Mammalian heat shock protein families. Expression and functions

Burel, Carole; Mezger, V.; Pinto, Maria Benegelânia; Rallu, Murielle; Trigon, Sylviane; Morange, M.

doi:10.1007/bf02118307

Cited by 98 publications

(52 citation statements)

References 67 publications

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“…These effects can be explained by the finding that HSPs exert an important protective role in the cells against apoptosis induced by several kinds of damaging agents 14,15,27,28 even if their function is still not completely defined. 13,29 Moreover, growth factors can inhibit both spontaneous 10,12 and injury-mediated apoptosis. 11 We have, moreover, found that the activity of JNK-1 and MAPK p38 was increased in IFNa-treated cells while EGF reduced the activity and the expression of the phosphorylated isoforms of JNK-1 and MAPK p38 in these cells.…”

Section: Discussionmentioning

confidence: 99%

Interferon-α induces apoptosis in human KB cells through a stress-dependent mitogen activated protein kinase pathway that is antagonized by epidermal growth factor

Caraglia¹,

Abbruzzese²,

Leardi

et al. 1999

Cell Death Differ

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We have demonstrated that interferon-a2-recombinant (IFNa) at growth inhibitory concentrations enhances the expression and signalling activity of the epidermal growth factor receptor (EGF-R) in human epidermoid carcinoma KB cells. Here we report that KB cells exposed to IFNa underwent apoptotic cell death and this effect was antagonized by EGF. We have also found that IFNa enhanced the expression of heat shock proteins (HSP) HSP-70, HSP-90 and HSP-27 and activated the NH 2 -terminal Jun kinase-1 (JNK-1) and p38 mitogen activated protein kinase, the target enzymes of a stress-dependent intracellular transduction pathway. Moreover, the overexpression of the wild-type JNK-1, obtained through plasmid transfection of KB cells, induced apoptosis which was potentiated by the exposure of wild-type JNK-1 (JNK-1 wt )-transfected cells to IFNa. All these effects were neutralized by the addition of EGF to parental and JNK-1 wt -transfected KB cells exposed to IFNa. In conclusion, EGF has a protective effect on KB cells from apoptosis while antagonizing a stress response elicited by IFNa and targeted on the stress pathway terminal kinases.

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Section: Discussionmentioning

confidence: 99%

Interferon-α induces apoptosis in human KB cells through a stress-dependent mitogen activated protein kinase pathway that is antagonized by epidermal growth factor

Caraglia¹,

Abbruzzese²,

Leardi

et al. 1999

Cell Death Differ

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“…Heat shock proteins (HSPs) participate in the response to proteotoxic stress, caused by elevated temperature and/or chemical insults (Burel et al 1992;Voellmy 1996). As chaperones, HSPs bind to and refold denatured cellular proteins or target ubiquitin ligases to damaged proteins, so that these can be recognized and degraded by the proteasome (Hirsch et al 2006).…”

Section: Systemically and Oscillator-driven Genesmentioning

confidence: 99%

Regulation of Circadian Gene Expression in Liver by Systemic Signals and Hepatocyte Oscillators

Kornmann

Schaad²,

Reinke³

et al. 2007

Cold Spring Harbor Symposia on Quantitative Biology

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“…As both these agents are mitogenic, it is difficult to relate this expression to proliferation as in some other systems (33)(34)(35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterization of Novel Genes Modulated in the Thyroid of Dogs Treated with Methimazole and Propylthiouracil

Wilkin¹,

Savonet²,

Radulescu³

et al. 1996

Journal of Biological Chemistry

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Induction of cell proliferation by mitogen or growth factor stimulation leads to the specific stimulation or repression of a large number of genes. To better understand differentiated epithelial cell growth regulation, we have initiated a study to identify genes which are regulated by the thyrotropin-dependent mitogenic pathway in dog thyroid cells. A thyroid cDNA library was prepared from a methimazole and propylthiouraciltreated dog and differentially screened with probes derived from control or stimulated thyroids. Among 19 clones isolated, 6 encode known proteins (inwardly rectifying potassium channel, nucleosome assembly protein, ribosomal protein L7, elongation factor 1␣, nonmuscle myosin light chain, and heat shock protein 90␤). The 13 others correspond to proteins whose function is unknown. Among them, 5 correspond to mRNAs whose expression was modulated by mitogenic stimulation of thyrocytes in primary culture. A preliminary characterization of two of these cDNAs is reported: clone 5, which might represent a novel, atypical protein kinase, and clone 3, which contains ankyrin-like repeats, suggesting that it might interact with other proteins.Induction of cell proliferation by mitogen or growth factor stimulation leads to the specific and sequential expression of a large number of genes (1-8): immediate early genes, induced rapidly and independently of de novo protein synthesis, delayed early genes whose transcriptional activation requires new protein synthesis, and others ending with the late G 1 genes, which are mainly enzymes involved in DNA synthesis. Conversely, the expression of other genes is also sequentially repressed after mitogenic stimulation (9 -11). Many of these regulated genes are proto-oncogenes or anti-oncogenes. Most of the known ones belong to two major classes of mitogenic pathways: the growth factors receptors tyrosine protein kinases and the phorbol ester protein kinases C cascades. A third signaling pathway, the cyclic AMP-dependent cascade, considered for a long time to be a general inhibitor of proliferation, stimulates proliferation in several epithelial cell types and in yeast (reviewed in Ref. 12). In thyroid cells, this pathway is activated by thyrotropin (TSH), 1 which is the main physiological agent regulating the thyroid gland (13,14). TSH and cyclic AMP promote cell proliferation, function, and differentiation while the mitogenic pathways elicited by EGF and tumor promoting phorbol esters are associated with the loss of expression of the differentiation specific genes (15-19). Several steps of the latter cascades are missing in the cyclic AMP pathway (14). The molecular mechanisms of this pathway are still largely unknown. We have therefore initiated a study aimed at the identification of genes that are regulated by cyclic AMP in thyroid cells.To identify new genes that might be regulated by the thyroid mitogenic pathways, we prepared a cDNA library from the thyroid of a dog treated in vivo with methimazole and propylthiouracil. The inhibition by these drugs of thyroid h...

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Mammalian heat shock protein families. Expression and functions

Cited by 98 publications

References 67 publications

Interferon-α induces apoptosis in human KB cells through a stress-dependent mitogen activated protein kinase pathway that is antagonized by epidermal growth factor

Interferon-α induces apoptosis in human KB cells through a stress-dependent mitogen activated protein kinase pathway that is antagonized by epidermal growth factor

Regulation of Circadian Gene Expression in Liver by Systemic Signals and Hepatocyte Oscillators

Identification and Characterization of Novel Genes Modulated in the Thyroid of Dogs Treated with Methimazole and Propylthiouracil

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