Predicted to enable GTP binding activity and calcium channel regulator activity. Predicted to be involved in small GTPase-mediated signal transduction. Predicted to be located in T-tubule. Predicted to be active in plasma membrane. Implicated in type 2 diabetes mellitus. Biomarker of congestive heart failure. [provided by Alliance of Genome Resources, Jul 2025]
Transcription factors with Perturb-seq knockdown data for RRAD. 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 = RRAD 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 RRAD, 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 |
|---|---|---|---|---|
| chr16:66,924,739–66,925,515 | at TSS | At TSS | 395 | |
| chr16:66,933,957–66,934,849 | 9.0 kb | Proximal (<10kb) | 931 |
Genomic view of the RRAD 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.