ArticleMolecular and cellular biology1997
The basic domain of myogenic basic helix-loop-helix (bHLH) proteins is the novel target for direct inhibition by another bHLH protein, Twist.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 165 citations in OpenAlex.
- Dual transcriptional and post-transcriptional regulation by the bHLH proteins Rtg1 and RtgX in Komagataella phaffii.Nucleic acids research · 2026Article
- Epithelial-to-mesenchymal transition transcription factors: New strategies for mesenchymal tissue regeneration.Cytokine & growth factor reviews · 2025Review
- Myogenesis gone awry: the role of developmental pathways in rhabdomyosarcoma.Frontiers in cell and developmental biology · 2024Review
- Twist alters the breast tumor microenvironment via choline kinase to facilitate an aggressive phenotype.Molecular and cellular biochemistry · 2023Article
- Homodimeric and Heterodimeric Interactions among Vertebrate Basic Helix-Loop-Helix Transcription Factors.International journal of molecular sciences · 2021Review
- Mechanisms of Binding Specificity among bHLH Transcription Factors.International journal of molecular sciences · 2021Review
- B-cell receptor-associated protein 31 promotes migration and invasion in ovarian cancer cells.Experimental and therapeutic medicine · 2021Article
- Twist activates miR-22 to suppress estrogen receptor alpha in breast cancer.Molecular and cellular biochemistry · 2021Article
- TWIST1 and chromatin regulatory proteins interact to guide neural crest cell differentiation.eLife · 2021Article
- Interaction between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion Negative Rhabdomyosarcoma.Nature communications · 2021Article
- Mutational burden and potential oligogenic model of TBX6-mediated genes in congenital scoliosis.Molecular genetics & genomic medicine · 2020Article
- Signaling Pathways Induced by Leptin during Epithelial⁻Mesenchymal Transition in Breast Cancer.International journal of molecular sciences · 2018Review
- Recessive MYF5 Mutations Cause External Ophthalmoplegia, Rib, and Vertebral Anomalies.American journal of human genetics · 2018Article
- Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia.Developmental cell · 2018Article
- Article
- Spatiotemporal expression of a twist homolog in the leech Helobdella austinensis.Development genes and evolution · 2017Article
- Article
- Id1 Expression Level Determines the Differentiation of Human Dental Pulp Stem Cells.Journal of dental research · 2014Article
- Twist reverses muscle cell differentiation through transcriptional down-regulation of myogenin.Bioscience reports · 2013Article
- Genome-wide binding of the basic helix-loop-helix myogenic inhibitor musculin has substantial overlap with MyoD: implications for buffering activity.Skeletal muscle · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In vertebrates, the basic helix-loop-helix (bHLH) protein Twist may be involved in the negative regulation of cellular determination and in the differentiation of several lineages, including myogenesis, osteogenesis, and neurogenesis. Although it has been shown that mouse twist (M-Twist) (i) sequesters E proteins, thus preventing formation of myogenic E protein-MyoD complexes and (ii) inhibits the MEF2 transcription factor, a cofactor of myogenic bHLH proteins, overexpression of E proteins and MEF2 failed to rescue the inhibitory effects of M-Twist on MyoD. We report here that M-Twist physically interacts with the myogenic bHLH proteins in vitro and in vivo and that this interaction is required for the inhibition of MyoD by M-Twist. In contrast to the conventional HLH-HLH domain interaction formed in the MyoD/E12 heterodimer, this novel type of interaction uses the basic domains of the two proteins. While the MyoD HLH domain without the basic domain failed to interact with M-Twist, a MyoD peptide containing only the basic and helix 1 regions was sufficient to interact with M-Twist, suggesting that the basic domain contacts M-Twist. The replacement of three arginine residues by alanines in the M-Twist basic domain was sufficient to abolish both the binding and inhibition of MyoD by M-Twist, while the domain retained other M-Twist functions such as heterodimerization with an E protein and inhibition of MEF2 transactivation. These findings demonstrate that M-Twist interacts with MyoD through the basic domains, thereby inhibiting MyoD.
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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.