Heat shock transcription factors regulate heat induced cell death in a rat histiocytoma

Prasad, Kolla V; Taiyab, Aftab; Jyothi, D; Srinivas, Usha K.; Sreedhar, Amere Subbarao

doi:10.1007/s12038-007-0058-4

Cited by 23 publications

(12 citation statements)

References 23 publications

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“…36 In mammalian cells, HSF2, a Sfl1 homolog, was suggested to induce autophagy upon heat shock although the molecular mechanism underlying its regulation was not characterized. 37 We show here that the overexpression of the Sfl1 protein greatly increases the expression of several ATG genes in yeast, especially ATG8, as well as autophagy activity in growing conditions. These results suggest that Sfl1 functions as a transcriptional activator of the autophagy pathway.…”

Section: Discussionmentioning

confidence: 65%

A large-scale analysis of autophagy-related gene expression identifies new regulators of autophagy

Bernard¹,

Jin²,

et al. 2015

Autophagy

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Autophagy is a pathway mediating vacuolar degradation and recycling of proteins and organelles, which plays crucial roles in cellular physiology. To ensure its proper cytoprotective function, the induction and amplitude of autophagy are tightly regulated, and defects in its regulation are associated with various diseases. Transcriptional control of autophagy is a critical aspect of autophagy regulation, which remains largely unexplored. In particular, very few transcription factors involved in the activation or repression of autophagy-related gene expression have been characterized. To identify such regulators, we analyzed the expression of representative ATG genes in a large collection of DNA-binding mutant deletion strains in growing conditions as well as after nitrogen or glucose starvation. This analysis identified several proteins involved in the transcriptional control of ATG genes. Further analyses showed a correlation between variations in expression and autophagy magnitude, thus identifying new positive and negative regulators of the autophagy pathway. By providing a detailed analysis of the regulatory network of the ATG genes our study paves the way for future research on autophagy regulation and signaling.

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Section: Discussionmentioning

confidence: 65%

A large-scale analysis of autophagy-related gene expression identifies new regulators of autophagy

Bernard¹,

Jin²,

et al. 2015

Autophagy

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“…Heat-induced changes in the biophysical properties of membranes can also result in alterations in water (48) or solute (8) permeability that could have secondary effects on membrane potential, action potential propagation, or contractile function. For example, swelling of muscle fibers, which has been shown to occur in cells at high temperature, could potentially have an influence on the lattice structure of the contractile machinery, and thus reduce force development (51).…”

Section: Discussionmentioning

confidence: 99%

Thermal tolerance of contractile function in oxidative skeletal muscle: no protection by antioxidants and reduced tolerance with eicosanoid enzyme inhibition

Oliver

Wright²,

Parinandi³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Mechanisms for the loss of muscle contractile function in hyperthermia are poorly understood. This study identified the critical temperature, resulting in a loss of contractile function in isolated diaphragm (thermal tolerance), and then tested the hypotheses 1) that increased reactive oxygen species (ROS) production contributes to the loss of contractile function at this temperature, and 2) eicosanoid metabolism plays an important role in preservation of contractile function in hyperthermia. Contractile function and passive force were measured in rat diaphragm bundles during and after 30 min of exposure to 40, 41, 42 or 43 degrees C. Between 40 and 42 degrees C, there were no effects of hyperthermia, but at 43 degrees C, a significant loss of active force and an increase in passive force were observed. Inhibition of ROS with the antioxidants, Tiron or Trolox, did not inhibit the loss of contractile force at 43 degrees C. Furthermore, treatment with dithiothreitol, a thiol (-SH) reducing agent, did not reverse the effects of hyperthermia. A variety of global lipoxygenase (LOX) inhibitors further depressed force during 43 degrees C and caused a significant loss of thermal tolerance at 42 degrees C. Cyclooxygenase (COX) inhibitors also caused a loss of thermal tolerance at 42 degrees C. Blockage of phospholipase with phospholipase A(2) inhibitors, bromoenol lactone or arachidonyltrifluoromethyl ketone failed to significantly prevent the loss of force at 43 degrees C. Overall, these data suggest that ROS do not play an apparent role in the loss of contractile function during severe hyperthermia in diaphragm. However, functional LOX and COX enzyme activities appear to be necessary for maintaining normal force production in hyperthermia.

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“…Upon stress, HSF-1 undergoes trimerization, hyperphosphorylation, translocation to the nucleus, and binding to heat shock elements and thereby activates heat shock gene transcription (20). Thus, HSF-1 activation could be indicated by the retarded migration bands in the Western blot assay due to its hyperphosphorylation.…”

Section: Cross-talk Between the Jnk2/c-jun Pathway And Hsf-1 Activatimentioning

confidence: 99%

p27 Suppresses Arsenite-induced Hsp27/Hsp70 Expression through Inhibiting JNK2/c-Jun- and HSF-1-dependent Pathways

Liu

Zhang

et al. 2010

Journal of Biological Chemistry

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p27 is an atypical tumor suppressor that can regulate the activity of cyclin-dependent kinases and G 0 -to-S phase transitions. More recent studies reveal that p27 may also exhibit its tumor-suppressive function through regulating many other essential cellular events. However, the molecular mechanisms underlying these anticancer effects of p27 are largely unknown. In this study, we found that depletion of p27 expression by either gene knock-out or knockdown approaches resulted in up-regulation of both Hsp27 and Hsp70 expression at mRNA-and promoter-derived transcription as well as protein levels upon arsenite exposure, indicating that p27 provides a negative signal for regulating the expression of Hsp27 and Hsp70. Consistently

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Heat shock transcription factors regulate heat induced cell death in a rat histiocytoma

Cited by 23 publications

References 23 publications

A large-scale analysis of autophagy-related gene expression identifies new regulators of autophagy

A large-scale analysis of autophagy-related gene expression identifies new regulators of autophagy

Thermal tolerance of contractile function in oxidative skeletal muscle: no protection by antioxidants and reduced tolerance with eicosanoid enzyme inhibition

p27 Suppresses Arsenite-induced Hsp27/Hsp70 Expression through Inhibiting JNK2/c-Jun- and HSF-1-dependent Pathways

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