ArticleNucleic acids research1996
CTF5--a new transcriptional activator of the NFI/CTF family.
Article in Nucleic acids research, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- Insulin-like growth factor 2 mRNA-binding protein 2-regulated alternative splicing of nuclear factor 1 C-type causes excessive granulosa cell proliferation in polycystic ovary syndrome.Cell proliferation · 2022Article
- MCPIP1-mediated NFIC alternative splicing inhibits proliferation of triple-negative breast cancer via cyclin D1-Rb-E2F1 axis.Cell death & disease · 2021Article
- Genetic Predisposition to Glioma Mediated by a MAPKAP1 Enhancer Variant.Cellular and molecular neurobiology · 2020Article
- Characterization and risk association of polymorphisms in Aurora kinases A, B and C with genetic susceptibility to gastric cancer development.BMC cancer · 2019Article
- Nucleosome distortion as a possible mechanism of transcription activation domain function.Epigenetics & chromatin · 2016Review
- Common patterns in type II restriction enzyme binding sites.Nucleic acids research · 2005Article
- A combination of MEF3 and NFI proteins activates transcription in a subset of fast-twitch muscles.Molecular and cellular biology · 1997Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NFI/CTF is a family of polypeptides involved in stimulating the initiation of adenovirus DNA replication and the activation of transcription driven by RNA polymerase II. Several naturally occurring NFI/CTF variants display distinctive transactivation activities in vivo. To define more precisely the role of the NFI/CTF family in regulating gene expression, we cloned the splice variant CTF5, analyzed transcriptional activation patterns in a yeast transcription assay, and compared it with other CTF proteins. CTF5, which lacks exons 9 and 10 including a CTD-like motif essential for transcriptional activation by full-length CTF1, enhances transcription to a greater extent than CTF1. In addition, CTF5 is even more active than CTF7, which lacks exons 7-9. These findings indicate that CTF proteins formed by differential splicing display a much broader range of transcriptional activities as observed previously.
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