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Ribobio co meriptm m6a transcriptome profiling kit
Meriptm M6a Transcriptome Profiling Kit, supplied by Ribobio co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transcriptomic+profiling/meriptm+m6a+transcriptome+profiling+kit/pm38725005-103-5-10
Average 90 stars, based on 1 article reviews
meriptm m6a transcriptome profiling kit - by Bioz Stars, 2026-09
90/100 stars

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Modification:

Article Title: FTO-mediated m6A modification elevates the MFN2 mRNA stability to suppress ovarian granulosa cell senescence.
Article Snippet: Although significant progress has been made in human-assisted reproductive technology in recent decades, fertility issues related to ovarian senescence remain a pressing challenge in reproductive medicine.. As granulosa cells play a critical role in supporting oocytes, understanding the mechanisms of ovarian granulosa cell senescence is crucial to addressing the decline in ovarian function and oocyte quality associated with ovarian senescence.. Previous studies have indicated that the mitochondrial fusion protein (MFN2) may play a key role in ovarian senescence and is linked to the outcomes of assisted reproductive technology.

Article Title: METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging.
Article Snippet: To explore the stability of Hspa1a mRNA in MC3T3-E1 NC and shMETTL3 cells, actinomycin D (Selleck) was added to the complete medium at 5 μg/ ml. .. Cells were collected at specified times, and RNA was extracted for qRTPCR to determine the half-life of Hspa1a. m6A RIP-qPCR and RIP-qPCR analysis The level of m6A modification on Hspa1a mRNA was detected using a MeRIPTM m6A Transcriptome Profiling Kit (RiboBio), following the same method as MeRIP-seq. ..

Article Title: METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging
Article Snippet: .. The level of m6A modification on Hspa1a mRNA was detected using a MeRIPTM m6A Transcriptome Profiling Kit (RiboBio), following the same method as MeRIP-seq. ..

Transfection:

Article Title: METTL3 regulates the proliferation, metastasis and EMT progression of bladder cancer through P3H4.
Article Snippet: Bladder cancer, the most common malignant tumor in the urinary system, exhibits significantly up-regulated expression of P3H4, which is associated with pathological factors.. The objective of this study was to elucidate the underlying mechanism of P3H4 in bladder cancer.. Initially, we analyzed P3H4 gene expression using the TCGA database and evaluated P3H4 levels in clinical samples and various bladder cell lines.



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(a-d) t-SNE performed on (a) PBMC immune frequencies, (b) PBMC gene expression, (c) immune frequencies and gene expression combined, and (d) plasma proteomics. (e) Clustering of transcriptomic data from our study and the Human Protein Atlas. (f) Distribution of Euclidean distance in transcriptomic profiles between collected samples (i) from the same participant within the first year (visit 1-4), (ii) from the same participant between year 1 and year 2 (visit 5-6), and (iii) from different participants. Wilcoxon tests were used for statistical analysis (ns, not significant; ****, P < 0.0001). (g) Euclidean distance between each transcriptomic profile from the last visit and the sample collected during the first year, divided into (i) pairs of samples from the same individual (light blue) and (ii) pairs of samples from different participants (red). (h) Distribution of intraclass correlation coefficient of immune cell profiling, transcriptomic and plasma proteomics. (i) Intraclass correlation coefficient of all 53 immune populations. (j) Intra- and inter-individual coefficients of variation of gene expression. (k) Examples of genes, immune populations and proteins showing individual expression profiles. Samples are colored according to their expression levels at visit 1 (orange: 0-25%, green: 25–50%, blue: 50–75%, purple: 75–100%). The highlighted dots indicate the median level of the corresponding group at that visit.

