ArticlePloS one2014
TBL2 is a novel PERK-binding protein that modulates stress-signaling and cell survival during endoplasmic reticulum stress.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- TBL2 Promotes Tumorigenesis via PRMT5/WDR77-Mediated AKT Activation in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Navigating the landscape of the unfolded protein response in CD8Frontiers in immunology · 2024Review
- Dose-Dependent Effect of Mitochondrial Superoxide Dismutase Gene Overexpression on Radioresistance of HEK293T Cells.International journal of molecular sciences · 2023Article
- Transducin Beta-Like 2 is a Potential Driver Gene that Adapts to Endoplasmic Reticulum Stress to Promote Tumor Growth of Lung Adenocarcinoma.Annals of surgical oncology · 2023Article
- Non-coding variants in VAMP2 and SNAP25 affect gene expression: potential implications in migraine susceptibility.The journal of headache and pain · 2023Article
- Modulation of NBAS-Related Functions in the Early Response to SARS-CoV-2 Infection.International journal of molecular sciences · 2023Article
- Neuron-specific translational control shift ensures proteostatic resilience during ER stress.The EMBO journal · 2022Article
- A prognostic signature model for unveiling tumor progression in lung adenocarcinoma.Frontiers in oncology · 2022Article
- An introduction to new robust linear and monotonic correlation coefficients.BMC bioinformatics · 2021Article
- TBL2 methylation is associated with hyper-low-density lipoprotein cholesterolemia: a case-control study.Lipids in health and disease · 2020Article
- Mechanisms, regulation and functions of the unfolded protein response.Nature reviews. Molecular cell biology · 2020Review
- PRKCSH contributes to tumorigenesis by selective boosting of IRE1 signaling pathway.Nature communications · 2019Article
- CNPY2 is a key initiator of the PERK-CHOP pathway of the unfolded protein response.Nature structural & molecular biology · 2017Article
- Inhibiting cytosolic translation and autophagy improves health in mitochondrial disease.Human molecular genetics · 2015Article
- Erratum: Proteostasis control by the unfolded protein response.Nature cell biology · 2015Article
- Cell intrinsic and extrinsic activators of the unfolded protein response in cancer: Mechanisms and targets for therapy.Seminars in cancer biology · 2015Review
- Proteostasis control by the unfolded protein response.Nature cell biology · 2015Review
- Molecular signal networks and regulating mechanisms of the unfolded protein response.Journal of Zhejiang University. Science. BReview
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Under ER stress, PKR-like ER-resident kinase (PERK) phosphorylates translation initiation factor eIF2α, resulting in repression of global protein synthesis and concomitant upregulation of the translation of specific mRNAs such as activating transcription factor 4 (ATF4). This PERK function is important for cell survival under ER stress and poor nutrient conditions. However, mechanisms of the PERK signaling pathway are not thoroughly understood. Here we identify transducin (beta)-like 2 (TBL2) as a novel PERK-binding protein. We found that TBL2 is an ER-localized type-I transmembrane protein and preferentially binds to the phosphorylated form of PERK, but not another eIF2α kinase GCN2 or ER-resident kinase IRE1, under ER stress. Immunoprecipitation analysis using various deletion mutants revealed that TBL2 interacts with PERK via the N-terminus proximal region and also associates with eIF2α via the WD40 domain. In addition, TBL2 knockdown can lead to impaired ATF4 induction under ER stress or poor nutrient conditions such as glucose and oxygen deprivation. Consistently, TBL2 knockdown rendered cells vulnerable to stresses similarly to PERK knockdown. Thus, TBL2 serves as a potential regulator of the PERK pathway.
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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.