Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA274568 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1787570.fastq.gz | Fastqsanger.gz | |||
| SRR1787580.fastq.gz | Fastqsanger.gz | |||
| SRR1787571.fastq.gz | Fastqsanger.gz | |||
| SRR1787581.fastq.gz | Fastqsanger.gz | |||
| SRR1787572.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:Bats as the only flying mammals incur a high metabolic cost during extended powered flight, which results in febrile-like temperatures without injury. Herein, we investigate the in vivo heat shock response (HSR) in the cave nectar bat Eonycteris spelaea. We demonstrate that E. spelaea exhibits enhanced physiological heat resistance, marked by reduced lethality, tissue damage and serum corticosterone levels in comparison to mice upon heat challenge. Additionally, E. spelaea did not exhibit an acute transcriptional response observed heat stress in mice. Instead, bats displayed a delayed and non-canonical HSR that did not involve the activation of classical heat shock related genes and pathways. This altered response in E. spelaea is attributed to the elevated basal expression of heat shock proteins, which we demonstrate to be a common characteristic exhibited by bats from diverse sub-orders, families and diets. Taken together, we demonstrate a distinct HSR in E. spelaea relative to the conventional model organism, mouse, which may provide insights to understand novel regulatory targets and effector proteins that underlie the mammalian heat shock response.
2025-04-02 | GSE261939 | GEO
Project description:Environmental stress, such as oxidative or heat stress, induces the activation of the heat shock response
(HSR) and leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular
chaperones to maintain cellular proteostasis. Controlled by highly intricate regulatory mechanisms,
having stress-induced activation and feedback regulations with multiple partners, the HSR is still
incompletely understood. In this context, we propose a minimal molecular model for the gene
regulatory network of the HSR that reproduces quantitatively different heat shock experiments both
on heat shock factor 1 (HSF1) and HSPs activities. This model, which is based on chemical kinetics
laws, is kept with a low dimensionality without altering the biological interpretation of the model
dynamics. This simplistic model highlights the titration of HSF1 by chaperones as the guiding line of
the network. Moreover, by a steady states analysis of the network, three different temperature stress
regimes appear: normal, acute, and chronic, where normal stress corresponds to pseudo thermal
adaption. The protein triage that governs the fate of damaged proteins or the different stress regimes
are consequences of the titration mechanism. The simplicity of the present model is of interest in
order to study detailed modelling of cross regulation between the HSR and other major genetic
networks like the cell cycle or the circadian clock.
Sivéry, A., Courtade, E., Thommen, Q. (2016). A minimal titration model of the mammalian dynamical heat shock response. Physical biology, 13(6), 066008.
2022-01-25 | MODEL2201210001 | BioModels
Project description:Antiviral therapies targeting the pandemic coronavirus disease 2019 (COVID 19) are urgently required. We studied an already approved botanical drug cepharanthine (CEP) in a cell culture model of GX_P2V, a severe acute respiratory syndrome coronavirus 2 (SARS CoV 2) related virus. RNA sequencing results showed the virus perturbed the expression of multiple cell stress responses such as endoplasmic reticulum (stress and HSF1 mediated heat shock response related genes and signaling pathways, of which heat shock response related genes and pathways were at the core. CEP was potent to reverse most dysregulated genes and pathways in infected cells mainly by interfering with cellular stress responses including ER stress unfolded protein response and HSF 1 mediated heat shock response . Additionally, single cell transcriptomes from COVID 19 patients (GSE150728 and GSE148829) also confirmed that cellular stress responses and stress induced autophagy play an important role in the development of COVID 19. In summary, this study uncovered the potential mechanisms of the anti-viral activities of CEP, providing evidence for CEP as a promising therapeutic option and modulating cellular stress could be a promising therapy for SARS CoV 2 infection.
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Project description:Intra Peritoneal Chemo Hyperthermia (IPCH) is a recently validated option for the treatment of peritoneal carcinomatosis from colorectal or ovarian origin. This therapeutic program demonstrated a significant improvement of the late stages (i.e. carcinomatosis) of the disease. From a clinical point of view, within the first 24 hours after IPCH, patients undergo a systemic inflammatory response syndrome, and therefore require to be monitored in an intensive care unit. From a metabolic perspective, preliminary data have been shown a significant "anaerobic style" disturbance of energetic metabolism, suggesting a deep cellular energetic deficit throughout IPCH process.
Putative contradictory effects of IPCH, like the increase of chemotherapy-related cellular toxicity due to heat and on the other hand the initiation of a stress protein response (heat shock response) which helps to reduce the cell injuries, leads to conduct a research project on the underlying mechanisms: consequences, in terms of patient’s care and follow-up, are of high relevance.
The primary goal is a multimodal assessment of the IPCH-related cell modifications: signaling pathways, apoptosis and antitumoral immune response.
