Involved in negative regulation of double-strand break repair via homologous recombination; positive regulation of double-strand break repair via nonhomologous end joining; and positive regulation of isotype switching. Located in actin cytoskeleton; nucleoplasm; and site of double-strand break. [provided by Alliance of Genome Resources, Jul 2025]
Transcription factors with Perturb-seq knockdown data for SHLD2. The Binding column indicates whether any binding evidence exists for this TF–gene pair (ChIP-seq or motif footprint peaks). The Mean coef is the average Perturb-seq regression coefficient across active gRNAs (positive = SHLD2 upregulated upon KD; negative = downregulated). The Outlier column indicates whether this gene is in the top or bottom 5% of all TF knockdown effects.
| TF | Mean coef | Binding | Outlier | TF→Gene link |
|---|
Open chromatin peaks (ATAC-seq) in the genomic neighbourhood of SHLD2, linked by TSS proximity or chromatin conformation (Multiome / HiCAR). Each element overlaps at least one TF ChIP-seq binding site — the TFs column shows how many distinct TFs bind that element.
| Accessibility | Element | Dist. to TSS | Link type | TFs |
|---|---|---|---|---|
| chr10:86,864,876–86,866,168 | 228.9 kb | Distal (>10kb) Multiome | 123 | |
| chr10:86,939,081–86,939,963 | 154.6 kb | Distal (>10kb) Multiome | 539 | |
| chr10:86,953,950–86,955,264 | 139.6 kb | Distal (>10kb) Multiome | 348 | |
| chr10:86,959,879–86,960,855 | 133.6 kb | Distal (>10kb) Multiome | 453 | |
| chr10:86,966,444–86,967,440 | 127.2 kb | Distal (>10kb) Multiome | 479 | |
| chr10:86,969,969–86,972,224 | 122.8 kb | Distal (>10kb) Multiome | 505 | |
| chr10:87,054,811–87,055,712 | 38.9 kb | Distal (>10kb) Multiome | 179 | |
| chr10:87,092,890–87,093,298 | 861 bp | At TSS | 374 | |
| chr10:87,093,833–87,095,937 | 895 bp | At TSS Multiome | 996 | |
| chr10:87,203,498–87,204,198 | 109.5 kb | Distal (>10kb) Multiome | 295 | |
| chr10:87,342,231–87,343,299 | 248.4 kb | Distal (>10kb) Multiome | 270 |
Genomic view of the SHLD2 locus showing ATAC-seq accessibility and RNA-seq expression across the ESC → DE time course, together with TF binding peaks and element-to-TSS loop connections.