway in diabetic complications. Additional datasets were analysed to understand the mechanisms of differential gene expression from an epigenetic perspective. Differentially expressed miRNAs were obtained to construct a miRNA-mRNA network from the miRNA profiles in the GSE57674 dataset. The miR-1237-3p/SH2B3, miR-1238-5p/ZNF652 and miR-766-3p/TGFBI axes may be involved in diabetic nephropathy. The methylation levels of the 345 genes were also tested based on the gene methylation profiles of the GSE121820 dataset. The top 20 hub genes in the PPI network were discerned using the CytoHubba tool. Correlation analysis with GFR showed that SYK, CXCL1, LYN, VWF, ANXA1, C3, HLA-E, RHOA, SERPING1, EGF and KNG1 may be involved in diabetic nephropathy. Eight small molecule compounds were identified as potential therapeutic drugs using Connectivity Map.
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PMID:Identification of C3 as a therapeutic target for diabetic nephropathy by bioinformatics analysis. 3277 79