ArticlePloS one2011
An atypical unfolded protein response in heat shocked cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Heat stress reveals bidirectional cross talk between the heat shock response and UPRER in C. elegans.G3 (Bethesda, Md.) · 2026Article
- Re-Evaluating Hot Mitochondria: Too Slow to Cool.Acta physiologica (Oxford, England) · 2026Review
- Heat shock factor-1 alleviates ER-stress in Caenorhabditis elegans.Scientific reports · 2026Article
- Single-nucleus RNA sequencing of human periventricular white matter in vascular dementia.bioRxiv : the preprint server for biology · 2024Article
- Endogenous fluorescent reporters for heat shock proteins are not detectable after stress induction.microPublication biology · 2024Article
- Neurodegenerative Proteinopathies Induced by Environmental Pollutants: Heat Shock Proteins and Proteasome as Promising Therapeutic Tools.Pharmaceutics · 2023Review
- TheInternational journal of molecular sciences · 2022Article
- Hijacking Cellular Stress Responses to Promote Lifespan.Frontiers in aging · 2022Review
- The function of the co-chaperone ERdj4 in diverse (patho-)physiological conditions.Cellular and molecular life sciences : CMLS · 2021Review
- Dietary thiols accelerate aging of C. elegans.Nature communications · 2021Article
- Quantitative Proteomic Analysis Revealed Broad Roles ofJournal of proteome research · 2021Article
- Harnessing the Proteostasis Network in Alcohol-associated Liver Disease.Current pathobiology reports · 2020Article
- Heat shock protein 70 (Hsp70) mediates Zika virus entry, replication, and egress from host cells.Emerging microbes & infections · 2019Article
- Evolution in chronic cold: varied loss of cellular response to heat in Antarctic notothenioid fish.BMC evolutionary biology · 2018Article
- Roles of heat shock factor 1 beyond the heat shock response.Cellular and molecular life sciences : CMLS · 2018Review
- TG2 regulates the heat-shock response by the post-translational modification of HSF1.EMBO reports · 2018Article
- A Futile Battle? Protein Quality Control and the Stress of Aging.Developmental cell · 2018Review
- The Hsp72 and Hsp90α mRNA Responses to Hot Downhill Running Are Reduced Following a Prior Bout of Hot Downhill Running, and Occur Concurrently within Leukocytes and the Vastus Lateralis.Frontiers in physiology · 2017Article
- Tumor suppressor BTG1 promotes PRMT1-mediated ATF4 function in response to cellular stress.Oncotarget · 2016Article
- The aggregation-prone intracellular serpin SRP-2 fails to transit the ER in Caenorhabditis elegans.Genetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe heat shock response (HSR) and the unfolded protein response (UPR) are both activated by proteotoxic stress, although in different compartments, and share cellular resources. How these resources are allocated when both responses are active is not known. Insight in possible crosstalk will help understanding the consequences of failure of these systems in (age-related) disease.
resultsIn heat stressed HEK293 cells synthesis of the canonical UPR transcription factors XBP1s and ATF4 was detected as well as HSF1 independent activation of the promoters of the ER resident chaperones HSPA5 (BiP) and DNAJB9 (ERdj4). However, the heat stress activation of the DNAJB9 promoter, a XBP1s target, was not blocked in cells expressing a dominant negative IRE1α mutant, and thus did not require XBP1s. Furthermore, the DNA element required for heat stress activation of the DNAJB9 promoter is distinct from the ATF4 and ATF6 target elements; even though inhibition of eIF2α phosphorylation resulted in a decreased activation of the DNAJB9 promoter upon heat stress, suggesting a role for an eIF2α phosphorylation dependent product.
conclusionsThe initial step in the UPR, synthesis of transcription factors, is activated by heat stress but the second step, transcriptional transactivation by these factors, is blocked and these pathways of the UPR are thus not productive. Expression of canonical ER chaperones is part of the response of heat stressed cells but another set of transcription factors has been recruited to regulate expression of these ER chaperones.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.