TGF-b utilizes a novel receptor activation mechanism to phosphorylate SMAD1/5 and regulate epithelial-to-mesenchymal transition
TGF-b treatment leads to the transcriptional regulation of many genes. However, the proportion of those that are dependent on SMAD1/5 is unknown. Here, we compared the transcriptional profile after TGF-b treatment in a parental clone and one in which SMAD1/5 had been deleted by CRISPR/Cas9 to identify SMAD1/5 dependent genes.
Provenance — who produced it, who reused it
Linked to 1 papers in the literature. Roles are inferred factual signals (who deposited the data vs who reused it), with counts — never a judgement about any author.
Deep data QC
100/100 · AStandardized, field-standard QC computed by touching the data — every metric states how it was obtained · evidence: measured
High-quality mouse RNA-seq (100/100) with exceptional coverage (838M reads) and outstanding mean base quality (39.1). Duplication of 30.46% is acceptable for RNA-seq; Q30 (95.2%) and minimal adapters (0.35%) support high-confidence differential expression analysis.
The A grade is a transparent weighted average. Each metric below scored from 0–100% against the published bulk-RNA-seq thresholds, weighted by its importance; nothing is hidden or subjective.
measured = computed from the data · extrapolated/reported = derived or from the repository · dq-1.0