Gadd153 Sensitizes Cells to Endoplasmic Reticulum Stress by Down-Regulating Bcl2 and Perturbing the Cellular Redox State

By K. McCullough, J. Martindale, L. Klotz, T. Aw, N. Holbrook. Molecular and Cellular Biology, 2001

1,966 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f92d32a7baf31fe69a54f45b0c804d0fd4f728b8

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In Cell Biology

1. R. Kaufman
2. D. Ron
3. J. Malhotra
4. G. Hotamışlıgil
5. Afshin Samali
6. A. Gorman
7. H. Harding
8. S. Oyadomari

In Epidemiology

1. R. Kaufman
2. J. Malhotra
3. D. Ron
4. Afshin Samali
5. A. Gorman
6. John Calvin Reed
7. H. Harding
8. I. Novoa

In Molecular Biology

1. R. Kaufman
2. D. Ron
3. J. Malhotra
4. G. Hotamışlıgil
5. H. Harding
6. Afshin Samali
7. A. Gorman
8. Kezhong Zhang

Citations in the corpus

• Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cellular Models of Parkinson's Disease (2002, background): “In addition, overexpression of CHOP sensitizes cells to ER stress, so their long-term survival after exposure to ER-stress-inducing agents is significantly lower (McCullough et al., 2001).”
• ER stress-induced cell death mechanisms. (2013, background): “Another possible mechanism by which CHOP induces apoptosis is via direct inhibition of Bcl-2 transcription [19] and induction of Bim expression [8].”
• Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Overexpression of the 29 kDa CHOP protein induces apoptosis through a mechanism that can be inhibited by BCL-2 (Ref”
• Endoplasmic Reticulum Stress in Liver Disease (2010, background): “Importantly, over expression of CHOP does not result in apoptosis, though it does sensitize cells to apoptosis [91].”
• The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “cellular redox state by depletion of cellular glutathione (138)”
• Endoplasmic reticulum stress: molecular mechanism and therapeutic targets (2023, background): “Activated CHOP immensely decreases Bcl2, in which BH4-Tat can alleviate the mitochondria membrane potential under ER stress, increases pro-apoptotic protein Bim, and activates caspases like caspase-9, -2, and -3.(40,41) Subsequently, mitochondrial outer membrane permeabilization facilitates the rele”
• A trip to the ER: coping with stress. (2004, background): “resistant to ER-stress-induced apoptosis [ 46 ,47], although the relative importance of CHOP, or any other protein implicated in the ER-stress-mediated apoptosis, remains unclear.”