ArticleMolecular genetics and genomics : MGG2010
Null mutations in Drosophila Optomotor-blind affect T-domain residues conserved in all Tbx proteins.
Article in Molecular genetics and genomics : MGG, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- An inherited TBX3 alteration in a prenatal case of ulnar-mammary syndrome: Clinical assessment and functional characterization in Drosophila melanogaster.Journal of cellular physiology · 2024Article
- Functionally distinct roles for T and Tbx6 during mouse development.Biology open · 2020Article
- Transcriptional repression of the ectodomain sheddase ADAM10 by TBX2 and potential implication for Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2019Article
- Optomotor-blind negatively regulates Drosophila eye development by blocking Jak/STAT signaling.PloS one · 2015Article
- Putative Breast Cancer Driver Mutations in TBX3 Cause Impaired Transcriptional Repression.Frontiers in oncology · 2015Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The T-box transcription factors TBX2 and TBX3 are overexpressed in many human cancers raising the need for a thorough understanding of the cellular function of these proteins. In Drosophila, there is one corresponding ortholog, Optomotor-blind (Omb). Currently, only two missense mutations are known for the two human proteins. Making use of the developmental defects caused by inactivation of omb, we have isolated and molecularly characterized four new omb mutations, three of them are missense mutations of amino acids fully conserved in all Tbx proteins. We interpret the functional defects in the framework of the known structure of the human TBX3 protein and provide evidence for loss of Omb DNA-binding activity in all three newly identified missense mutations.
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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.