ArticleScientific reports2018
An essential role for the nuclear protein Akirin2 in mouse limb interdigital tissue regression.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Epigenetic regulation of vertebrate limb development: from field specification to tissue morphogenesis.Epigenetics · 2026Review
- Comparative transcriptomics in serial organs uncovers early and pan-organ developmental changes associated with organ-specific morphological adaptation.Nature communications · 2025Article
- Role of nuclear protein Akirin in the modulation of female reproduction inFrontiers in physiology · 2024Article
- Article
- Function of cofactor Akirin2 in the regulation of gene expression in model human Caucasian neutrophil-like HL60 cells.Bioscience reports · 2021Article
- Akirin proteins in development and disease: critical roles and mechanisms of action.Cellular and molecular life sciences : CMLS · 2020Review
- Epithelial Migration and Non-adhesive Periderm Are Required for Digit Separation during Mammalian Development.Developmental cell · 2020Article
- Akirin Is Required for Muscle Function and Acts Through the TGF-β Sma/Mab Signaling Pathway inG3 (Bethesda, Md.) · 2020Article
- Functional Characterization of the Lin28/let-7 Circuit During Forelimb Regeneration inFrontiers in cell and developmental biology · 2020Article
- Overlap of Genetic Risk between Interstitial Lung Abnormalities and Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2019Article
- Akirin2 is modulated by miR-490-3p and facilitates angiogenesis in cholangiocarcinoma through the IL-6/STAT3/VEGFA signaling pathway.Cell death & disease · 2019Article
- A Review of the Genetics and Pathogenesis of Syndactyly in Humans and Experimental Animals: A 3-Step Pathway of Pathogenesis.BioMed research international · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of interdigital tissue regression requires the interplay of multiple spatiotemporally-controlled morphogen gradients to ensure proper limb formation and release of individual digits. Disruption to this process can lead to a number of limb abnormalities, including syndactyly. Akirins are highly conserved nuclear proteins that are known to interact with chromatin remodelling machinery at gene enhancers. In mammals, the analogue Akirin2 is essential for embryonic development and critical for a wide variety of roles in immune function, meiosis, myogenesis and brain development. Here we report a critical role for Akirin2 in the regulation of interdigital tissue regression in the mouse limb. Knockout of Akirin2 in limb epithelium leads to a loss of interdigital cell death and an increase in cell proliferation, resulting in retention of the interdigital web and soft-tissue syndactyly. This is associated with perdurance of Fgf8 expression in the ectoderm overlying the interdigital space. Our study supports a mechanism whereby Akirin2 is required for the downregulation of Fgf8 from the apical ectodermal ridge (AER) during limb development, and implies its requirement in signalling between interdigital mesenchymal cells and the AER.
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