Heat Shock Factor Protein 1 (HSF1) ELISA Kits

Caenorhabditis elegans (C. elegans) Heat Shock Factor Protein 1 (HSF1) interaction partners

1. hsf-1 is essential for regulating cytoskeletal integrity during aging.

2. mTOR Target S6 Kinase Arrests Development in Caenorhabditis elegans When the Heat-Shock Transcription Factor Is Impaired

3. autophagy contributes to stress resistance and hormesis, and reveal a requirement for autophagy in HSF-1-regulated functions in the heat-shock response, proteostasis and ageing.

4. Heat shock transcription factor HSF-1 (HSF-1) is required for the learned avoidance behavior of toward Pseudomonas aeruginosa strain PA14 .

5. a critical role for autophagy in C. elegans stress resistance and hormesis, and reveal a requirement for autophagy in HSF-1 regulated functions in the heat-shock response, proteostasis, and aging.

6. xyloketal derivatives bound to the DNA binding domain of HSF-1, promoted the conformation of HSF-1, thus strengthened the interaction between the HSF-1 and related DNA. ALA-67, ASN-74 and LYS-80 of binding region might be the key amino residues during the interaction.

7. These functions of HPK-1/HSF-1 undergo rapid down-regulation once animals reach reproductive maturity. We show that HPK-1 fortifies proteostasis and extends longevity by an additional independent mechanism: induction of autophagy.

8. Diminution in phenotypic variation for both gene expression and life span at 25 degrees C may be a consequence of low level hsf-1-dependent expression of HSP-16.2 and other chaperones at the higher temperature.

9. We demonstrate that while DAF-16/FOXO is dispensable, the age-dependent suppression of cilia phenotypes in IFT mutants requires cell-autonomous functions of the HSF1 heat shock factor and the Hsp90 chaperone

10. HSF-1 is a codeterminant of both alcohol and nicotine sensitivity in C. elegans and that this phenotype requires the small HSP, HSP-16.48. HSP-16.48 function in drug sensitivity is unrelated to a chaperone action during the heat shock stress response.

11. Heat-stress-enhanced ascaroside production appears to be mediated at least in part by HSF-1, which seems to be important in adaptation strategies for coping with heat stress in this nematode.

12. FUdR treatment can modulate the HSR and proteostasis, and should be used with caution when used to inhibit reproduction.

13. Excitation of the AFD thermosensory neurons is sufficient to activate HSF1 in another cell, even in the absence of temperature increase. Excitation of the AFD thermosensory neurons enhances serotonin release.

14. hsf-1 RNAi suppressed the restoration of thrashing reduced by heat stress. In contrast, hsf-1 knockdown cancelled prevention of movement reduction in a daf-2 mutant, but didn't suppress thrashing restoration in daf-2 mutant.

15. we engaged C. elegans mutants and identified that the p38 MAPK signaling, insulin/IGF-1 signaling (IIS), and HSF-1 play pivotal roles in the WCESP-mediated host immune response

16. HSF-1 has a prominent role in cytoskeletal integrity, ensuring cellular function during stress and aging. Overexpression of pat-10 increased actin filament stability, thermotolerance, and longevity, indicating that in addition to chaperone regulation, HSF-1 has a prominent role in cytoskeletal integrity, ensuring cellular function during stress and aging.

17. HSF-1 represses the expression of daf-7 encoding a TGF-beta ligand, to induce young larvae to enter the dauer stage, a developmentally arrested, non-feeding, highly stress-resistant, long-lived larval form triggered by crowding and starvation.

18. required for daf-2-insulin/IGF-1 receptor mutations to extend life-span

19. downstream transcription factors, heat shock factor 1, and DAF-16 regulate opposing disaggregation and aggregation activities to promote cellular survival in response to constitutive toxic Abeta(1-42) aggregation

20. Increased temperature results in the activation of a conserved pathway involving the heat-shock (HS) transcription factor (HSF)-1 that enhances immunity in the invertebrate Caenorhabditis elegans.

Mouse (Murine) Heat Shock Factor Protein 1 (HSF1) interaction partners

1. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence.

2. HSF1 phosphorylation at both Ser303 (S303) and Ser307 (S307) has been shown to repress HSF1 transcriptional activity under normal physiological growth conditions. Our results confirmed that loss of phosphorylation in HSF1(303A/307A) cells and tissues increases protein stability but also markedly sensitizes HSF1 activation under normal and heat- or nutrient-induced stress conditions.

