ArticleHuman genetics2004
Regulation of the MID1 protein function is fine-tuned by a complex pattern of alternative splicing.
Article in Human genetics, 2004. 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.
- Perspective in Alternative Splicing Coupled to Nonsense-Mediated mRNA Decay.International journal of molecular sciences · 2020Review
- Review
- RNA Degradation in Neurodegenerative Disease.Advances in neurobiology · 2018Review
- Differential Transcriptome Networks between IDO1-Knockout and Wild-Type Mice in Brain Microglia and Macrophages.PloS one · 2016Article
- The RNA-binding protein Rbfox2: an essential regulator of EMT-driven alternative splicing and a mediator of cellular invasion.Oncogene · 2014Article
- A pronounced evolutionary shift of the pseudoautosomal region boundary in house mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2012Article
- Reduced Mid1 Expression and Delayed Neuromotor Development in daDREAM Transgenic Mice.Frontiers in molecular neuroscience · 2012Article
- Article
- Stochastic noise in splicing machinery.Nucleic acids research · 2009Article
- Structural implication of splicing stochastics.Nucleic acids research · 2009Article
- Alternative polyadenylation signals and promoters act in concert to control tissue-specific expression of the Opitz Syndrome gene MID1.BMC molecular biology · 2007Article
- SVC: structured visualization of evolutionary sequence conservation.Nucleic acids research · 2005Article
- The Vertebrate Genome Annotation (Vega) database.Nucleic acids research · 2005Article
- The importance of being divisible by three in alternative splicing.Nucleic acids research · 2005Article
- Article
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical features of Opitz BBB/G syndrome are confined to defects of the developing ventral midline, whereas the causative gene, MID1, is ubiquitously expressed. Therefore, a non-redundant physiological function of the MID1 product appears to be developmentally restricted. Here, we report the identification of several alternative MID1 exons in human, mouse and fugu. We show that splice variants of the MID1 gene that are comparable in terms of function occur in the three organisms, suggesting an important role in the regulation of the MID1 protein function. Accordingly, we observed differential MID1 transcript patterns in a tissue-specific manner by Northern blot and RT-PCR. The identified splice variants cause loss-of-function effects via several mechanisms. Some introduce a stop codon followed by a novel poly(A(+)) tail, leading to the formation of C-terminally truncated proteins. Dominant negative effects through altered binding to the MID1-interacting protein alpha4 in vitro could be demonstrated in a couple of cases. Others carry premature termination codons without poly(A(+)) tails. These are degraded by nonsense mediated mRNA decay (NMD). Our data reveal a mechanism conserved in human, mouse and fugu that regulates developmentally restricted MID1 activity and suggest NMD to be critical in the translational regulation of a ubiquitously transcribed mRNA.
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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.