Non-canonical Notch signaling activates IL-6/JAK/STAT signaling in breast tumor cells and is controlled by p53 and IKKβ
Notch signaling is frequently hyperactivated in breast cancer, but how the enhanced signaling contributes to the tumor process is less well understood. In this report, we identify the proinflammatory cytokine interleukin-6 (IL-6) as a novel Notch target in breast tumor cells. Enhanced Notch signaling upregulated IL-6 expression at the transcriptional level, leading to activation of autocrine and paracrine JAK/STAT signaling. IL-6 upregulation was mediated by non-canonical Notch signaling, as it...
Provenance — who produced it, who reused it
Linked to 2 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.
- Non-canonical Notch signaling activates IL-6/JAK/STAT signaling... 2012 · 141 cites
1 further paper cites this accession but reuse could not be confirmed.
Deep data QC
metadata only · no data-level QC for this typeStandardized, field-standard QC computed by touching the data — every metric states how it was obtained
No quantitative QC rubric exists for this data type yet, so it is deliberately left unscored — this is an honest "not applicable", not a poor rating.
measured = computed from the data · extrapolated/reported = derived or from the repository · dq-1.0 · provisional — verify independently
Scientific quality
Based on hands-on reproduction of the papers that use this dataset. A reproducible paper that stands on this data is positive evidence; a flagged one is a prompt to look closer — never a verdict on the dataset itself without the evidence.