1,804,261 research outputs found
Proceedings of the sixth SFB-375 Ringberg workshop 'Astroteilchenphysik'
No full textSIGLEAvailable from TIB Hannover: RS 2508(6) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman
miR-375-3p damaged osteogenesis by inducing cell apoptosis.
No full text(A) Relative expression levels of RUNX2 in MC3T3-E1 cells treated with miR-375-3p mimics. (B) Relative expression levels of SOST in MC3T3-E1 cells treated with miR-375-3p mimics. (C) Representative TUNEL staining images of MC3T3-E1 cells. More TUNEL positive staining cells (Red) were found after the cells were transfected with miR-375-3p mimics. (D) Quantification of TUNEL-positive cells. * p < 0.05, ** p < 0.01. n = 3/group.</p
miR-375-3p targeted LRP5 and β-catenin.
No full text(A) The binding sites between miR-375-3p and the 3’UTR of LRP5 and β-catenin. (B) The relative luciferase activity of MC3T3-E1 cells transfected with luciferase-wild type (or mutant) LRP5 plasmids and miR-375-3p mimics. (C) The relative luciferase activity of MC3T3-E1 cells transfected with luciferase-wild type (or mutant) β-catenin plasmids and miR-375-3p mimics. * p < 0.05. ** p < 0.01, NS, not significant. n = 3/group.</p
Bulletin No. 375 - Alfalfa Varieties for Wyoming
No full textBulletin No. 375 - Alfalfa Varieties for Wyomin
Dispelling the Myths Behind First-author Citation Counts
No full textWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
Additional file 3: of A novel miR-375-HOXB3-CDCA3/DNMT3B regulatory circuitry contributes to leukemogenesis in acute myeloid leukemia
No full textFigure S1. The expression of miR-126 and miR-375 in normal controls, CpG islands around the region encoding miR-375, and expression of pre-miR-375. (A) The expressions of miR-126 and miR-375 were detected in all CD34+ cells from 20 normal controls (NC). Housekeeping gene U6 is used as a reference. The lowest expression of miR-375 in one NC was set to 1.0 and then the expressions of miR-375 and miR-126 in all other specimens were normalized by this lowest specimen. The fold change of miR-375 and miR-126 were calculated by Student’s t-test. (B) CpG islands around the region encoding pre-miR-375 were analyzed by MethPrimer software. (C) The expression of pre-miR-375 was detected by qRT-PCR in HL-60 and THP1 cells, which were transduced with MSCV-miR-375 or MSCV-NC. *P < 0.01 versus MSCV-NC. (TIFF 221 kb
E2F transcription factor 1 is involved in the phenotypic modulation of esophageal squamous cell carcinoma cells via microRNA-375
No full textE2F family of transcription factors modulates multiple cellular functions associated with cell cycle and apoptosis. Here, we focused on the relevance of E2F1 to esophageal squamous cell carcinoma (ESCC) and identification of E2F1-mediated network in this study. Query of Gene Expression Omnibus database revealed that E2F1 was the core gene that was upregulated in ESCC. E2F1 downregulation inhibited ESCC cell activity. microRNA (miR)-375 was confirmed to be a downstream target of E2F1. E2F1 bound to miR-375 promoter and inhibited miR-375 transcription. Moreover, miR-375 inhibitor mitigated the repressive impacts of si-E2F1 on ESCC cells in part. Further study showed that sestrin 3 (SESN3) could interact with miR-375, and its knockdown annulled the stimulative effect of miR-375 inhibitor on ESCC development. Finally, E2F1 and SESN3 downregulation inhibited the phosphatidylinositol 3 kinase (PI3K)/AKT pathway activity in cells, while miR-375 inhibitor promoted PI3K/AKT pathway activation. These findings suggest that E2F1 inhibited miR-375 expression and promoted SESN3 expression to activate the PI3K/AKT pathway in ESCC.</p
Additional file 9: of A novel miR-375-HOXB3-CDCA3/DNMT3B regulatory circuitry contributes to leukemogenesis in acute myeloid leukemia
No full textFigure S6. An illustration of miR-375-HOXB3-CDCA3/DNMT3B regulatory circuitry. (A) In normal hematological cells or leukemic cells treated with AZA, miR-375 expression is increased because of DNA hypomethylation. Upregulation of miR-375 inhibits HOXB3 expression, resulting in the arrest of proliferation and reduction of colony formation via decreasing the expression of CDCA3. Moreover, the decreased expression of HOXB3 can not increase and recruit DNMT3B to bind in the pre-miR-375 promoter and maintains the hypomethylation of pre-miR-375, which finally leads to the upregulated expression of miR-375, in turn. (TIFF 592Â kb
miR-375-3p arrested the expression of LRP5 and β-catenin.
No full text(A) Relative expression levels of LRP5 in MC3T3-E1 cells upon transfection of miR-375-3p mimics or inhibitors. (B) Relative expression levels of β-catenin in MC3T3-E1 cells upon transfection of miR-375-3p mimics or inhibitors. (C) Representative staining images of MC3T3-E1 cells. Less green cells were found after the cells were transfected with miR-375-3p mimics. * p < 0.05. ** p < 0.01. n = 3/group.</p
- …