The assessment criteria include Heat shock protein expression (blood/cell ratio) compared to baseline values, apoptosis and immune response before/after IPCH.
The scheduled sample size is 30 patients having an IPCH and 30 patients contraindicated per surgery.
| 2131952 | ecrin-mdr-crc
Project description:Global warming has great impacts on plant growth and development. Heat shock transcription factors are the master regulators of heat stress response to alleviate protein misfolding in the cytosol in plants. However, how plants deal with accumulation of misfolded proteins in the endoplasmic reticulum (ER) under heat stress conditions is less understood, especially in crops such as in rice. Here we report a positive feed-back loop mediated by the membrane-associated transcription factors NTL3 and bZIP74 in heat stress response in rice. In response to heat stress, the ER-membrane-associated bZIP74 is activated and up-regulate the expression of NTL3 in rice; NTL3 encodes an ER-membrane-associated transcription factor that is activated and regulate downstream genes including bZIP74 involved in protein folding and reactive oxygen species scavenging. Loss-of-function mutations of NTL3 are sensitive to heat stress while inducible expression of the processed form of NTL3 increases heat stress tolerance in rice seedlings. Our work reveals the important role of NTL3 in ER stress response for heat stress tolerance in rice.
2020-04-20 | GSE122021 | GEO
Project description:4-Hydroxynonenal (HNE), a cytotoxic and diffusible electrophile generated by the spontaneous decomposition of oxidized lipids, has a suspected role in neurodegenerative and inflammatory disease processes. In addition to promoting cell death, elevated levels of HNE lead to the engagement of cytoprotective signaling pathways, including the heat shock, antioxidant, DNA damage, and ER stress responses. Activation of the heat shock response, mediated by the transcription factor heat shock factor 1 (HSF1), is critical for maintaining cellular viability in the presence of HNE. Accordingly, silencing HSF1 expression using siRNA enhances the toxicity of HNE. Microarray analysis of samples from control and HSF1-silenced cells was performed to investigate which associated changes in gene could be responsible for the decrease in cellular viability.
2008-10-01 | GSE12762 | GEO
Project description:Analysis of the coordinated transcriptional reponse to heat shock and ER stress
2015-09-04 | GSE65636 | GEO
Project description:Analysis of the coordinated transcriptional reponse to heat shock and ER stress mRNA profiles of NIH3T3 cells which stably expressing DD-sfGFP were generated by deep sequencing, in triplicate, using Illumina HiSeq. The samples were collected from indicated timepoints after exposed to either heat stress or ER stress.
2015-09-04 | E-GEOD-65636 | biostudies-arrayexpress
Project description:Proctor2005 - Actions of chaperones and their
role in ageing
This model is described in the article:
Modelling the actions of
chaperones and their role in ageing.
Proctor CJ, Soti C, Boys RJ,
Gillespie CS, Shanley DP, Wilkinson DJ, Kirkwood TB.
Mech. Ageing Dev. 2005 Jan; 126(1):
119-131
Abstract:
Many molecular chaperones are also known as heat shock
proteins because they are synthesised in increased amounts
after brief exposure of cells to elevated temperatures. They
have many cellular functions and are involved in the folding of
nascent proteins, the re-folding of denatured proteins, the
prevention of protein aggregation, and assisting the targeting
of proteins for degradation by the proteasome and lysosomes.
They also have a role in apoptosis and are involved in
modulating signals for immune and inflammatory responses.
Stress-induced transcription of heat shock proteins requires
the activation of heat shock factor (HSF). Under normal
conditions, HSF is bound to heat shock proteins resulting in
feedback repression. During stress, cellular proteins undergo
denaturation and sequester heat shock proteins bound to HSF,
which is then able to become transcriptionally active. The
induction of heat shock proteins is impaired with age and there
is also a decline in chaperone function. Aberrant/damaged
proteins accumulate with age and are implicated in several
important age-related conditions (e.g. Alzheimer's disease,
Parkinson's disease, and cataract). Therefore, the balance
between damaged proteins and available free chaperones may be
greatly disturbed during ageing. We have developed a
mathematical model to describe the heat shock system. The aim
of the model is two-fold: to explore the heat shock system and
its implications in ageing; and to demonstrate how to build a
model of a biological system using our simulation system
(biology of ageing e-science integration and simulation
(BASIS)).
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000091.
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2024-09-02 | BIOMD0000000091 | BioModels
Project description:HSF1 is a major transcriptional regulator of heat shock responses. Many cells activate HSF1 in response to heat shock temperatures (>42oC) and other cellular stress causing agents. Unlike other cell types, T cells activate HSF1 in response to T cell activation or when exposed to febrile (40oC) temperatures, suggesting a role for HSF1 beyond the heat-shock response. We used microarray analysis and HSF1 knock-out mice to study the HSF1 mediated gene regulation in activated T cells under normal and fever temperatures.
2012-09-20 | GSE41005 | GEO