Disease relevance of Heat-Shock Response

• The dnaK protein modulates the heat-shock response of Escherichia coli [1].
• Membrane physical state controls the signaling mechanism of the heat shock response in Synechocystis PCC 6803: identification of hsp17 as a "fluidity gene" [2].
• Several known inducers of the heat shock response (heat stress, arsenite, and heavy metals) were shown to cause a significant elevation of c-fos mRNA in HeLa cells [3].
• Surprisingly, we show that this aggregate-prone protein with a polyalanine expansion can also protect against polyglutamine toxicity, which can be explained by induction of heat-shock response [4].
• A heat-shock response was also seen in an oculopharyngeal muscular dystrophy mouse model expressing an authentic polyalanine-expanded protein [4].

Psychiatry related information on Heat-Shock Response

• Geldanamycin activates a heat shock response and inhibits huntingtin aggregation in a cell culture model of Huntington's disease [5].
• An abnormal APP heat shock response could increase accumulation of A beta, the APP metabolite found in Alzheimer's disease amyloid plaques [6].

High impact information on Heat-Shock Response

• Heat shock factor and the heat shock response [7].
• Like RNA polymerase II, topoisomerase I is recruited to heat-shock genes during the heat-shock response [8].
• Effect of sodium salicylate on the human heat shock response [9].
• During attenuation of the heat shock response, transcription of heat shock genes returns to basal levels and HSF1 reverts to an inert monomer [10].
• Alteration in the level of HSBP1 expression in C. elegans has severe effects on survival of the animals after thermal and chemical stress, consistent with a role for HSBP1 as a negative regulator of the heat shock response [11].

Chemical compound and disease context of Heat-Shock Response

• The heat shock response of Mycobacterium tuberculosis has been characterized in detail by one- and two-dimensional polyacrylamide gel electrophoresis after metabolic labeling with [35S]methionine and 14C-amino acids [12].
• Previously, we reported that prolactin (PRL)-dependent Nb2 lymphoma cells exhibit an aberrant heat shock response because of cysteine protease-mediated fragmentation of the heat shock transcription factor (HSF) [13].
• These results show that both the cold shock response induced by some antibiotics and the heat shock response induced by ethanol may lead to enhanced expression of certain heterologous proteins in E. coli [14].
• Inhibition of the heat shock response and synthesis of glucose-regulated proteins in Ca2+-deprived rat hepatoma cells [15].
• The aim of this study was to investigate whether repeated exposure to hyperthermia or to the stress protein activating cyclopentenone prostaglandin 15-deoxy-delta(12,14)-prostaglandin J2 (15dPGJ2) leads to adaptation of the cells, attenuation of the heat shock response, and abrogation of the protective effect [16].

Biological context of Heat-Shock Response

• These results reveal that the repression of heat shock gene transcription, which occurs during attenuation, is due to the association of Hsp70 with the HSF1 transactivation domain, thus providing a plausible explanation for the role of molecular chaperones in at least one key step in the autoregulation of the heat shock response [10].
• We propose that Bag1 functions in the heat-shock response to coordinate cell growth signals and mitogenesis, and that Hsp70 functions as a sensor in stress signalling [17].
• Among the genes whose expression is regulated by this protein are those that participate in nitrogen metabolism, carbon metabolism, electron transport, inositol metabolism, heat shock response, meiosis, and sporulation [18].
• The cloned CYP1 promoter confers heat-inducible expression upon a reporter gene, and transcriptional induction is mediated through sequences similar to the consensus heat shock response element [19].
• Transcriptional activation of the heat shock genes during the heat shock response in Drosophila has been intimately linked to phosphorylation of histone H3 at serine 10, whereas repression of non-heat-shock genes correlates with dephosphorylation of histone H3 [20].

Anatomical context of Heat-Shock Response

• Attenuation of the heat shock response in HeLa cells is mediated by the release of bound heat shock transcription factor and is modulated by changes in growth and in heat shock temperatures [21].
• To establish a biological role for HSBP1, the homologous Caenorhabditis elegans protein was overexpressed in body wall muscle cells and was shown to block activation of the heat shock response from a heat shock promoter-reporter construct [11].
• Concurrent collapse of keratin filaments, aggregation of organelles, and inhibition of protein synthesis during the heat shock response in mammary epithelial cells [22].
• Null cells lacking HSF3, yet expressing normal levels of HSF1, exhibited a severe reduction in the heat shock response, as measured by inducible expression of heat shock genes, and did not exhibit thermotolerance [23].
• The influence of cell hydration and taurine on the heat shock response was studied in primary rat hepatocytes [24].

Associations of Heat-Shock Response with chemical compounds

• This heat-shock response was blocked by actinomycin D added before heat exposure [25].
• We report that induction of the heat shock response in cortical cultures protects neurons from glutamate-induced excitotoxicity [26].
• The 1,25-(OH)2D3-induced amplification of the heat shock response likely represents a mechanism for counteracting the Ca2+-associated enhanced susceptibility to oxidative injury due to 1,25-(OH)2D3 [27].
• We looked for gene(s) which, when present in multicopy, prevent the constitutive heat shock response associated with htrC mutant bacteria or caused by the presence of puromycin [28].
• These same adenylylated nucleotides accumulate after exposure to ethanol, an agent also known to induce the heat-shock response in a variety of cells [29].

Gene context of Heat-Shock Response

• Expression of genes under the control of known heat shock-inducible promoter elements (HSEs and STREs) was not compromised in PKC1 pathway mutants, indicating that this pathway mediates a novel aspect of the yeast heat shock response [30].
• In contrast, nonsteroidal antiinflammatory drugs triggered only an incomplete heat shock response, with HSF1 activation but not hsp70 induction, whereas steroids and immunosuppressive drugs did not affect the heat shock response at all [31].
• Overexpression of DROJ1 in Drosophila SL2 cells delays the onset of the heat shock response [32].
• Hsp78 appears to act in concert with other mitochondrial chaperone proteins since a conditioning pretreatment of the cells to induce the cellular heat shock response is required to maintain mitochondrial functions under severe temperature stress [33].
• We show that the Gcn5/Ada complex is selectively required for the unfolded protein response but not for the heat shock response [34].

Analytical, diagnostic and therapeutic context of Heat-Shock Response

• Analysis of protein binding to a consensus heat shock element (HSE) by electrophoretic mobility shift assay suggests that the induction of the heat shock response by TBT was attributable to activation of the heat shock transcription factor (HSTF) [35].
• The magnitude of heat shock response determined by Northern blotting did not always correlate with the level of HSF1 expression, suggesting that not only HSF1 but also HSF3 may be a major factor mediating stress signals to heat shock gene expression in the chicken [36].
• In the present study, mouse embryos from inbred strains known to differ in terms of their sensitivity to heat-induced exencephaly were treated in vivo and their heat shock response determined using SDS-PAGE electrophoretic techniques [37].
• Western blot analysis of the products showed that degradation of rscuPA was much larger at 37 degrees C than at 30 degrees C. Using E. coli CAG630 carrying the htpR mutation, which avoids heat shock response, for expression of rscuPA eliminated the instability of the product at both temperatures [38].
• Ketamine can provide protective effects, through its anti-inflammatory properties, as shown in animal models of septic shock and endotoxemia, and has elicited the heat-shock response (HSR) in experimental studies [39].

References