ArticleNucleic acids research1997
Inhibition of muscle-specific gene expression by Id3: requirement of the C-terminal region of the protein for stable expression and function.
Article in Nucleic acids research, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- A prevalent disease-associated SNP in the humanNAR molecular medicine · 2026Article
- Vitamin A retinoic acid contributes to muscle stem cell and mitochondrial function loss in old age.JCI insight · 2025Article
- APOBEC2 safeguards skeletal muscle cell fate through binding chromatin and regulating transcription of non-muscle genes during myoblast differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- EZH2 modulates retinoic acid signaling to ensure myotube formation during development.FEBS letters · 2022Article
- Regulation of Transcription Factors by Reactive Oxygen Species and Nitric Oxide in Vascular Physiology and Pathology.Antioxidants & redox signaling · 2017Review
- Id4 suppresses MMP2-mediated invasion of glioblastoma-derived cells by direct inactivation of Twist1 function.Oncogene · 2015Article
- Loss of Id3 increases VCAM-1 expression, macrophage accumulation, and atherogenesis in Ldlr-/- mice.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis.Molecular cell · 2012Article
- A systems approach and skeletal myogenesis.Comparative and functional genomics · 2012Article
- The transcriptional repressor ID2 can interact with the canonical clock components CLOCK and BMAL1 and mediate inhibitory effects on mPer1 expression.The Journal of biological chemistry · 2010Article
- Id3 is a novel atheroprotective factor containing a functionally significant single-nucleotide polymorphism associated with intima-media thickness in humans.Circulation research · 2010Article
- Inhibitor of DNA binding-1 promotes the migration and proliferation of endothelial progenitor cells in vitro.Molecular and cellular biochemistry · 2010Article
- A systems approach reveals that the myogenesis genome network is regulated by the transcriptional repressor RP58.Developmental cell · 2009Article
- Suppression of chondrogenesis by Id helix-loop-helix proteins in murine embryonic orofacial tissue.Differentiation; research in biological diversity · 2009Article
- UVB upregulates the bax promoter in immortalized human keratinocytes via ROS induction of Id3.Experimental dermatology · 2009Article
- Identification of novel MyoD gene targets in proliferating myogenic stem cells.Molecular and cellular biology · 2002Article
- Article
- Increased myogenic repressor Id mRNA and protein levels in hindlimb muscles of aged rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2002Article
- Article
- Id2 promotes apoptosis by a novel mechanism independent of dimerization to basic helix-loop-helix factors.Molecular and cellular biology · 1998Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have examined the role of an Id-like protein, Id3 (also known as HLH462), in the regulation of muscle-specific gene expression. Id proteins are believed to block expression of muscle-specific genes by preventing the dimerization between ubiquitous bHLH proteins (E proteins) and myogenic bHLH proteins such as MyoD. Consistent with its putative role as an inhibitor of differentiation, Id3 mRNA was detected in proliferating skeletal muscle cells, was further induced by basic fibroblast growth factor (bFGF) and was down-regulated in differentiated muscle cultures. Overexpression of Id3 efficiently inhibited the MyoD-mediated activation of the muscle-specific creatine kinase (MCK) reporter gene. Deletion analysis indicated that the C-terminal 15 amino acids of Id3 are critical for the full inhibitory activity while deleting up to 42 residues from the C-terminus of the related protein, Id2, did not affect its ability to inhibit the MCK reporter gene. Chimeric protein containing the N-terminal region of Id3 and the C-terminus of Id2 was also non-functional in transfected cells. In contrast, wild-type Id3, the C-terminal mutants, and the Id3/Id2 chimera could all interact with the E-protein E47in vitro. Additional studies indicated that truncation of the Id3 C-terminus might have adversely affected the expression level of the mutant proteins but the Id3/Id2 chimera was stably expressed. Taken together, our results revealed a more complex requirement for the expression and proper function of the Id family proteins than was hitherto expected.
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