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Smad4-p65 interactions drive BMP-mediated protection against inflammatory cell death [4C-Seq]

GSE315066 Mus musculus (mouse) Other 12 samples Submitted 2026/02/18 Platform GPL24247
At a glance

mouse · 12 samples

Organism
Mus musculus (mouse)
Samples
12 samples: 6 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI.
Summary (written by the submitters)
Inflammation-induced osteoblast death undermines bone homeostasis and can aggravate bone-destructive diseases, yet how pro-survival BMP signaling intersects with inflammatory TNF–NF-κB signaling remains poorly defined. Here we show that BMP4 protects mouse osteoblasts from TNF-α–triggered apoptosis and cytotoxic death and that this cytoprotection requires both Smad4 and NF-κB p65.
Read the full summary ↓
Integrative epigenomic profiling (ChIP-seq/ATAC-seq/RNA-seq) reveals extensive Smad4–p65 co-occupancy and identifies Samd9l as a prominent TNF-α–inducible gene that is selectively repressed by BMP4. Two Smad4/p65-bound distal elements physically contact the Samd9l promoter, exhibit TNF-responsive enhancer activity, and are required for Samd9l induction, as demonstrated by 4C-seq and CRISPR/dCas9-based chromatin closing/opening. Functionally, Samd9l depletion attenuates TNF-α–driven caspase activation and cytotoxicity in osteoblasts and enhances BMP2-driven ectopic bone formation in vivo. Cross-species mapping suggests that the two mouse regulatory elements converge into a single promoter-proximal composite element at the human SAMD9L locus, supporting a conserved inflammatory control node. Together, these findings define a BMP4–Smad4 mechanism that reshapes NF-κB enhancer outputs to limit osteoblast death and nominate the SAMD9L regulatory circuit as a therapeutic entry point for inflammatory bone loss.
This dataset
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Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗
3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE315066_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Whole study · RAW.tar ↓

Also filed as BioProject PRJNA1394952. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
6 conditions, mostly in duplicate
OB_none_OC1 ×2 OB_TNFa_OC1 ×2 OB_TNFa+BMP4_OC1 ×2 OB_none_OC2 ×2 OB_TNFa_OC2 ×2 OB_TNFa+BMP4_OC2 ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 12 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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