ArticleGenome research2025
Aberrant homeodomain-DNA cooperative dimerization underlies distinct developmental defects in two dominant
Article in Genome research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Decoding the mechanisms of cooperative DNA binding by the Paired-like homeodomain family.Nature communications · 2026Article
- Aberrant retinal structure and vasculature in mouse models of dominant retinopathies caused by CRX homeodomain mutations.Scientific reports · 2026Article
- Aberrant retinal structure and vasculature in mouse models of dominant retinopathies caused bybioRxiv : the preprint server for biology · 2026Article
- PreclinicalbioRxiv : the preprint server for biology · 2026Article
- Human CRX regulates photoreceptor cells development via bidirectional transcriptional control in retinal organoids.Stem cell reports · 2026Article
- Decoding the mechanisms of cooperative DNA binding by the Paired-like homeodomain family.bioRxiv : the preprint server for biology · 2025Article
- The ALX4 dimer structure provides insight into how disease alleles impact function.Nature communications · 2025Article
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Abstract
Paired-class homeodomain (HD) transcription factors (TFs) play essential roles in vertebrate development, and their mutations are linked to human diseases. One unique feature of a paired-class HD is cooperative dimerization on specific palindrome DNA sequences. Yet, the functional significance of HD cooperative dimerization in animal development and its dysregulation in diseases remains elusive. Using the retinal TF cone-rod homeobox (CRX) as a model, we have studied how blindness-causing mutations in the paired HD, p.E80A and p.K88N, alter CRX's cooperative dimerization, leading to gene misexpression and photoreceptor developmental deficits in dominant manners. CRX
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