Transcriptomic response to adult hypothalamic deletion of Snord116
Snord116 deletion mouse models recapitulate aspects of the Prader-Willi Syndrome. In this study, we examine the gene expression changes in the mediobasal hypothalamus for mice which have an adult onset deletion of Snord116 in the mediobasal hypothalamus.
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.
- Hypothalamic loss of Snord116 recapitulates the hyperphagia of P... 2018 · 103 cites
Deep data QC
90/100 · AStandardized, field-standard QC computed by touching the data — every metric states how it was obtained · evidence: measured
Bulk RNA-seq (mouse). Grade A: high base quality (Q30=96.7%, base quality=39.3) offset by moderate-to-high PCR duplication (56.2%). While above the B threshold, duplication at this level will noticeably increase noise in abundance estimates, especially for minor transcripts. Usable for robust genes but recommend duplicate-aware analysis or validation for low-abundance targets.
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