ArticleiScience2022
Fine-tuned KDM1A alternative splicing regulates human cardiomyogenesis through an enzymatic-independent mechanism.
Article in iScience, 2022. 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, 14 citations in OpenAlex.
- Uncoupling histone modification crosstalk by engineering lysine demethylase LSD1.Nature chemical biology · 2025Article
- Enhancing the Maturation of Human Pluripotent Stem Cell-Derived Cardiomyocytes with an n-Type Organic Semiconductor Coating.ACS applied materials & interfaces · 2024Article
- An autoinhibitory switch of the LSD1 disordered region controls enhancer silencing.Molecular cell · 2024Article
- Asynchronous microexon splicing ofbioRxiv : the preprint server for biology · 2024Article
- Unsupervised ensemble-based phenotyping enhances discoverability of genes related to left-ventricular morphology.Nature machine intelligence · 2024Article
- Demethylase-independent roles of LSD1 in regulating enhancers and cell fate transition.Nature communications · 2023Article
- Catsnap: a user-friendly algorithm for determining the conservation of protein variants reveals extensive parallelisms in the evolution of alternative splicing.The New phytologist · 2023Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histone demethylase KDM1A is a multi-faceted regulator of vital developmental processes, including mesodermal and cardiac tube formation during gastrulation. However, it is unknown whether the fine-tuning of KDM1A splicing isoforms, already shown to regulate neuronal maturation, is crucial for the specification and maintenance of cell identity during cardiogenesis. Here, we discovered a temporal modulation of ubKDM1A and KDM1A+2a during human and mice fetal cardiac development and evaluated their impact on the regulation of cardiac differentiation. We revealed a severely impaired cardiac differentiation in KDM1A
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