Temperature Shock

Heat shock - Organisms when placed in a high temperature that is sublethal respond by producing a series of proteins and discontinuing synthesis of all other proteins. This pretreatment allows the organism to survive high temperatures that would be lethal without pretreatment.

Heat shock proteins _ HSP

Table 1 Phenotypes of multicellular eukaryotes, and the cells and tissues that they comprise,
for which Hsps are necessary and/or sufficienta
Protein Phenotype
Hsp10 Cellular: tolerance of ischemia (no phenotype) (308); tolerance of ischemia when
co-expressed with Hsp60 (308)
Hsp27 Cellular: resistance to chemotherapeutic drugs (309); resistance to hydrogen
peroxide (310, 311); resistance to hydrogen peroxide (no phenotype) (312);
resistance to ultraviolet radiation (no phenotype) (312); resistance of tumor
cells to monocytes (311); sensitivity to lymphokine-activated killer cells (no
phenotype) (311); tolerance of hyperthermia (312–316); resistance to tumor
necrosis factor (317) (310); tolerance of ischemia (318); resistance of actin
polymers to cytochalasin (314); accelerated nuclear protein aggregation (319);
accelerated decline of thermal radiosensitization (319)
Crystallin Cellular: tolerance of hyperthermia (320, 321); tolerance of ischemia (318);
resistance to tumor necrosis factor (310); resistance to hydrogen peroxide (310)
Hsp60 Cellular: tolerance of hyperthermia (no phenotype) (322, 323); tolerance of
ischemia (no phenotype) (308, 322, 323); tolerance of ischemia when
co-expressed with Hsp10 (308)
Hsp65 Cellular: tumor regression (324); loss of tumorigenicity (325)
Tissue/organ: regression of malignant tumors (324)
Hsp70 Cellular: tolerance of hyperthermia (326) (316, 322, 323, 327–342); tolerance of
ischemia/hypoxia (322, 323, 340, 343–345); recovery from translational and
transcriptional inhibition following heat shock (335); regulation of heat-shock
response (331, 346, 347); tolerance of endotoxin (348); reduced protein
denaturation upon heat exposure (349); tumorigenicity (350); cell proliferation
(351, 164); resistance to hydrogen peroxide (311); resistance of tumor cells to
monocytes (311); sensitivity to lymphokine-activated killer cells (no phenotype)
(311); escape from drug-induced cell cycle arrest (352); protein glycosylation
(353); tolerance of ultraviolet radiation (354); apoptosis (351, 355, 356);
resistance to apoptosis (no phenotype) (328, 329)
Tissue/organ: recovery of contractility after ischemia (345, 357–359); reduction
in myocardial infarct size (345, 359); reduction of hyperthermic damage to
midgut (221); resistance of heart to ischemic injury (357–359); resistance of
hippocampus to ischemic injury (360)
Organismal: tolerance of hyperthermia (18–20, 109, 156, 203, 221, 224, 278, 361);
growth and development (222); regulation of heat-shock response (361);
persistence in nature (no phenotype) (277)
Hsc70 Organismal: tolerance of hyperthermia (203)
Hsp72 Cellular: apoptosis (no phenotype) (362); protection against heat-induced nuclear
protein aggregation (319); protection against hypoxia (363); protection against
thermal radiosensitization (319)
Tissue/organ: reduction in myocardial infarct size (364)
Grp78 Cellular: protein secretion (229–231)
Protein Phenotype
Hsp90 Cellular: tolerance of hyperthermia (322, 323, 328, 329, 340); tolerance of
ischemia (no phenotype) (322, 323, 340); apoptosis (362); apoptosis
(no phenotype) (328, 329); cell proliferation and cell cycle control (365);
glucocorticoid receptor function (205)
Hsp100 Organismal: host infection in Leishmania (126)
Hsp101 Cellular: tolerance of hyperthermia (366)
Many Hsps Cellular: recovery of cell proliferation after heat shock (367); recovery from
chromosome damage after heat shock (367–369); tolerance of hyperthermia
(370, 371); tolerance of ischemia (336)
HSF Organismal: oogenesis and development (372); thermotolerance (372, 373)
aIn all cited work, specific Hsps have undergone experimental or natural manipulation.