Cholesterol pathway inhibition induces TGFβ signaling to promote basal differentiation in pancreatic cancer
Oncogenic transformation alters the metabolism of cellular lipids to sustain tumor growth. We define a reciprocal mechanism by which cholesterol metabolism controls the formation and differentiation of pancreatic ductal adenocarcinoma (PDAC). Disruption of distal cholesterol biosynthesis by conditional inactivation of Nsdhl, or treatment with cholesterol-lowering statins caused murine pancreatic carcinomas induced by KrasG12D expression and homozygous Trp53 loss to undergo a differentiation...
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
51/100 · FStandardized, field-standard QC computed by touching the data — every metric states how it was obtained · evidence: measured
Mouse 150 bp paired-end RNA-seq with moderate quality metrics (Q30: 68.6%, mean quality 32.3), representing lower-tier sequencing reliability common in older or cost-optimized studies. The 36% GC content is notably depressed, potentially indicating GC-bias or sample-specific transcript composition. Search terms: mouse bulk RNA-seq, paired-end transcriptomics.
The F 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