A mitochondrial specific stress response in mammalian cells

By Quan Zhao, Jianghui Wang, Ilya Levichkin, S. Stasinopoulos, M. Ryan, N. Hoogenraad. EMBO Journal, 2002

1,004 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/173faf71a93edebe362adc9ed3987c3b50653d9c

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In Cell Biology

1. R. Kaufman
2. D. Ron
3. H. Harding
4. F. Urano
5. A. Dillin
6. Suzanne C Wolff
7. Jenni Durieux
8. D. Finley

In Molecular Biology

1. D. Ron
2. R. Kaufman
3. H. Harding
4. F. Urano
5. A. Suomalainen
6. A. Dillin
7. D. Finley
8. Robert W. Williams

Citations in the corpus

• Multi-omics analysis identifies ATF4 as a key regulator of the mitochondrial stress response in mammals (2017, methodology): “Surprisingly, under the conditions used, we did not detect activation of the prototypical UPRmt, which is generally characterized by the induction of the chaperones HSP60 and HSP10 and the protease CLPP, among others, and which has been mainly described in invertebrates and cellular models as the pr”
• The NAD+/sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling (2013, neutral): “H) The NAD+ precursor NR (E and G; 1 mM) and the PARP inhibitor AZD2281 (F and H; 1 mM) induce UPRmt, as evidenced by CLPP expression, in a timedependent fashion in AML12 cells.”
• TRB3, a novel ER stress‐inducible gene, is induced via ATF4–CHOP pathway and is involved in cell death (2005, background): “TRB3 downregulates CHOP-dependent transcriptional activity It has been shown that several CHOP-inducible genes have been induced during ER stress or mitochondrial stress via novel CHOP-binding sequence (Wang et al, 1998; Zhao et al, 2002) (Figure 3A).”
• Compartment-specific perturbation of protein handling activates genes encoding mitochondrial chaperones (2004, background): “The stress-induced transcription factor CHOP was shown to play an important role in this signaling pathway (Zhao et al., 2002).”
• Genome-Wide and Functional Annotation of Human E3 Ubiquitin Ligases Identifies MULAN, a Mitochondrial E3 that Regulates the Organelle's Dynamics and Signaling (2008, background): “So far, the most definitive link connecting NF-kB activation to mitochondria is through MAVS, a MOM-resident protein that participates in the host innate immune response to viral infection [29].”
• The Cell Non-Autonomous Nature of Electron Transport Chain-Mediated Longevity (2011, positive): “The Mitochondrial Unfolded Protein Response Is Required for ETC-Mediated Longevity In response to a mitochondrial perturbation there exists a stress response mechanism that is communicated to the nucleus to increase the expression of mitochondrial associated protein chaperones, such as HSP-6 andHSP-”
• A new pathway for mitochondrial quality control: mitochondrial‐derived vesicles (2014, methodology): “Using a different approach, the Youle lab employed a non-cleavable mutant of ornithine carbamyl transferase (Jin & Youle, 2013), first used to induce the mitochondrial unfolded protein response by Nick Hoogenraad (Zhao et al, 2002).”
• Mitochondria: In Sickness and in Health (2012, background): “UPRmt originates in mitochondria from the accumulation of unassembled respiratory complex subunits and is communicated to the nucleus via an unknown mechanism where it culminates in the regulated expression of mitochondrial protein chaperones, such as HSP-60 (Benedetti et al., 2006; Haynes et al., 2”