Similar Datasets
Project description:Lymphoblastoid cells trisomic for chromosome 21 activate the heat shock response more robustly than disomic cells.
2023-04-21 | GSE173537 | GEO
Project description:We utilize ribosome profiling to directly monitor translation in E. coli at 30 °C and investigate how this changes after 10-20 minutes of heat shock at 42 °C. Translation is controlled by the interplay of several RNA hybridization processes, which are expected to be temperature sensitive. We observe that translation efficiencies are robustly maintained after thermal heat shock and after mimicking the heat shock response transcriptional program at 30 °C.
2016-11-19 | GSE90056 | GEO
Project description:The transcriptional response to heat shock is essential for cells to function effectively under stress. This is a highly heritable trait but the nature and extent of inter-individual variation in heat shock response are not well established. This dataset consists of the global transcription profiles for a panel of lymphoblastoid cell lines established from 60 founder individuals in the Yoruba HapMap population that have been exposed to heat shock. RNA was extracted from resting cells as well as cells that were exposed to heat shock at 42°C for 1 hour and then allowed to recover for 6 hours at 37°C. In combination with the HapMap genotypes for these individuals this enables the study of the effect of genetic variation on the heat shock response.
2016-08-26 | E-MTAB-4953 | biostudies-arrayexpress
Project description:Poly(A)+ RNA extracted from WBCs obtained from chromosome 21 disomic (D21) and trisomic (T21) individuals to identify consistent changes in gene expression across individuals.
2019-09-12 | GSE128621 | GEO
Project description:Poly(A)+ RNA extracted from WBCs obtained from chromosome 21 disomic (D21) and trisomic (T21) individuals to identify consistent changes in gene expression across individuals.
2019-09-12 | GSE128614 | GEO
Project description:Human trisomies can alter cellular phenotypes and produce congenital abnormalities such as Down Syndrome (DS). Here we have generated induced pluripotent stem cells (iPSCs) from DS fibroblasts, and introduced a TKNEO transgene into one copy of chromosome 21 by gene targeting. When selecting against TKNEO, spontaneous chromosome loss was the most common cause for survival, with a frequency of ~10-4, while point mutations, epigenetic silencing, and TKNEO deletions occurred at lower frequencies in this unbiased comparison of inactivating mutations. Mitotic recombination events resulting in extended loss of heterozygosity were not observed in DS iPSCs. The disomic cells that we derived proliferated faster and produced more endothelia in vivo than their otherwise isogenic trisomic counterparts, but hematopoietic differentiation, pluripotency and survival were statistically unchanged. Our study describes the first targeted removal of a human trisomy, which could prove useful in both clinical and research applications. RNA samples were from two trisomic iPSC clone (C2-4, C3-5) and four derived disomic subclones (C2-4-3, C2-4-4 and C3-5-11, C3-5-13). Duplicate RNA samples from human embyonic stem cells (H1) were included as control.
2012-10-23 | E-GEOD-38931 | biostudies-arrayexpress
Project description:Individuals with Trisomy 21 (T21) exhibit numerous hematological abnormalities, including reductions in numbers of circulating B and T lymphocytes. To elucidate molecular mechanisms underlying these phenotypes, we differentiated human isogenic disomic and trisomic pluripotent cells, and observed that trisomic cells showed defects in B cell, but not T, cell differentiation. Global gene expression of differentiated, trisomic B cells revealed reduced expression of genes encoding endothelin signaling components, namely the Endothelin Receptor B (Ednrb), and its ligand Endothelin1 (Edn1).. Depletion of Ednrb mRNA in cord blood CD34+ cells led to defective B cell differentiation, supporting an hypothesis that low expression of Ednrb in T21 contributes to intrinsic lymphoid defects. Further evidence for the role of the Ednrb pathway in B cell differentiation was obtained through CRISPR/Cas9 gene targeting in disomic and trisomic iPS cells. Knockout of Ednrb in both cell backgrounds reduced the capacity for B cell differentiation. Collectively, this work identifies downregulation of Ednrb as a causative factor for impaired B lymphocyte generation in trisomic cells, which may contribute to defects in immune function associated with T21. Furthermore, a novel role for endothelin signaling in regulation of B cell development has been identified.
2018-05-30 | GSE110064 | GEO
Project description:Whole-genome analysis of heat shock factor binding sites in Drosophila melanogaster. Heat shock factor IP DNA or Mock IP DNA from heat shocked Kc 167 cells compared to whole cell extract on Agilent 2x244k tiling arrays.
2011-01-05 | GSE19744 | GEO
Project description:Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules).
2011-11-09 | GSE24197 | 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