Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.11.2 (prolyl hydroxylase)
 1,814 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers. In this study, our objective was to identify differentially regulated proteins in ESCC using isobaric tag for relative and absolute quantification (iTRAQ) technique and liquid chromatography-tandem mass spectrometry (LC-MS/MS). We compared the protein expression profiles of ESCC tumor tissues with the corresponding adjacent normal tissue from three patients. It was determined that 72 and 57 unique proteins were significantly up-regulated and down-regulated in all three samples. In addition, there were 431 significantly differentially regulated proteins having at least two biological samples. This subject found some of the differential proteins, such as prolyl 4-hydroxylase subunit alpha-1, prolyl 4-hydroxylase subunit alpha-2, and calponin-2, immunoglobulin superfamily containing leucine-rich repeat protein, and prolyl 3-hydroxylase1, which were few studies about them in ESCC. In order to determine the results, we performed another independent experiment. Our results indicated quantitative proteomics, as a robust discovery tool for the identification, differentially regulated proteins in cancers.
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PMID:iTRAQ-based quantitative proteomic analysis of esophageal squamous cell carcinoma. 2633 Feb 93

We have previously reported that miR-17~92 is critically involved in the pathogenesis of pulmonary hypertension (PH). We also identified two novel mR-17/20a direct targets, PDZ and LIM domain protein 5 (PDLIM5) and prolyl hydroxylase 2 (PHD2), and elucidated the signaling pathways by which PDLIM5 and PHD2 regulate functions of pulmonary artery smooth muscle cells (PASMCs). In addition, we have shown that plasminogen activator inhibitor-1 (PAI-1) is also downregulated in PASMCs that overexpress miR-17~92. However, it is unclear whether PAI-1 is a direct target of miR-17~92 and whether it plays a role in regulating the PASMC phenotype. In this study, we have identified PAI-1 as a novel target of miR-19a/b, two members of the miR-17~92 cluster. We found that the 3'-untranslated region (UTR) of PAI-1 contains a miR-19a/b binding site and that miR-19a/b can target this site to suppress PAI-1 protein expression. MiR-17/20a, two other members of miR-17~92, may also indirectly suppress PAI-1 expression through PDLIM5. PAI-1 is a negative regulator of miR-17~92-mediated PASMC proliferation. Silencing of PAI-1 induces Smad2/calponin signaling in PASMCs, suggesting that PAI-1 is a negative regulator of the PASMC contractile phenotype. We also found that PAI-1 is essential for the metabolic gene expression in PASMCs. Furthermore, although there is no significant change in PAI-1 levels in PASMCs isolated from idiopathic pulmonary arterial hypertension and associated pulmonary arterial hypertension patients, PAI-1 is downregulated in hypoxia/Sugen-induced hypertensive rat lungs. These results suggest that miR-17~92 regulates the PASMC contractile phenotype and proliferation coordinately and synergistically by direct and indirect targeting of PAI-1.
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PMID:PAI-1 is a novel component of the miR-17~92 signaling that regulates pulmonary artery smooth muscle cell phenotypes. 2964 96