ArticlePloS one2013
A hypomorphic lsd1 allele results in heart development defects in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Genomic analyses implicate noncoding de novo variants in congenital heart disease.Nature genetics · 2020Trial
- Review
- Lysine-specific histone demethylase 1a regulates nephron development and long-term transcriptional programming.JCI insight · 2026Article
- Lysine-specific demethylase 1a is obligatory for gene regulation during kidney development.bioRxiv : the preprint server for biology · 2025Article
- Review
- Epigenetic repression ofiScience · 2024Article
- An Updated Review on the Significance of DNA and Protein Methyltransferases and De-methylases in Human Diseases: From Molecular Mechanism to Novel Therapeutic Approaches.Current medicinal chemistry · 2024Review
- SPR-1/CoREST facilitates the maternal epigenetic reprogramming of the histone demethylase SPR-5/LSD1.Genetics · 2023Article
- The H2A.Z and NuRD associated protein HMG20A controls early head and heart developmental transcription programs.Nature communications · 2023Article
- Epigenetics in Congenital Heart Disease.Journal of the American Heart Association · 2022Review
- Epigenetic Regulation of Heart Failure: Cell Type Matters.Circulation research · 2021Article
- Identification of Rpl29 as a major substrate of the lysine methyltransferase Set7/9.The Journal of biological chemistry · 2018Article
- Gene discovery for Mendelian conditions via social networking: de novo variants in KDM1A cause developmental delay and distinctive facial features.Genetics in medicine : official journal of the American College of Medical Genetics · 2016Article
- Epigenetic mechanisms in heart development and disease.Drug discovery today · 2015Review
- Association of DNMT1 Gene Polymorphisms with Congenital Heart Disease in Child Patients.Pediatric cardiology · 2015Article
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysine-specific demethylase 1 (Lsd1/Aof2/Kdm1a), the first enzyme with specific lysine demethylase activity to be described, demethylates histone and non-histone proteins and is essential for mouse embryogenesis. Lsd1 interacts with numerous proteins through several different domains, most notably the tower domain, an extended helical structure that protrudes from the core of the protein. While there is evidence that Lsd1-interacting proteins regulate the activity and specificity of Lsd1, the significance and roles of such interactions in developmental processes remain largely unknown. Here we describe a hypomorphic Lsd1 allele that contains two point mutations in the tower domain, resulting in a protein with reduced interaction with known binding partners and decreased enzymatic activity. Mice homozygous for this allele die perinatally due to heart defects, with the majority of animals suffering from ventricular septal defects. Molecular analyses revealed hyperphosphorylation of E-cadherin in the hearts of mutant animals. These results identify a previously unknown role for Lsd1 in heart development, perhaps partly through the control of E-cadherin phosphorylation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.