ArticleMolecular and cellular biology1996
Flanking sequences modulate the cell specificity of M-CAT elements.
Article in Molecular and cellular biology, 1996. 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, 74 citations in OpenAlex.
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- Identification of cis-regulatory modules in promoters of human genes exploiting mutual positioning of transcription factors.Nucleic acids research · 2013Article
- Unbiased discovery of interactions at a control locus driving expression of the cancer-specific therapeutic and diagnostic target, mesothelin.Journal of proteome research · 2012Article
- Genome-wide mapping of Sox6 binding sites in skeletal muscle reveals both direct and indirect regulation of muscle terminal differentiation by Sox6.BMC developmental biology · 2011Article
- Members of the TEAD family of transcription factors regulate the expression of Myf5 in ventral somitic compartments.Developmental biology · 2011Article
- RTEF-1, an upstream gene of hypoxia-inducible factor-1α, accelerates recovery from ischemia.The Journal of biological chemistry · 2011Article
- Structural analysis of the cancer-specific promoter in mesothelin and in other genes overexpressed in cancers.The Journal of biological chemistry · 2011Article
- Structural and functional insights into the TEAD-YAP complex in the Hippo signaling pathway.Protein & cell · 2010Article
- dMyc functions downstream of Yorkie to promote the supercompetitive behavior of hippo pathway mutant cells.PLoS genetics · 2010Article
- Overexpression of TEAD-1 in transgenic mouse striated muscles produces a slower skeletal muscle contractile phenotype.The Journal of biological chemistry · 2008Article
- Myocyte-specific M-CAT and MEF-1 elements regulate G-protein gamma 3 gene (gamma3) expression in cardiac myocytes.DNA and cell biology · 2008Article
- Transcriptional enhancer factor 1 (TEF-1/TEAD1) mediates activation of IFITM3 gene by BRGl.FEBS letters · 2008Article
- TEF-1 and C/EBPbeta are major p38alpha MAPK-regulated transcription factors in proliferating cardiomyocytes.The Biochemical journal · 2006Article
- The transcriptional co-activator TAZ interacts differentially with transcriptional enhancer factor-1 (TEF-1) family members.The Biochemical journal · 2005Article
- Sp3 proteins negatively regulate beta myosin heavy chain gene expression during skeletal muscle inactivity.Molecular and cellular biology · 2004Article
- Transcription enhancer factor 1 binds multiple muscle MEF2 and A/T-rich elements during fast-to-slow skeletal muscle fiber type transitions.Molecular and cellular biology · 2003Article
- TEAD/TEF transcription factors utilize the activation domain of YAP65, a Src/Yes-associated protein localized in the cytoplasm.Genes & development · 2001Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
M-CAT elements mediate both muscle-specific and non-muscle-specific transcription. We used artificial promoters to dissect M-CAT elements derived from the cardiac troponin T promoter, whose regulation is highly striated muscle specific. We show that muscle-specific M-CAT-dependent expression requires two distinct components: the core heptameric M-CAT motif (5'-CATTCCT-3'), which constitutes the canonical binding site for TEF-1-related proteins, and specific sequences immediately flanking the core motif that bind an additional factor(s). These factors are found in higher-order M-CAT DNA-protein complexes with TEF-1 proteins. Non-muscle-specific promoters are produced when the sequences flanking the M-CAT motif are removed or modified to match those of non-muscle-specific promoters such as the simian virus 40 promoter. Moreover, a mutation of the 5'-flanking region of the cardiac troponin T M-CAT-1 element upregulated expression in nonmuscle cells. That mutation also disrupts a potential E box that apparently does not bind myogenic basic helix-loop-helix proteins. We propose a model in which M-CAT motifs are potentially active in many cell types but are modulated through protein binding to specific flanking sequences. In nonmuscle cells, these flanking sequences bind a factor(s) that represses M-CAT-dependent activity. In muscle cells, on the other hand, the factor(s) binding to these flanking sequences contributes to both the cell specificity and the overall transcriptional strength of M-CAT-dependent promoters.
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