Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.2 (PDK1)
 2,238 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MicroRNAs are small non-coding RNAs that posttranscriptionally regulate mRNA expression. hsa-miR-6165 which was previously discovered in our group is located in the forth intron of p75NTR gene and its function is still under investigation. As P75NTR has diverse cellular functions, some of the complexity of its function could be attributed to the internally located microRNA. Our analysis revealed that treatment of HCT116 cells with 5-azacytidine promoted differential expression of hsa-miR-6165 from its host gene which is consistent with the bioinformatic prediction of an independent promoter for hsa-miR-6165. In addition, hsa-miR-6165 promoter is capable of driving GFP reporter gene in HeLa cells. The putative target gene expression level which was detected using RT-qPCR is inversely proportional to the expression level of hsa-miR-6165 during NT2 cell neural differentiation. Furthermore, hsa-miR-6165 overexpression resulted in significant downregulation of ABLIM-1, PVRL1, and PDK1 target genes, while it attenuates NT2 neural differentiation. Hsa-miR-6165 overexpression in SW480 cells also resulted in significant downregulation of PKD1, DAGLA, and PLXNA2 putative target genes, while it increases the sub-G1 cell population of SW480 and HEK293T cells as detected by flow cytometry. Overall, in this study, we report an independent promoter for hsa-miR-6165 which is active in HeLa cells. Additionally, hsa-miR-6165 targets ABLIM-1, PVRL1, PKD1, PLXNA2, and PDK1 genes, and unlike in HEK293T and SW480 cells, hsa-miR-6165 overexpression does not affect HeLa cells while its downregulation reduces sub-G1 cell population. Our results validate that hsa-miR-6165 affects the cell cycle progression and could increase apoptosis in human cell lines.
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PMID:Expression and Function of hsa-miR-6165 in Human Cell Lines and During the NT2 Cell Neural Differentiation Process. 2895 60

In the current study we compared the molecular signature of expanded mesenchymal stromal cells (MSCs) derived from selected CD271+ bone marrow mononuclear cells (CD271-MSCs) and MSCs derived from non-selected bone marrow mononuclear cells by plastic adherence (PA-MSCs). Transcriptome analysis demonstrated for the first time the upregulation of 115 and downregulation of 131 genes in CD271-MSCs. Functional enrichment analysis showed that the upregulated genes in CD271-MSCs are significantly enriched for extracellular matrix (tenascin XB, elastin, ABI family, member 3 (NESH) binding protein, carboxypeptidase Z, laminin alpha 2 and nephroblastoma overexpressed) and cell adhesion (CXCR7, GPNMB, MYBPH, SVEP1, ARHGAP6, TSPEAR, PIK3CG, ABL2 and NCAM1). CD271-MSCs expressed higher gene transcript levels that are involved in early osteogenesis/chondrogenesis/adipogenesis (ZNF145, FKBP5). In addition, increased transcript levels for early and late osteogenesis (DPT, OMD, ID4, CRYAB, SORT1), adipogenesis (CTNNB1, ZEB, LPL, FABP4, PDK4, ACDC), and chondrogenesis (CCN3/NOV, CCN4/WISP1, CCN5/WISP2 and ADAMTS-5) were detected. Interestingly, CD271-MSCs expressed increased levels of hematopoiesis associated genes (CXCL12, FLT3L, IL-3, TPO, KITL). Down-regulated genes in CD271-MSCs were associated with WNT and TGF-beta signaling, and cytokine/chemokine signaling pathways. In addition to their capacity to support hematopoiesis, these results suggest that CD271-MSCs may contain more osteo/chondro progenitors and/or feature a greater differentiation potential.
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PMID:Molecular signature of human bone marrow-derived mesenchymal stromal cell subsets. 3074 27