Predicted to enable ATP hydrolysis activity and microtubule severing ATPase activity. Predicted to be involved in cell division and microtubule cytoskeleton organization. Predicted to act upstream of or within locomotory behavior. Predicted to be located in nuclear matrix. [provided by Alliance of Genome Resources, Jul 2025]
Transcription factors with Perturb-seq knockdown data for FIGN. 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 = FIGN 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 FIGN, 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 |
|---|---|---|---|---|
| chr2:163,730,013–163,730,146 | 5.9 kb | Proximal (<10kb) | 23 | |
| chr2:163,734,929–163,735,300 | 711 bp | At TSS | 180 | |
| chr2:163,735,784–163,737,415 | 284 bp | At TSS Multiome | 815 |
Genomic view of the FIGN 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.