ArticlePloS one2011
The putative RNA helicase HELZ promotes cell proliferation, translation initiation and ribosomal protein S6 phosphorylation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- HELZ is a RNA-DNA helicase that resolves R loops to facilitate homologous recombination repair.Nature communications · 2026Article
- HELZ-BRCA2 complex resolves R-loops to drive transcription-coupled homologous recombination.Nature communications · 2026Article
- AMPK modulates a DEAH box RNA-helicase to attenuate TOR signaling and establish developmental quiescence in Caenorhabditis elegans.PLoS biology · 2025Article
- Article
- Map2k6 is a potent genetic modifier of arterial rupture in vascular Ehlers-Danlos syndrome mice.JCI insight · 2025Article
- Enhancing Genomic Prediction Accuracy for Body Conformation Traits in Korean Holstein Cattle.Animals : an open access journal from MDPI · 2024Article
- Targeting Zinc Finger Proteins with Exogenous Metals and Molecules: Lessons learned from Tristetraprolin, a CCCH type Zinc Finger.European journal of inorganic chemistry · 2021Article
- RNA Helicases as Shadow Modulators of Cell Cycle Progression.International journal of molecular sciences · 2021Review
- HELZ directly interacts with CCR4-NOT and causes decay of bound mRNAs.Life science alliance · 2019Article
- Article
- Dietary intake alters gene expression in colon tissue: possible underlying mechanism for the influence of diet on disease.Pharmacogenetics and genomics · 2016Article
- Article
- Hyperphosphorylation of ribosomal protein S6 predicts unfavorable clinical survival in non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2015Article
- Divergence of RNA localization between rat and mouse neurons reveals the potential for rapid brain evolution.BMC genomics · 2014Article
- Dubowitz syndrome is a complex comprised of multiple, genetically distinct and phenotypically overlapping disorders.PloS one · 2014Article
- Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The hypoxia-inducible transcription factor (HIF) is a key component of the cellular adaptation mechanisms to hypoxic conditions. HIFα subunits are degraded by prolyl-4-hydroxylase domain (PHD) enzyme-dependent prolyl-4-hydroxylation of LxxLAP motifs that confer oxygen-dependent proteolytic degradation. Interestingly, only three non-HIFα proteins contain two conserved LxxLAP motifs, including the putative RNA helicase with a zinc finger domain HELZ. However, HELZ proteolytic regulation was found to be oxygen-independent, supporting the notion that a LxxLAP sequence motif alone is not sufficient for oxygen-dependent protein destruction. Since biochemical pathways involving RNA often require RNA helicases to modulate RNA structure and activity, we used luciferase reporter gene constructs and metabolic labeling to demonstrate that HELZ overexpression activates global protein translation whereas RNA-interference mediated HELZ suppression had the opposite effect. Although HELZ interacted with the poly(A)-binding protein (PABP) via its PAM2 motif, PABP was dispensable for HELZ function in protein translation. Importantly, downregulation of HELZ reduced translational initiation, resulting in the disassembly of polysomes, in a reduction of cell proliferation and hypophosphorylation of ribosomal protein S6.
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What OpenQuestion holds
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.