3. The upregulation of miR-195a-3p due to HSF1 deficiency impaired cardiac angiogenesis by regulating AMPKalpha2/VEGF signaling.

4. The results suggest that HSF1 and NRF2 suppress heme-induced and heat-induced HO-1 expression, respectively.

5. Hypercapnia-mediated inhibition of NF-kappaB cytokine production is dependent on HSF1 expression and/or activation.

6. Variations in brain defects result from cellular mosaicism in the activation of Hsf1 heat shock signaling.

7. Downregulation of miR-199b-5p induced differentiation of Bone-marrow mesenchymal stem cells toward cardiomyocyte-like cells partly via the HSF1/HSP70 signaling pathway.

8. RIP140 is a co-repressor of HSF1, and it regulates neuronal stress response.

9. The results collectively suggest that in the pressure overload heart failure model, HSF1 promoted formation of macrophages by inducing upregulation of HIF-1 expression, through which heart failure was ameliorated.

10. These results provide new insight into HSF1 as a novel host factor for dengue virus infection through its role in facilitating autophagy-regulated viral replication in the brains.

11. HSF1 activity is decreased in fibrotic hearts. HSF1 inhibits phosphorylation and nuclear distribution of Smad3 via direct binding to Smad3. Active Smad3 blocks the anti-fibrotic effect of HSF1.

12. the expression level of NFATc2, miR-208b and miR-499 suggested that these responses were suppressed in HSF1-null mice

13. identify 4 huntingtin-targeting miRNAs viz. miR-125b, miR-146a, miR-150 and miR-214 as candidate miRNAs responsible for observed inhibitory effect of HSF1 on huntingtin expression.

14. HSF1 plays an important role in the occurrence of UVR-B-induced cataracts, possibly via regulation of HSPs such as HSP25.

15. Targeted deletion of HSF1 results in changes of locomotor function associated with changes in cerebellar calbindin protein levels. These findings suggest a role of HSF1 in regular Purkinje cell calcium homeostasis.

16. this study shows that HSF1 overexpression protects against TDP-43 pathology by upregulation of chaperones, especially HSP70, rather than enhancing autophagy

17. Acetylation of the protein triggers TDP-43 pathology in cultured cells and mouse skeletal muscle, which can be cleared through an HSF1-dependent chaperone mechanism that disaggregates the protein.

18. These findings provide insight into the role of HSF1 in Leydig cell steroidogenesis, suggesting that it maintains cholesterol transport by recovering StAR under chronic heat stress.

19. In mammalian cell lines, only heat shock-induced but not basal expression of chaperones is dependent on the mammalian Hsf1 homolog.

20. Upregulating HSF1 relieves the tau toxicity in N2a-TauRD DeltaK280 by reducing CHOP and increasing HSP70 a5 (BiP/GRP78). Our work reveals how the bidirectional crosstalk between the two stress response systems promotes early tau pathology and identifies HSF1 being one likely key player in both systems.

Human Heat Shock Factor Protein 1 (HSF1) interaction partners

1. A 90-bp sequence around the intronic single nucleotide polymorphism rs2802292 has enhancer functions, and that the rs2802292 G-allele creates a novel HSE binding site for HSF1, which induces FOXO3 expression in response to diverse stress stimuli.

2. These data support the hypothesis that fibronectin is stress-responsive and a functional HSF1 target gene.

3. HSF1 stimulated GLS1-dependent mTOR activation to promote colorectal carcinogenesis.

4. We show that prior to heat shock, the HSF1-PARP13-PARP1 complex binds to the HSP70 promoter. In response to heat shock, activated and auto-PARylated PARP1 dissociates from HSF1-PARP13 and is redistributed throughout the HSP70 locus.

5. These findings suggest that NRF2 and HSF1 have opposing roles during autophagy, and illustrate the existence of tight mechanistic links between the cellular stress responses.

6. Study compared the effect of different heavy metals, concerning their potential to activate HSF1 with a sensitive artificial heat shock reporter cell line, consisting of heat shock elements (HSE). Results indicate that the importance of the individual binding sites for HSF1 is determined by their sequence similarity to the consensus sequence and their position relative to the transcription start site.

