ArticleNucleic acids research2014
Transcription factor abundance controlled by an auto-regulatory mechanism involving a transcription start site switch.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- ZNF143 is a transcriptional regulator of nuclear-encoded mitochondrial genes that acts independently of looping and CTCF.Molecular cell · 2025Article
- SOXC Transcription Factors as Diagnostic Biomarkers and Therapeutic Targets for Arthritis.International journal of molecular sciences · 2023Review
- Genome-wide inference reveals that feedback regulations constrain promoter-dependent transcriptional burst kinetics.Nucleic acids research · 2023Article
- SOX4 and RELA Function as Transcriptional Partners to Regulate the Expression of TNF- Responsive Genes in Fibroblast-Like Synoviocytes.Frontiers in immunology · 2022Article
- Two paralogous znf143 genes in zebrafish encode transcriptional activator proteins with similar functions but expressed at different levels during early development.BMC molecular and cell biology · 2020Article
- ZNF143 in Chromatin Looping and Gene Regulation.Frontiers in genetics · 2020Review
- The RNA exosome nuclease complex regulates human embryonic stem cell differentiation.The Journal of cell biology · 2019Article
- Selective Activation of AlternativeGenes · 2018Article
- Zinc finger protein 143 expression is closely related to tumor malignancy via regulating cell motility in breast cancer.BMB reports · 2017Article
- Genetic disruption of the sh3pxd2a gene reveals an essential role in mouse development and the existence of a novel isoform of tks5.PloS one · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A transcriptional feedback loop is the simplest and most direct means for a transcription factor to provide an increased stability of gene expression. In this work performed in human cells, we reveal a new negative auto-regulatory mechanism involving an alternative transcription start site (TSS) usage. Using the activating transcription factor ZNF143 as a model, we show that the ZNF143 low-affinity binding sites, located downstream of its canonical TSS, play the role of protein sensors to induce the up- or down-regulation of ZNF143 gene expression. We uncovered that the TSS switch that mediates this regulation implies the differential expression of two transcripts with an opposite protein production ability due to their different 5' untranslated regions. Moreover, our analysis of the ENCODE data suggests that this mechanism could be used by other transcription factors to rapidly respond to their own aberrant expression level.
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Registered trials
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.