ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2014
Krüppel -like factor 8 is a stress-responsive transcription factor that regulates expression of HuR.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Electroacupuncture Relieves HuR/KLF9-Mediated Inflammation to Enhance Neurological Repair after Spinal Cord Injury.eNeuro · 2023Article
- RNA-binding proteins and their role in kidney disease.Nature reviews. Nephrology · 2022Review
- Suppression of epithelial-mesenchymal transition in hepatocellular carcinoma cells by Krüppel-like factor 4.Oncotarget · 2016Article
- EMMPRIN, SP1 and microRNA-27a mediate physcion 8-O-β-glucopyranoside-induced apoptosis in osteosarcoma cells.American journal of cancer research · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsHuR is an RNA-binding protein that regulates the post-transcriptional life of thousands of cellular mRNAs and promotes cell survival. HuR is expressed as two mRNA transcripts that are differentially regulated by cell stress. The goal of this study is to define factors that promote transcription of the longer alternate form.
methodsEffects of transcription factors on HuR expression were determined by inhibition or overexpression of these factors followed by competitive RT-PCR, gel mobility shift, and chromatin immunoprecipitation. Transcription factor expression patterns were identified through competitive RT-PCR and Western analysis. Stress responses were assayed in thapsigargin-treated proximal tubule cells and in ischemic rat kidney.
resultsA previously described NF-κB site and a newly identified Sp/KLF factor binding site were shown to be important for transcription of the long HuR mRNA. KLF8, but not Sp1, was shown to bind this site and increase HuR mRNA levels. Cellular stress in cultured or native proximal tubule cells resulted in a rapid decrease of KLF8 levels that paralleled those of the long HuR mRNA variant.
conclusionsThese results demonstrate that KLF8 can participate in regulating expression of alternate forms of HuR mRNA along with NF-κB and other factors, depending on cellular contexts.
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