ArticleNature communications2014
Receptor-interacting protein 140 attenuates endoplasmic reticulum stress in neurons and protects against cell death.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- Deubiquitination of RIPK3 by OTUB2 potentiates neuronal necroptosis after ischemic stroke.EMBO molecular medicine · 2025Article
- Gut microbiota-derived acetic acids promoted sepsis-induced acute respiratory distress syndrome by delaying neutrophil apoptosis through FABP4.Cellular and molecular life sciences : CMLS · 2024Article
- Reduced insulin signaling in neurons induces sex-specific health benefits.Science advances · 2023Article
- Comprehensive characterization of putative genetic influences on plasma metabolome in a pediatric cohort.Human genomics · 2022Article
- Receptor-Interacting Protein 140 Enhanced Temozolomide-Induced Cellular Apoptosis Through Regulation of E2F1 in Human Glioma Cell Lines.Neuromolecular medicine · 2022Article
- HREM, RNAseq and Cell Cycle Analyses Reveal the Role of the G2/M-Regulatory Protein, WEE1, on the Survivability of Chicken Embryos during Diapause.Biomedicines · 2022Article
- Regulation of exosome secretion by cellular retinoic acid binding protein 1 contributes to systemic anti-inflammation.Cell communication and signaling : CCS · 2021Article
- Endophilin A2-mediated alleviation of endoplasmic reticulum stress-induced cardiac injury involves the suppression of ERO1α/IPInternational journal of biological sciences · 2021Article
- Receptor-interacting protein 140 as a co-repressor of Heat Shock Factor 1 regulates neuronal stress response.Cell death & disease · 2017Article
- Notoginsenoside R1 Alleviates Oxygen-Glucose Deprivation/Reoxygenation Injury by Suppressing Endoplasmic Reticulum Calcium Release via PLC.Scientific reports · 2017Article
- Expression and Regulatory Network Analysis of miR-140-3p, a New Potential Serum Biomarker for Autism Spectrum Disorder.Frontiers in molecular neuroscience · 2017Article
- Receptor-Interacting Protein 140 Orchestrates the Dynamics of Macrophage M1/M2 Polarization.Journal of innate immunity · 2016Article
- Retinoic Acid Induces Ubiquitination-Resistant RIP140/LSD1 Complex to Fine-Tune Pax6 Gene in Neuronal Differentiation.Stem cells (Dayton, Ohio) · 2016Article
- cGMP/Protein Kinase G Signaling Suppresses Inositol 1,4,5-Trisphosphate Receptor Phosphorylation and Promotes Endoplasmic Reticulum Stress in Photoreceptors of Cyclic Nucleotide-gated Channel-deficient Mice.The Journal of biological chemistry · 2015Article
- Behavioral stress reduces RIP140 expression in astrocyte and increases brain lipid accumulation.Brain, behavior, and immunity · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Inositol 1, 4, 5-trisphosphate receptor (IP3R)-mediated Ca(2+) release from the endoplasmic reticulum (ER) triggers many physiological responses in neurons, and when uncontrolled can cause ER stress that contributes to neurological disease. Here we show that the unfolded protein response (UPR) in neurons induces rapid translocation of nuclear receptor-interacting protein 140 (RIP140) to the cytoplasm. In the cytoplasm, RIP140 localizes to the ER by binding to the IP3R. The carboxyl-terminal RD4 domain of RIP140 interacts with the carboxyl-terminal gate-keeping domain of the IP3R. This molecular interaction disrupts the IP3R's 'head-tail' interaction, thereby suppressing channel opening and attenuating IP3R-mediated Ca(2+) release. This contributes to a rapid suppression of the ER stress response and provides protection from apoptosis in both hippocampal neurons in vitro and in an animal model of ER stress. Thus, RIP140 translocation to the cytoplasm is an early response to ER stress and provides protection against neuronal death.
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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.