TRB3, a novel ER stress‐inducible gene, is induced via ATF4–CHOP pathway and is involved in cell death

By Nobumichi Ohoka, Satoshi Yoshii, T. Hattori, K. Onozaki, H. Hayashi. EMBO Journal, 2005

1,022 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c6c830666d9b0a42e84670a80cd2b1b6f4ad6fbc

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In Cell Biology

1. J. Malhotra
2. R. Kaufman
3. Shiyu Wang
4. H. Chae
5. Hyung-Ryong Kim
6. Afshin Samali
7. A. Gorman
8. M. Cnop

In Molecular Biology

1. J. Malhotra
2. R. Kaufman
3. Shiyu Wang
4. Afshin Samali
5. A. Gorman
6. H. Chae
7. Hyung-Ryong Kim
8. A. K. Cardozo

Citations in the corpus

• ER stress: Autophagy induction, inhibition and selection (2015, background): “Transcription factor ATF4 translocates to the nucleus and activates a set of UPR target genes involved in amino acid metabolism, antioxidant responses, autophagy, and apoptosis.(133,232) Induction.”
• Mediators of endoplasmic reticulum stress‐induced apoptosis (2006, background): “However, during prolonged ER stress, TRB3 induction is much more robust and is thought to act as an Akt inhibitor, therefore pushing the cell in the direction of apoptosis (Ohoka et al, 2005).”
• The integrated stress response (2016, neutral): “These interactions of ATF4, with other transcription factors or interacting partners, influence the outcome of ISR signaling; for example, interactions with ATF3 enhance cellular efforts to re-establish homeostasis, while interactions with CHOP promote cell death upon ER stress [131,132].”
• The impact of the unfolded protein response on human disease (2012, background): “CHOP up-regulates apoptosis-related genes including DR5 (Yamaguchi and Wang, 2004), Trb3 (Ohoka et al., 2005), BIM (Puthalakath et al.”
• The eIF2α/ATF4 pathway is essential for stress-induced autophagy gene expression (2013, background): “CHOP can (i) heterodimerize with C/EBP and function as a negative or positive trans-activator (23,46,60); (ii) cooperate with ATF4 to activate TRB3 transcription during ER stress (53); and (iii) negatively regulate ATF4-dependent transcription of the ASNS gene (18).”
• Endoplasmic Reticulum Stress in Liver Disease (2010, background): “Another proapoptotic protein, TRB3, is transcriptionally induced in tunicamycin treated cells and is CHOP-dependent for its expression [99].”
• The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “The binding site of CHOP overlaps the amino acid response elements in the TRB3 promoter, and the specific regions in CHOP and TRB3 are responsible for their interaction (69).”
• The eIF2α kinases: their structures and functions (2013, neutral): “ATF4 also upregulates the pro-apoptotic transcription factor CHOP, also known as GADD153, [143, 216], and Tribbles 3 (TRB3) [141], a pseudokinase that contributes to cell death under certain conditions in part by inhibiting the AKT pathway [20].”
• Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, neutral): “Trb3 encodes a human orthologue of Drosophila tribble, and Trb3 -knockdown cells are resistant to ER stress-induced apoptosis (100).”
• The endoplasmic reticulum and the unfolded protein response. (2007, background): “TRB3 (Tribbles homolog 3) encodes a human ortholog of Drosophila tribble, and TRB3-knock-down cells are resistant to ER stress-induced apoptosis [65].”