Molecular Chaperones and the Nuclear Response to Stress

Author(s):  
Lynn Boyd ◽  
Katherine M. Sampuda
2004 ◽  
pp. 1002-1005 ◽  
Author(s):  
Barbara Despres ◽  
Pierre Goloubinoff

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Anmin Yu ◽  
Ping Li ◽  
Ting Tang ◽  
Jiancai Wang ◽  
Yuan Chen ◽  
...  

Hsp70s (heat shock protein 70s) are a class of molecular chaperones that are highly conserved and ubiquitous in organisms ranging from microorganisms to plants and humans. Most research on Hsp70s has focused on the mechanisms of their functions as molecular chaperones, but recently, studies on stress responses are coming to the forefront. Hsp70s play key roles in cellular development and protecting living organisms from environmental stresses such as heat, drought, salinity, acidity, and cold. Moreover, functions of human Hsp70s are related to diseases including neurological disorders, cancer, and virus infection. In this review, we provide an overview of the specific roles of Hsp70s in response to stress, particularly abiotic stress, in all living organisms.


2008 ◽  
Vol 42 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Eirini Meimaridou ◽  
Sakina B Gooljar ◽  
J Paul Chapple

Molecular chaperones are best recognized for their roles in de novo protein folding and the cellular response to stress. However, many molecular chaperones, and in particular the Hsp70 chaperone machinery, have multiple diverse cellular functions. At the molecular level, chaperones are mediators of protein conformational change. To facilitate conformational change of client/substrate proteins, in manifold contexts, chaperone power must be closely regulated and harnessed to specific cellular locales – this is controlled by cochaperones. This review considers specialized functions of the Hsp70 chaperone machinery mediated by its cochaperones. We focus on vesicular trafficking, protein degradation and a potential role in G protein-coupled receptor processing.


2020 ◽  
Vol 63 (10) ◽  
pp. 3311-3325
Author(s):  
Brittany L. Perrine ◽  
Ronald C. Scherer

Purpose The goal of this study was to determine if differences in stress system activation lead to changes in speaking fundamental frequency, average oral airflow, and estimated subglottal pressure before and after an acute, psychosocial stressor. Method Eighteen vocally healthy adult females experienced the Trier Social Stress Test (TSST) to activate the hypothalamic–pituitary–adrenal axis. The TSST includes public speaking and performing mental arithmetic in front of an audience. At seven time points, three before the stressor and four after the stressor, the participants produced /pa/ repetitions, read the Rainbow Passage, and provided a saliva sample. Measures included (a) salivary cortisol level, (b) oral airflow, (c) estimated subglottal pressure, and (d) speaking fundamental frequency from the second sentence of the Rainbow Passage. Results Ten of the 18 participants experienced a hypothalamic–pituitary–adrenal axis response to stress as indicated by a 2.5-nmol/L increase in salivary cortisol from before the TSST to after the TSST. Those who experienced a response to stress had a significantly higher speaking fundamental frequency before and immediately after the stressor than later after the stressor. No other variable varied significantly due to the stressor. Conclusions This study suggests that the idiosyncratic and inconsistent voice changes reported in the literature may be explained by differences in stress system activation. In addition, laryngeal aerodynamic measures appear resilient to changes due to acute stress. Further work is needed to examine the influence of other stress systems and if these findings hold for dysphonic individuals.


1961 ◽  
Vol 37 (4) ◽  
pp. 565-576 ◽  
Author(s):  
Richard A. Miller

ABSTRACT Four per cent formaldehyde, insulin, or epinephrine in oil was injected for 5 days into pigeons subjected to varying degrees of hypophysectomy alone or together with large lesions in the median eminence and hypothalamus. Adrenals atrophied after the removal of the pars distalis alone or together with the neurohypophysis in untreated pigeons but showed markedly hypertrophic interrenal tissue (cortex in mammals) after treatment with formaldehyde or insulin. The slope of the dose-response curve was similar in operated and unoperated pigeons. The accumulation of bile in the liver parenchyma, which may occur after removal of the pars distalis, is an endogenous stress which was associated regularly with adrenal hypertrophy. After very large lesions of the median eminence and ventral hypothalamus in addition to total hypophysectomy, adrenals hypertrophied rather than atrophied, and the response to formaldehyde paralleled that in intact and »hypohysectomized« pigeons. Interrenal tissue was stimulated regularly; chromaffin tissue was partially degranulated, sometimes showed hyperplasia with colchicine, but only occasionally appeared hypertrophied. Epinephrine in nearly lethal doses caused only minimal adrenal enlargement. After adrenal denervation followed by hypophysectomy, the adrenals were still stimulated by formaldehyde. It appears that the interrenal tissue of the pigeon responds to a humoral stimulus not of hypophyseal origin in the absence of the hypophyseal-hypothalamic system.


1962 ◽  
Vol 39 (1) ◽  
pp. 79-86 ◽  
Author(s):  
J. R. Hodges ◽  
Joan Vernikos-Danellis

ABSTRACT Pituitary and blood corticotrophin (ACTH) concentrations were estimated in adrenalectomized rats maintained on cortisol or crude adrenocortical extract (ACE) with and without ascorbic acid. Blood ACTH levels were also determined in similarly treated animals after subjection to mild stress. Thirty days after adrenalectomy there were marked rises in pituitary and blood corticotrophin concentration which were prevented by daily treatment with small doses of cortisol or ACE. In contrast to intact animals, adrenalectomized rats exhibited markedly increased adrenocorticotrophic responses to mild stress. This pituitary hyperexcitability was not diminished by replacement therapy with corticoids alone but was considerably reduced by ascorbic acid given in conjunction with ACE. It is suggested that corticoids control the rate at which ACTH is synthesised in the pituitary gland and that other factors, including ascorbic acid, control the excitability of the pituitary gland in its adrenocorticotrophic response to stress.


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