Journal: Blood

Article Title: p16 INK4a deficiency promotes IL-4-induced polarization and inhibits proinflammatory signaling in macrophages

doi: 10.1182/blood-2010-10-313106

Figure Lengend Snippet: Microarray analysis using mRNA from p16−/− BMDM compared to p16+/+ BMDM showed (A) decreased mRNA expression of classically activated macrophages-associated genes and (B) increased mRNA expression of alternatively activated macrophages-associated genes. Data is expressed as fold change relative to p16+/+ BMDM. (C) Differential gene expression in p16−/− BMDM relative to p16+/+ BMDM was correlated with the changes induced in IL-4-induced p16+/+ AAMφ. The figure shows 2log values of the probesets significantly (p<0.05) regulated only in p16−/− BMDM (red dots), only in IL-4-polarized p16+/+ AAMφ (green dots) and by both conditions (blue dots), compared to p16+/+ BMDM. The X-axis represents differences in gene expression induced by IL-4, whereas the Y-axis represents the effect of p16INKa-deficiency. These comparisons are depicted in the schematic representation of the protocol in the corresponding colors. Pearson Correlation analysis was done for probesets differentially expressed by both conditions (blue). (D) Heat map of p16+/+ BMDM, p16−/− BMDM, IL-4-polarized p16+/+ and p16−/− AAMφ gene expression profiles. Colors fluctuate from blue (poorly expressed) to green (intermediate expression) and yellow (high expression). Additional information regarding gene description, fold induction, and p-value can be found in Table S3.

Article Snippet: We thank E. Vallez for mouse breeding, J. Brozek (Genfit SA, Loos, France) for microarray raw data analysis, T. Coevoet, N. Jouy and A. Lucas for technical assistance.

Techniques: Microarray, Expressing, Gene Expression

Journal: Blood

Article Title: p16 INK4a deficiency promotes IL-4-induced polarization and inhibits proinflammatory signaling in macrophages

doi: 10.1182/blood-2010-10-313106

Figure Lengend Snippet: Representation of the relative microarray intensity values from a selection of down-regulated genes in p16+/+ and p16−/− BMDM with or without polarization (AAMφ) by 15 ng/mL IL-4 from day 0 of differentiation. Statistically significant differences are indicated (a: p<0.05 compared to p16+/+ BMDM; b: p<0.05 compared to p16−/− BMDM; c: p<0.05 compared to p16+/+ AAMφ.)

Article Snippet: We thank E. Vallez for mouse breeding, J. Brozek (Genfit SA, Loos, France) for microarray raw data analysis, T. Coevoet, N. Jouy and A. Lucas for technical assistance.

Techniques: Microarray, Selection

Journal: BMC Ophthalmology

Article Title: MiRNAs regulate oxidative stress related genes via binding to the 3′ UTR and TATA-box regions: a new hypothesis for cataract pathogenesis

doi: 10.1186/s12886-017-0537-9

Figure Lengend Snippet: Heatmap shows differentially expressed mRNAs in cataractous lens samples compared with transparent lens samples. Six separate microarray assays were performed to determine the genome-wide mRNA expression in the central epithelium of transparent and cataractous human lenses. Microarray data were processed by CapitalBio Corporation. Heatmap shows differentially expressed mRNAs in cataractous lens samples compared with transparent lens samples. Relative expression value from high to low was shown by gradient of red to green in the heatmap. Colors indicate relative mRNA expression. Red and green indicate higher or lower expression of mRNAs relative to those in transparent lens samples, respectively. FDR (false discovery rate) adjusted p -value <0.05

Article Snippet: Microarray raw data were processed at CapitalBio Corporation.

