ArticleMolecular and cellular biology1993
E1A-mediated inhibition of myogenesis correlates with a direct physical interaction of E1A12S and basic helix-loop-helix proteins.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- The N terminus of adenovirus type 12 E1A inhibits major histocompatibility complex class I expression by preventing phosphorylation of NF-kappaB p65 Ser276 through direct binding.Journal of virology · 2010Article
- Intrinsic structural disorder in adenovirus E1A: a viral molecular hub linking multiple diverse processes.Journal of virology · 2008Review
- Muscle-regulated expression and determinants for neuromuscular junctional localization of the mouse RIalpha regulatory subunit of cAMP-dependent protein kinase.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- The retinoblastoma gene family members pRB and p107 coactivate the AP-1-dependent mouse tissue factor promoter in fibroblasts.Oncogene · 2000Article
- Suppression of E1A-mediated transformation by the p50E4F transcription factor.Molecular and cellular biology · 1999Article
- p21(CIP1) and p57(KIP2) control muscle differentiation at the myogenin step.Genes & development · 1999Article
- Suppression of adenovirus E1A-induced apoptosis by mutated p53 is overcome by coexpression with Id proteins.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- A cellular repressor of E1A-stimulated genes that inhibits activation by E2F.Molecular and cellular biology · 1998Article
- E1A represses apolipoprotein AI enhancer activity in liver cells through a pRb- and CBP-independent pathway.Nucleic acids research · 1998Article
- Database of mutations within the adenovirus 5 E1A oncogene.Nucleic acids research · 1998Article
- The basic domain of myogenic basic helix-loop-helix (bHLH) proteins is the novel target for direct inhibition by another bHLH protein, Twist.Molecular and cellular biology · 1997Article
- Molecular mechanisms of myogenic coactivation by p300: direct interaction with the activation domain of MyoD and with the MADS box of MEF2C.Molecular and cellular biology · 1997Article
- Cyclin-mediated inhibition of muscle gene expression via a mechanism that is independent of pRB hyperphosphorylation.Molecular and cellular biology · 1996Article
- A novel E1A domain mediates skeletal-muscle-specific enhancer repression independently of pRB and p300 binding.Molecular and cellular biology · 1996Article
- Skeletal muscle cells lacking the retinoblastoma protein display defects in muscle gene expression and accumulate in S and G2 phases of the cell cycle.The Journal of cell biology · 1996Article
- Expression of E1A in terminally differentiated muscle cells reactivates the cell cycle and suppresses tissue-specific genes by separable mechanisms.Molecular and cellular biology · 1996Article
- Induction of DNA synthesis and apoptosis in cardiac myocytes by E1A oncoprotein.The Journal of cell biology · 1996Article
- E1a induces the expression of epithelial characteristics.The Journal of cell biology · 1994Article
- The cellular transcription factor USF cooperates with varicella-zoster virus immediate-early protein 62 to symmetrically activate a bidirectional viral promoter.Molecular and cellular biology · 1994Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The observation that adenovirus E1A gene products can inhibit differentiation of skeletal myocytes suggested that E1A may interfere with the activity of myogenic basic helix-loop-helix (bHLH) transcription factors. We have examined the ability of E1A to mediate repression of the muscle-specific creatine kinase (MCK) gene. Both the E1A12S and E1A13S products repressed MCK transcription in a concentration-dependent fashion. In contrast, amino-terminal deletion mutants (d2-36 and d15-35) of E1A12S were defective for repression. E1A12S also repressed expression of a promoter containing a multimer of the MCK high-affinity E box (the consensus site for myogenic bHLH protein binding) that was dependent, in C3H10T1/2 cells, on coexpression of a myogenin bHLH-VP16 fusion protein. A series of coprecipitation experiments with glutathione S-transferase fusion and in vitro-translated proteins demonstrated that E1A12S, but not amino-terminal E1A deletion mutants, could bind to full-length myogenin and E12 and to deletion mutants of myogenin and E12 that spare the bHLH domains. Thus, the bHLH domains of myogenin and E12, and the high-affinity E box, are targets for E1A-mediated repression of the MCK enhancer, and domains of E1A required for repression of muscle-specific gene transcription also mediate binding to bHLH proteins. We conclude that E1A mediates repression of muscle-specific gene transcription through its amino-terminal domain and propose that this may involve a direct physical interaction between E1A and the bHLH region of myogenic determination proteins.
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