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Updated: May 8, 2026
07:42
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
ING1 induces apoptosis through direct effects at the mitochondria
P Bose1, S Thakur, S Thalappilly
1Department of Biochemistry and Molecular Biology, Southern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
Cell Death & Disease
|September 7, 2013
Summary
The ING1 tumor suppressor protein moves to mitochondria upon cellular stress, interacting with BAX to trigger apoptosis independently of p53. This reveals a new role for ING1 in programmed cell death.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- The ING family, including ING1, are tumor suppressors involved in epigenetic regulation, DNA repair, and apoptosis.
- ING1 interacts with PCNA and 14-3-3 proteins, influencing its cellular localization and function.
- Previous studies suggested ING1 affects apoptosis in a p53-dependent manner.
Purpose of the Study:
- To investigate the role of ING1 in apoptosis induction and its subcellular localization.
- To determine if ING1's mitochondrial translocation and apoptotic function are p53-dependent.
- To elucidate the interaction of ING1 with other apoptotic regulators like BAX.
Main Methods:
- Studied ING1 translocation to mitochondria in response to apoptosis-inducing stimuli in primary fibroblasts and epithelial cell lines.
- Assessed the correlation between ING1 mitochondrial translocation and apoptosis induction in breast cancer cell lines after UV treatment.
- Investigated endogenous ING1-BAX interaction and colocalization using biochemical and imaging techniques.
- Utilized bioinformatics and sequence analysis to identify potential functional domains and interactions.
Main Results:
- ING1 translocates to mitochondria in response to apoptotic stimuli, independent of p53 status.
- ING1 directly interacts with and colocalizes with the pro-apoptotic protein BAX in a UV-inducible manner.
- Mitochondria-targeted ING1 enhances apoptosis induction compared to wild-type ING1.
- Bioinformatic analysis suggests interactions between yeast ING proteins and mitochondrial proteins, and ING1 possesses a BH3-like domain.
Conclusions:
- Stress-induced ING1 relocalization to mitochondria, mediated by 14-3-3 proteins, promotes apoptosis through BAX interaction.
- ING1 plays a direct role in regulating mitochondrial membrane permeability and apoptosis.
- This study redefines the understanding of ING1's function in the cytoplasm and its contribution to programmed cell death.
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