HDAC4 protects cells from ER stress induced apoptosis through interaction with ATF4
Abstract
Histone deacetylase 4 (HDAC4) is involved in the regulation of many fundamental cell processes such as proliferation, differentiation, and survival via the modification of their substrates or protein-protein interactions. In this study, we found that HDAC4 could be upregulated under ER stress. There exists a direct interaction between HDAC4 and activating transcription factor 4 (ATF4). In vitro, overexpression of HDAC4 caused the retention of ATF4 in cytoplasm and inhibition of ATF4 transcriptional activity. ER stress could promote cell apoptosis through the upregulation of ATF4 levels and its target genes such as CHOP and TRB3. This effect was exacerbated by downregulation of HDAC4 levels. These results demonstrated that HDAC4 played an important role in the regulation of ER stress-induced apoptosis through interacting with ATF4 and inhibiting its transcriptional activity.
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Cytoplasmic HDAC4 may have neuroprotective effects.
“HDAC4 in the cytoplasm may have neuroprotective effects.145–147”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [146]
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Yuan, M., Yang, B., Rothschild, G., Mann, J. J., Sanford, L. D., Tang, X., Huang, C., Wang, C., & Zhang, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01519-z · Cited by 246 · see citing works
Puangmalai, N., Sengupta, U., Bhatt, N., Gaikwad, S., Montalbano, M., Bhuyan, A., Garcia, S., McAllen, S., Sonawane, M., Jerez, C., et al. (2022) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2022.101766 · Cited by 68 · see citing works
- Authors
- Zhang, P., Sun, Q., Zhao, C., Ling, S., Li, Q., Chang, Y.-Z., & Li, Y.
- Affiliations
- China Astronaut Research and Training Center (CN)
- Hebei Normal University (CN)
- Corresponding author
- Chang, Yan-Zhong
- Li, Yingxian
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2014-03
- Volume
- 26
- Issue
- 3
- Pages
- 556-563
- ISSN
- 0898-6568 (ISSN-L)
- OpenAlex
- W2082409505
- Cited by
- 54
- References
- 0
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 11 · 2023: 3 · 2022: 5 · 2021: 8 · 2020: 1 · 2019: 6 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 5 · 2014: 3
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cellular Signalling (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation Projects (31325012, 31170811, 31271225)
- Advanced Space Medico-engineering Research Project of China (2012SY54B1602)
- National Basic Research Program of China 973 program (2011CB711003)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- HDAC4, endoplasmic reticulum stress, apoptosis, ATF4, protein-protein interaction, transcriptional activity, CHOP, TRB3, endoplasmic reticulum stress response
- MeSH terms
- Calcium-Transporting ATPases, Animals, Cell Line, Endoplasmic Reticulum, Enzyme Inhibitors, Glycosylation, Histone Deacetylases, Humans, Phosphorylation, Repressor Proteins, Transcription, Genetic, Signal Transduction, Transcriptional Activation, Eukaryotic Initiation Factor-2, Up-Regulation, 3T3 Cells, Apoptosis, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Thapsigargin, eIF-2 Kinase, RNA Interference, RNA, Small Interfering, Mice, Activating Transcription Factor 4, Transcription Factor CHOP, HEK293 Cells, Endoplasmic Reticulum Stress
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