Journal: bioRxiv

Article Title: Systems-level longitudinal immune profiling reveals individualized immunotypes and genetic associations

doi: 10.64898/2026.03.21.713378

Figure Lengend Snippet: (a-d) t-SNE performed on (a) PBMC immune frequencies, (b) PBMC gene expression, (c) immune frequencies and gene expression combined, and (d) plasma proteomics. (e) Clustering of transcriptomic data from our study and the Human Protein Atlas. (f) Distribution of Euclidean distance in transcriptomic profiles between collected samples (i) from the same participant within the first year (visit 1-4), (ii) from the same participant between year 1 and year 2 (visit 5-6), and (iii) from different participants. Wilcoxon tests were used for statistical analysis (ns, not significant; ****, P < 0.0001). (g) Euclidean distance between each transcriptomic profile from the last visit and the sample collected during the first year, divided into (i) pairs of samples from the same individual (light blue) and (ii) pairs of samples from different participants (red). (h) Distribution of intraclass correlation coefficient of immune cell profiling, transcriptomic and plasma proteomics. (i) Intraclass correlation coefficient of all 53 immune populations. (j) Intra- and inter-individual coefficients of variation of gene expression. (k) Examples of genes, immune populations and proteins showing individual expression profiles. Samples are colored according to their expression levels at visit 1 (orange: 0-25%, green: 25–50%, blue: 50–75%, purple: 75–100%). The highlighted dots indicate the median level of the corresponding group at that visit.

Article Snippet: Moreover, we downloaded the transcriptomic profiles available from the Human Protein Atlas ( https://www.proteinatlas.org/humanproteome/blood ) and used them to verify the expression patterns of key genes across cell types.

Techniques: Gene Expression, Clinical Proteomics, Expressing

(a) t-SNE sample clustering based on transcriptomic profiles of genes in the PBMC association network. (b) Immune frequencies patterns across the three sample clusters. (c) Distribution of (top) innate immune cell frequencies and (bottom) CD4:CD8 ratio across the three clusters. (d) Immune frequencies of the modules in the PBMC network, divided by sample clusters. (e) Number of up- and down-regulated genes in each module (FDR<0.05) obtained from differential expression analysis between each cluster and the remaining two. (f-h) t-SNE clustering colored based on CD4:CD8+ T cells ratio, and immune frequencies of the B cells, cytotoxic and myeloid modules. (j) (Top) CRP levels of participant P3920. (Bottom) Sample clusters of participants across visits; highlighted in black are the samples from participant P3920. (k) Pattern of clinical variables across the three clusters. (l) Patterns of the 30 proteins with the most significant up-regulation in any of the three clusters. SBP, systolic blood pressure; DBP, diastolic blood pressure; TNT, troponin T; CRP, C-reactive protein; HDL, high density lipoprotein; ALAT, alanine aminotransferase; GGT, gamma-glutamyl transferase. P-values are calculated by Wilcoxon tests in c-d; ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: bioRxiv

Article Title: Systems-level longitudinal immune profiling reveals individualized immunotypes and genetic associations

doi: 10.64898/2026.03.21.713378

Figure Lengend Snippet: (a) t-SNE sample clustering based on transcriptomic profiles of genes in the PBMC association network. (b) Immune frequencies patterns across the three sample clusters. (c) Distribution of (top) innate immune cell frequencies and (bottom) CD4:CD8 ratio across the three clusters. (d) Immune frequencies of the modules in the PBMC network, divided by sample clusters. (e) Number of up- and down-regulated genes in each module (FDR<0.05) obtained from differential expression analysis between each cluster and the remaining two. (f-h) t-SNE clustering colored based on CD4:CD8+ T cells ratio, and immune frequencies of the B cells, cytotoxic and myeloid modules. (j) (Top) CRP levels of participant P3920. (Bottom) Sample clusters of participants across visits; highlighted in black are the samples from participant P3920. (k) Pattern of clinical variables across the three clusters. (l) Patterns of the 30 proteins with the most significant up-regulation in any of the three clusters. SBP, systolic blood pressure; DBP, diastolic blood pressure; TNT, troponin T; CRP, C-reactive protein; HDL, high density lipoprotein; ALAT, alanine aminotransferase; GGT, gamma-glutamyl transferase. P-values are calculated by Wilcoxon tests in c-d; ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: Moreover, we downloaded the transcriptomic profiles available from the Human Protein Atlas ( https://www.proteinatlas.org/humanproteome/blood ) and used them to verify the expression patterns of key genes across cell types.

Techniques: Quantitative Proteomics