ArticleMolecular and cellular biology1993
fos/jun repression of cardiac-specific transcription in quiescent and growth-stimulated myocytes is targeted at a tissue-specific cis element.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 54 citations in OpenAlex.
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- CMV enhancer may not be suitable for tissue-specific enhancement of promoters in cancer gene therapy.Cancer gene therapy · 2020Article
- The Kruppel-like transcription factor KLF13 is a novel regulator of heart development.The EMBO journal · 2006Article
- Modulation of MLC-2v gene expression by AP-1: complex regulatory role of Jun in cardiac myocytes.Molecular and cellular biochemistry · 2001Article
- CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo.The Journal of clinical investigation · 2000Article
- Nerve growth factor and epidermal growth factor stimulate clusterin gene expression in PC12 cells.The Biochemical journal · 1999Article
- The C-terminal domain of c-fos is required for activation of an AP-1 site specific for jun-fos heterodimers.Molecular and cellular biology · 1998Article
- Opposing effects of Jun kinase and p38 mitogen-activated protein kinases on cardiomyocyte hypertrophy.Molecular and cellular biology · 1998Article
- Identification of a cis-acting regulatory element conferring inducibility of the atrial natriuretic factor gene in acute pressure overload.The Journal of clinical investigation · 1997Article
- DNA binding and transactivation properties of Fos variants with homodimerization capacity.Nucleic acids research · 1997Article
- Angiotensin II type1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- The atrial natriuretic factor promoter is a downstream target for Nkx-2.5 in the myocardium.Molecular and cellular biology · 1996Article
- Localization of the Catf1 transcription factor gene to mouse chromosome 19.Mammalian genome : official journal of the International Mammalian Genome Society · 1995Article
- An AP1 binding site upstream of the kappa immunoglobulin intron enhancer binds inducible factors and contributes to expression.Nucleic acids research · 1994Article
- A hormone-encoding gene identifies a pathway for cardiac but not skeletal muscle gene transcription.Molecular and cellular biology · 1994Article
- Developmental stage-specific regulation of atrial natriuretic factor gene transcription in cardiac cells.Molecular and cellular biology · 1994Article
- A nuclear pathway for alpha 1-adrenergic receptor signaling in cardiac cells.The EMBO journal · 1993Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Unlike that of skeletal muscle cells in which growth and differentiation appear mutually exclusive, growth stimulation of cardiac cells is characterized by transient expression of early response nuclear proto-oncogenes as well as induction of several cardiac-specific markers. This observation led to the speculation that these proto-oncogenes, particularly c-fos and c-jun, might act as positive regulators of cardiac transcription. We have examined the role of c-jun and c-fos in basal and growth-stimulated cardiac transcription, using the cardiac-specific atrial natriuretic factor (ANF) gene as a marker. The results indicate that c-jun and c-fos are negative regulators of ANF transcription. Inducers of jun and fos activity, such as mitogens and growth factors, inhibited endogenous ANF transcripts. In transient cotransfection assays, jun and fos were able to trans-repress the ANF promoter in both quiescent and alpha 1-adrenergic stimulated myocytes. This repression was specific to myocyte cultures and was not observed in nonmuscle cells. Deletion analysis indicated that repression does not require typical AP-1-binding sites (tetradecanoyl phorbol acetate response elements) or serum response elements but is targeted at a cardiac-specific element within the ANF promoter. Various Fos-related proteins, including Fra-1, Fos B, and v-Fos, were able to trans-repress ANF transcription. In addition, C-terminal c-fos mutants which no longer repress transcription of such early growth response genes as c-fos and EGR-1 retained the ability to repress ANF transcription. Repression by c-jun occurs via the N-terminal activation domain and does not require the DNA-binding domain, suggesting that proto-oncogene repression involves interaction with one or more limiting cardiac-specific coactivators.
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