This gene encodes a member of the plexin family. Plexins are transmembrane receptors for semaphorins, a large family of proteins that regulate axon guidance, cell motility and migration, and the immune response. The encoded protein and its ligand regulate melanocyte adhesion, and viral semaphorins may modulate the immune response by binding to this receptor. The encoded protein may be a tumor suppressor protein for melanoma. Alternatively spliced transcript variants have been observed for this gene. [provided by RefSeq, Jan 2011]
Transcription factors with Perturb-seq knockdown data for PLXNC1. 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 = PLXNC1 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 PLXNC1, 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 |
|---|---|---|---|---|
| chr12:94,140,659–94,140,859 | 7.7 kb | Proximal (<10kb) | 73 | |
| chr12:94,147,883–94,150,737 | 189 bp | At TSS Multiome | 794 | |
| chr12:94,260,806–94,261,454 | 112.6 kb | Distal (>10kb) Multiome HiCAR | 104 | |
| chr12:94,263,934–94,264,564 | 115.7 kb | Distal (>10kb) Multiome HiCAR | 188 | |
| chr12:94,389,628–94,390,387 | 241.4 kb | Distal (>10kb) Multiome | 205 | |
| chr12:94,459,523–94,460,634 | 311.4 kb | Distal (>10kb) Multiome HiCAR | 909 | |
| chr12:94,560,633–94,561,227 | 412.4 kb | Distal (>10kb) Multiome HiCAR | 348 | |
| chr12:94,872,875–94,874,146 | 725.0 kb | Distal (>10kb) Multiome HiCAR | 358 |
Genomic view of the PLXNC1 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.