7. Results show that the expression of HSF1 in both cancer-associated fibroblasts (CAFs) and tumor cells was positively associated with poor prognosis and oral squamous cell carcinoma (OSCC). Moreover, HSF1 expression in CAFs induced tumor cells to undergo partial EMT and enhanced the proliferation, migration and invasion of cancer cells. Its knockdown in CAFs reduced tumor growth.

8. miR-644a promotes apoptosis in HCC cells by inhibiting HSF1

9. HSF1 binds a heat shock element of lncRNA NEAT1 to promote formation of paraspeckles.

10. the mechanistic basis of HSF1 gene regulation in cancer cells and provide molecular evidence supporting a direct interaction between HSF1 and NRF2

11. High HSF1 expression is associated with glioblastoma.

12. Combining genetic knockdown of GKAP and pharmacological inhibition of NMDAR, study implicates FMRP and HSF1 as downstream effectors, which along with GKAP demonstrably support invasiveness of PanNET and pancreatic ductal adenocarcinoma cancer cells.

13. Dickkopf-3 (DKK3) is a heat shock transcription factor 1 protein (HSF1) effector that modulates the pro-tumorigenic behaviour of cancer-associated fibroblasts (CAFs), and DKK3 orchestrates a concomitant activation of beta-catenin and YAP oncogene protein (YAP)/tafazzin protein (TAZ).

14. that high heat shock factor 1 expression is significantly correlated with advanced tumour progression and poor prognosis

15. HSF1 may be closely associated with the proliferation and motility of gastric cancer cells and poor prognosis of patients with gastric cancer. Accordingly, HSF1 could serve as a prognostic marker for gastric cancer.

16. HSF1 positively regulates the transcription of latent HIV

17. A strong reduction in heat shock transcription factor 1 (HSF1) levels was evident in Huntington's Disease (HD).

18. Variations in brain defects result from cellular mosaicism in the activation of Hsf1 heat shock signaling.

19. Studies indicate that heat shock factor 1 (HSF1) acts in diverse stress-induced cellular processes and molecular mechanisms.

20. In response to DNA damage, activated and auto-poly-ADP-ribosylated PARP1 dissociates from HSF1-PARP13, and redistributes to DNA lesions and DNA damage-inducible gene loci.

Cow (Bovine) Heat Shock Factor Protein 1 (HSF1) interaction partners

1. The association between the HSF 1 expression and antioxidative activity through correlation analysis was found to be non-significant, though enzymatic activity appeared to behave in a similar fashion in both breeds at 5% level of significance, thus ruling out the role of HSF1 expression level on the activity of enzymes involved in oxidative stress in vitro in zebu and crossbred cattle.

2. As the 4693-T mutation caused the disruption of microRNA target binding (resulting in the relief of the transcriptional repression), the HSF1 gene is useful in dairy cattle thermal tolerant breeding.

Chlamydomonas reinhardtii (C. reinhardtii) Heat Shock Factor Protein 1 (HSF1) interaction partners

1. HSF1 is a key trans-acting factor for counteracting transgene promoter silencing in Chlamydomonas.

2. Data show that activated HSF1 and CRR1 transcription factors mediate the acetylation of histones H3/4, nucleosome eviction, remodeling of the H3K4 mono- and dimethylation marks, and transcription initiation/elongation.

3. data suggest that HSF1 is a key regulator of the stress response in Chlamydomonas

Rabbit Heat Shock Factor Protein 1 (HSF1) interaction partners

1. Data suggest that myocardial HSF1 and HSP70 (70 kDa heat-shock protein) can be up-regulated by dietary factors (here, antioxidant taurine as a dietary supplement administered to counteract effects of atherogenic diet).

Pig (Porcine) Heat Shock Factor Protein 1 (HSF1) interaction partners

1. The results indicate that Heat shock protein 70 (Hsp70) mediates distinct stress-related functions in different tissues during transportation. Heat shock factor-1 (HSF-1) levels were reduced at 1 and 4 h only in the hearts of transported pigs.

Zebrafish Heat Shock Factor Protein 1 (HSF1) interaction partners

1. that zHsf1 plays a positive role in HS-driven expression of zper2 in the dark but seems to act as an attenuator in the presence light

2. The transcriptional up-regulation of unc45b, hsp90aa1.1 and smyd1b is specific to zebrafish mutants with myosin folding defects, and is not triggered in other zebrafish myopathy models

3. data suggest that HSF1 is involved in regulating constitutive lens specific expression of hsp70 in the embryonic zebrafish