Involved in several processes, including cardiac muscle cell proliferation; negative regulation of smooth muscle cell apoptotic process; and positive regulation of protein kinase C activity. Located in Golgi membrane and extracellular space. Part of COPI vesicle coat. [provided by Alliance of Genome Resources, Jul 2025]
Transcription factors with Perturb-seq knockdown data for DIPK2A. 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 = DIPK2A 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 DIPK2A, 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 |
|---|---|---|---|---|
| chr3:143,805,063–143,806,295 | 166.1 kb | Distal (>10kb) Multiome | 164 | |
| chr3:143,970,615–143,973,789 | 60 bp | At TSS Multiome | 1038 | |
| chr3:145,111,045–145,111,877 | 1139.6 kb | Distal (>10kb) Multiome HiCAR | 100 | |
| chr3:145,111,987–145,114,289 | 1141.4 kb | Distal (>10kb) Multiome HiCAR | 149 |
Genomic view of the DIPK2A 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.