ER-stress-induced transcriptional regulation increases protein synthesis leading to cell death

By Jaeseok Han, Sung Hoon Back, Junguk Hur, Yu-Hsuan Lin, Robert D. Gildersleeve, J. Shan, Celvie L. Yuan, Dawid Krokowski, Shiyu Wang, M. Hatzoglou and 3 more. Nature Cell Biology, 2013

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Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d41e25de9c309e708d589b5661dd89d6d5dccedd

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Citations in the corpus

Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer (2017, neutral): “Subsequently, ATF4 and CHOP cooperatively induce multiple genes involved in amino acid biosynthesis, amino acid transport, and the intracellular recycling system autophagy (B’Chir et al., 2013; Han et al., 2013).”
Metabolic control of cell death (2014, background): “In the course of ER stress, the eukaryotic translation initiation factor 2a (eIF2a) kinase 3 (best known as PERK) phosphorylates eIF2a, restricting the translation of a majority of proteinswhile stimulating the synthesis of activating transcription factor 4 (ATF4) and DNA damage– inducible transcrip”
Insulin resistance: Review of the underlying molecular mechanisms (2018, background): “ER stress in beta cells disrupts insulin synthesis and sensitivity (Han et al., 2013).”
ER stress: Autophagy induction, inhibition and selection (2015, background): “1B).(144,145) For instance, bufalin, an active component of Bufo gargarizan venom and a treatment for malignant glioma, causes ER stress-mediated ATP depletion and upregulation of AMPK activity with increased autophagy and overall survival of glioma cells.”
A multiplexed single-cell CRISPR screening platform enables systematic dissection of the unfolded protein response (2016, result): “As expected from previous work (Acosta-Alvear et al., 2007; Han et al., 2013; Lee et al., 2003; Shoulders et al., 2013), epistasis analysis using combinatorial depletions of PERK, ATF6, and IRE1α revealed both distinct and overlapping programs of gene expression.”
The integrated stress response (2016, neutral): “…expression of genes involved in amino acid transport and biosynthesis, Kaufman and colleagues showed that in response to ER stress, ATF4 and CHOP interact to regulate common genes involved in cellular amino acid metabolic processes, mRNA translation, and the unfolded protein response (UPR) [122].”
The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “ATF4 translocates to the nucleus, which increases the expression of CHOP and ATF3.”
Multi-omics analysis identifies ATF4 as a key regulator of the mitochondrial stress response in mammals (2017, result): “Of note, some of the up-regulated genes (13/59) also were potential CHOP targets; however, because all those genes were also ATF4 targets and CHOP only overlapped with half of them, we hypothesized that CHOP activation is a downstream event in this context (Fig.”
Endoplasmic reticulum stress: molecular mechanism and therapeutic targets (2023, background): “Then, eukaryotic translation initiation factor 2α (eIF2α), a ubiquitous translation initiation factor, is inactivated by phosphorylation under the activation of PERK, alleviating translation, reducing protein synthesis, and contributing to protein load reduction.(13) If ER stress persists, ATF4 mRNA”