Techniques: Microarray, Genome Wide, Expressing

Journal: Frontiers in Immunology

Article Title: Deep analysis of skin molecular heterogeneities and their significance on the precise treatment of patients with psoriasis

doi: 10.3389/fimmu.2024.1326502

Figure Lengend Snippet: Overview of data processing steps. From the public databases, nine microarray datasets containing 250 patients with psoriasis were selected. According to the established methodologies, DEGs were filtered, and enrichment analysis, PPI network analysis, and supervised clustering were performed. Finally, the Xgboost classifier was constructed to predict the responses of stratified subtypes to commonly used biologics. DEGs, differentially expressed genes; GO, Gene Ontology; GSEA, Gene-set enrichment analysis; KEGG, Kyoto Encyclopedia of Genes and Genomes; MCODE, Molecular Complex Detection; PPI, protein–protein interaction.

Article Snippet: Normalized matrix files are downloaded directly from Illumina into raw microarray data.

Techniques: Microarray, Construct

Journal: Oncogene

Article Title: Identification of CASZ1 nuclear export signal (NES) reveals potential mechanisms for loss of CASZ1 tumor suppressor activity in neuroblastoma

doi: 10.1038/onc.2016.179

Figure Lengend Snippet: (A) IPA assay of CASZ1b targets in SY5Y cells determined by microarray showed gene enrichment in the categories of molecular and cellular functions with a key subcategory being cell growth and proliferation (threshold represents p=0.05). (B) GSEA assay indicated the positive enrichment of genes involved neurological system process (left panel), and negative enrichment of genes regulated by MYC (right panel). NES, normalized enrichment score; Nom, nominal; FDR, false discovery rate. (C) Transcriptional activity assay of cytoplasmic localized K37A mutant and loss of NuRD binding mutant L31A in SY5Y cells by realtime PCR. a, Left panel: western blot analysis of CASZ1b and mutant proteins from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment; right panel: realtime PCR analysis of CASZ1b and mutant mRNA levels from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment. b-f, realtime PCR result verified the regulation of TH, NGFR, CD9, MYC and KIT by CASZ1b in SY5Y cells after 24 h Tet treatment. Compared to wild type CASZ1b, K37 almost completely lost transcriptional activity at regulating all these genes in SY5Y cells (data are shown as means ± S.E.M., *: p<0.05). Compared to wild type CASZ1b, L37 significantly decreased transcriptional activity at regulating TH, NGFR and MYC, but had a slight increase at regulating CD9 and no effect on KIT (data are shown as means ± S.E.M., *: p<0.05).

Article Snippet: Gene set enrich analysis (GSEA) ( , ) was performed using the whole gene list generated by uploading the raw microarray data to Partek Genomics Suite 6.6.

Techniques: Microarray, Activity Assay, Mutagenesis, Binding Assay, Western Blot

Journal: Toxicological Sciences

Article Title: Chronic Hexavalent Chromium Exposure Upregulates the RNA Methyltransferase METTL3 Expression to Promote Cell Transformation, Cancer Stem Cell-Like Property, and Tumorigenesis

doi: 10.1093/toxsci/kfac023

Figure Lengend Snippet: Total RNA N6-methyladenosine (m6A) modification levels are significantly increased in chronic hexavalent chromium [Cr(VI)] exposure-transformed human bronchial epithelial cells and chronic chromate-exposed mouse lung tissues. A, The heatmap from m6A microarray analysis showing the extent of total messenger RNA m6A methylation in passage-matched control cells (BEAS-2B-Control) and chronic Cr(VI) exposure-transformed cells [BEAS-2B-Cr(VI)]. B and C, Relative total RNA m6A levels measured by using the EpiQuik m6A RNA Methylation Quantification Kit. The total RNA m6A levels in Cr(VI)-transformed cells (B) or chromate-exposed mouse lung tissues (C) are expressed relative to the passage-matched control cells (means ± SD, n = 3) (B) or vehicle control-exposed mouse lungs (means ± SD, n = 6) (C), respectively. *p < .05.

Article Snippet: The microarray raw data were further analyzed by Arraystar Inc. and the microarray raw data were deposited to the National Center for Biotechnology Information’s data repository (GSE186605).

Techniques: Modification, Transformation Assay, Microarray, Methylation, Control