This gene, which encodes a non-protein coding transcript, exhibits differential DNA methylation between the two parental alleles at an adjacent CpG island, and is expressed only from the paternal allele. It is believed to be one of the causative genes for transient neonatal diabetes mellitus (TNDM), which is a rare disease characterized by intrauterine growth retardation, dehydration, and failure to thrive due to a lack of normal insulin secretion. [provided by RefSeq, Oct 2010]
Transcription factors with Perturb-seq knockdown data for HYMAI. 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 = HYMAI 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 HYMAI, 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 |
|---|---|---|---|---|
| chr6:144,007,258–144,007,418 | 843 bp | At TSS | 104 | |
| chr6:144,007,743–144,008,869 | at TSS | At TSS | 500 | |
| chr6:144,013,517–144,013,734 | 5.3 kb | Proximal (<10kb) | 268 |
Genomic view of the HYMAI 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.