ArticleNature communications2018
Kruppel-like factor 4-dependent Staufen1-mediated mRNA decay regulates cortical neurogenesis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Krüppel-Like Factors Modulate Susceptibility To Neuropsychiatric Disorders.Molecular neurobiology · 2025Review
- Subversion of mRNA degradation pathways by EWSR1::FLI1 represents a therapeutic vulnerability in Ewing sarcoma.Nature communications · 2025Article
- Decoding transcriptional identity during neuron-astroglia cell fate driven by RAR-specific agonists.NAR molecular medicine · 2025Article
- Gene expression profiling, prognosis, and immune microenvironment of KLF4 in malignancies.PloS one · 2025Article
- Dynamically regulated transcription factors are encoded by highly unstable mRNAs in theRNA (New York, N.Y.) · 2023Article
- Identification of candidate genes for developmental colour agnosia in a single unique family.PloS one · 2023Article
- Emerging Roles of RNA-Binding Proteins in Neurodevelopment.Journal of developmental biology · 2022Review
- Identification and coregulation pattern analysis of long noncoding RNAs following subacute spinal cord injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
- RNA-binding protein signaling in adult neurogenesis.Frontiers in cell and developmental biology · 2022Review
- The multifunctional RNA-binding protein Staufen1: an emerging regulator of oncogenesis through its various roles in key cellular events.Cellular and molecular life sciences : CMLS · 2021Review
- Baihui (DU20)-penetrating-Qubin (GB7) acupuncture regulates microglia polarization through miR-34a-5p/Klf4 signaling in intracerebral hemorrhage rats.Experimental animals · 2021Article
- Role of circular RNA expression in the pathological progression after spinal cord injury.Neural regeneration research · 2021Article
- Article
- NF-κB-activated SPRY4-IT1 promotes cancer cell metastasis by downregulating TCEB1 mRNA via Staufen1-mediated mRNA decay.Oncogene · 2021Article
- Glucocorticoid counteracts cellular mechanoresponses by LINC01569-dependent glucocorticoid receptor-mediated mRNA decay.Science advances · 2021Article
- Multi-Tissue Multi-Omics Nutrigenomics Indicates Context-Specific Effects of Docosahexaenoic Acid on Rat Brain.Molecular nutrition & food research · 2020Article
- IGF2BP2 stabilized FBXL19-AS1 regulates the blood-tumour barrier permeability by negatively regulating ZNF765 by STAU1-mediated mRNA decay.RNA biology · 2020Article
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
- TRA2A-induced upregulation of LINC00662 regulates blood-brain barrier permeability by affecting ELK4 mRNA stability in Alzheimer's microenvironment.RNA biology · 2020Article
- Leptin stimulates synaptogenesis in hippocampal neurons via KLF4 and SOCS3 inhibition of STAT3 signaling.Molecular and cellular neurosciences · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Kruppel-like factor 4 (Klf4) is a zinc-finger-containing protein that plays a critical role in diverse cellular physiology. While most of these functions attribute to its role as a transcription factor, it is postulated that Klf4 may play a role other than transcriptional regulation. Here we demonstrate that Klf4 loss in neural progenitor cells (NPCs) leads to increased neurogenesis and reduced self-renewal in mice. In addition, Klf4 interacts with RNA-binding protein Staufen1 (Stau1) and RNA helicase Ddx5/17. They function together as a complex to maintain NPC self-renewal. We report that Klf4 promotes Stau1 recruitment to the 3'-untranslated region of neurogenesis-associated mRNAs, increasing Stau1-mediated mRNA decay (SMD) of these transcripts. Stau1 depletion abrogated SMD of target mRNAs and rescued neurogenesis defects in Klf4-overexpressing NPCs. Furthermore, Ddx5/17 knockdown significantly blocked Klf4-mediated mRNA degradation. Our results highlight a novel molecular mechanism underlying stability of neurogenesis-associated mRNAs controlled by the Klf4/Ddx5/17/Stau1 axis during mammalian corticogenesis.
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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 Socratic graph.