Abstract
Eukaryotic organisms have evolved complex and robust cellular stress response pathways to ensure maintenance of proteostasis and survival during fluctuating environmental conditions. Highly conserved stress response pathways can be triggered and coordinated at the cell-autonomous and cell-nonautonomous level by proteostasis transcription factors, including HSF1, SKN-1/NRF2, HIF1, and DAF-16/FOXO that combat proteotoxic stress caused by environmental challenges. While these transcription factors are often associated with a specific stress condition, they also direct “noncanonical” transcriptional programs that serve to integrate a multitude of physiological responses required for development, metabolism, and defense responses to pathogen infections. In this review, we outline the established function of these key proteostasis transcription factors at the cell-autonomous and cell-nonautonomous level and discuss a newly emerging stress responsive transcription factor, PQM-1, within the proteostasis network. We look beyond the canonical stress response roles of proteostasis transcription factors and highlight their function in integrating different physiological stimuli to maintain cytosolic organismal proteostasis.
Award Identifier / Grant number: NC/P001203/1
Funding statement: National Centre for the Replacement Refinement and Reduction of Animals in Research, Funder Id: http://dx.doi.org/10.13039/501100010757, NC3Rs Grant number: NC/P001203/1.
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Articles in the same Issue
- Frontmatter
- Reviews
- Redefining proteostasis transcription factors in organismal stress responses, development, metabolism, and health
- Proteostasis in thermogenesis and obesity
- Research Articles/Short Communications
- Protein Structure and Function
- Citrate synthase desuccinylation by SIRT5 promotes colon cancer cell proliferation and migration
- Membranes, Lipids, Glycobiology
- Core 1 O-N-acetylgalactosamine (O-GalNAc) glycosylation in the human cell nucleus
- Cell Biology and Signaling
- LncRNA ELFN1-AS1 promotes esophageal cancer progression by up-regulating GFPT1 via sponging miR-183-3p
- Vemurafenib downmodulates aggressiveness mediators of colorectal cancer (CRC): Low Molecular Weight Protein Tyrosine Phosphatase (LMWPTP), Protein Tyrosine Phosphatase 1B (PTP1B) and Transforming Growth Factor β (TGFβ)
- Osteopontin enhances the migration of lung fibroblasts via upregulation of interleukin-6 through the extracellular signal-regulated kinase (ERK) pathway
- A role of heparan sulphate proteoglycan in the cellular uptake of lipocalins ß-lactoglobulin and allergen Fel d 4
- A progesterone receptor membrane component 1 antagonist induces large vesicles independent of progesterone receptor membrane component 1 expression
Articles in the same Issue
- Frontmatter
- Reviews
- Redefining proteostasis transcription factors in organismal stress responses, development, metabolism, and health
- Proteostasis in thermogenesis and obesity
- Research Articles/Short Communications
- Protein Structure and Function
- Citrate synthase desuccinylation by SIRT5 promotes colon cancer cell proliferation and migration
- Membranes, Lipids, Glycobiology
- Core 1 O-N-acetylgalactosamine (O-GalNAc) glycosylation in the human cell nucleus
- Cell Biology and Signaling
- LncRNA ELFN1-AS1 promotes esophageal cancer progression by up-regulating GFPT1 via sponging miR-183-3p
- Vemurafenib downmodulates aggressiveness mediators of colorectal cancer (CRC): Low Molecular Weight Protein Tyrosine Phosphatase (LMWPTP), Protein Tyrosine Phosphatase 1B (PTP1B) and Transforming Growth Factor β (TGFβ)
- Osteopontin enhances the migration of lung fibroblasts via upregulation of interleukin-6 through the extracellular signal-regulated kinase (ERK) pathway
- A role of heparan sulphate proteoglycan in the cellular uptake of lipocalins ß-lactoglobulin and allergen Fel d 4
- A progesterone receptor membrane component 1 antagonist induces large vesicles independent of progesterone receptor membrane component 1 expression