Prostaglandin A1 enhances c-fos expression and activating protein-1 activity

Ishikawa, Takahiro; Sekine, Nobuo; Hata, Keisuke; Igarashi, Tetsuya; Fujita, Toshiro

doi:10.1016/s0303-7207(00)00241-0

Cited by 8 publications

(3 citation statements)

References 46 publications

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“…The complex controls the expression of numerous genes implicated in cell cycle regulation, as well as cell migration and death. Upon proteotoxicity, HFS1 binds to an HSE located in the Fos1 promoter, and Fos1 expression is increased in a HFS1-dependent manner, (Tables 1 and S1) [134,135]. HSF2 also activates Fos1 transcription [136].…”

Section: Hsf-1 In Cell Growth and Proliferationmentioning

confidence: 99%

Roles of heat shock factor 1 beyond the heat shock response

Barna

Csermely

Vellai

2018

Cell. Mol. Life Sci.

148

108

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Various stress factors leading to protein damage induce the activation of an evolutionarily conserved cell protective mechanism, the heat shock response (HSR), to maintain protein homeostasis in virtually all eukaryotic cells. Heat shock factor 1 (HSF1) plays a central role in the HSR. HSF1 was initially known as a transcription factor that upregulates genes encoding heat shock proteins (HSPs), also called molecular chaperones, which assist in refolding or degrading injured intracellular proteins. However, recent accumulating evidence indicates multiple additional functions for HSF1 beyond the activation of HSPs. Here, we present a nearly comprehensive list of non-HSP-related target genes of HSF1 identified so far. Through controlling these targets, HSF1 acts in diverse stress-induced cellular processes and molecular mechanisms, including the endoplasmic reticulum unfolded protein response and ubiquitin-proteasome system, multidrug resistance, autophagy, apoptosis, immune response, cell growth arrest, differentiation underlying developmental diapause, chromatin remodelling, cancer development, and ageing. Hence, HSF1 emerges as a major orchestrator of cellular stress response pathways.

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Section: Hsf-1 In Cell Growth and Proliferationmentioning

confidence: 99%

Roles of heat shock factor 1 beyond the heat shock response

Barna

Csermely

Vellai

2018

Cell. Mol. Life Sci.

148

108

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“…Expression of FOS is induced by growth factors, cytokines and cellular stress . Treatment of cells with stimuli that induce the heat shock response, such as heat, arsenite, cadmium and prostaglandin A1, leads to an increase in FOS mRNA, which requires stress‐induced binding of heat shock transcription factor HSF1 to the heat shock element (HSE) in the FOS promoter . The FOS HSE is also constitutively bound by HSF2, a member of the HSF family, which serves to maintain normal FOS expression .…”

Section: Introductionmentioning

confidence: 99%

The proto-oncogeneJUNis a target of the heat shock transcription factor HSF1

Sawai

Ishikawa

Ota

et al. 2013

FEBS J

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The transcription factor activator protein‐1 (AP‐1) participates in many aspects of cell physiology, such as cellular proliferation, transformation, and death. AP‐1 is a dimeric complex that primarily contains Jun and Fos family members. Here, we report that JUN is a target of heat shock transcription factor HSF1. HSF1 is the master regulator of genes encoding molecular chaperones, and is involved in cellular processes such as the stress response, cell differentiation, aging and carcinogenesis. In HeLa cells, JUN transcription was rapidly induced by heat treatment. We found that HSF1 bound to the JUN promoter and was necessary for its efficient response to heat shock. In heat‐shocked cells, c‐Jun‐mediated gene expression was induced slowly following accumulation of c‐Jun protein. Forced expression of active HSF1 in cells resulted in an increase in c‐Jun expression and activation of c‐Jun target genes. These results show that HSF1 regulates JUN expression, thereby modulating AP‐1 activity.

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“…The interactions of cyPG with various protein targets and biochemical processes along the AP-1 activation pathway provide an example of the complexity of the mechanism of action of these prostanoids. (A) cyPG have been reported to modulate the activity of various kinases, including ERK, JNK and p38 [124][125][126], which in turn have an impact on the activity of the promoters of AP-1 components, such as c-fos and c-jun, thus contributing to the regulation of their cellular levels [35,127]. (B) Activation of PPAR by cyPG may result in inhibition of AP-1 activity by protein-protein interaction, sequestration of cofactors, or impairment of DNA binding [52].…”

Section: Biological Effects and Mechanisms Of Action Of Cypgmentioning

confidence: 99%