Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1996 Aug;16(8):4273-80.
doi: 10.1128/MCB.16.8.4273.

Signals from the stressed endoplasmic reticulum induce C/EBP-homologous protein (CHOP/GADD153)

X Z Wang  1 , B Lawson, J W Brewer, H Zinszner, A Sanjay, L J Mi, R Boorstein, G Kreibich, L M Hendershot, D Ron
Affiliations

Signals from the stressed endoplasmic reticulum induce C/EBP-homologous protein (CHOP/GADD153)

X Z Wang et al. Mol Cell Biol. 1996 Aug.

Abstract

The gene encoding C/EBP-homologous protein (CHOP), also known as growth arrest and DNA-damage-inducible gene 153 (GADD153), is activated by agents that adversely affect the function of the endoplasmic reticulum (ER). Because of the pleiotropic effects of such agents on other cellular processes, the role of ER stress in inducing CHOP gene expression has remained unclear. We find that cells with conditional (temperature-sensitive) defects in protein glycosylation (CHO K12 and BHK tsBN7) induce CHOP when cultured at the nonpermissive temperature. In addition, cells that are defective in initiating the ER stress response, because of overexpression of an exogenous ER chaperone, BiP/GRP78, exhibit attenuated inducibility of CHOP. Surprisingly, attenuated induction of CHOP was also noted in BiP-overexpressing cells treated with methyl methanesulfonate, an agent thought to activate CHOP by causing DNA damage. The roles of DNA damage and growth arrest in the induction of CHOP were therefore reexamined. Induction of growth arrest by culture to confluence or treatment with the enzymatic inhibitor N-(phosphonacetyl)-L-aspartate did not induce CHOP. Furthermore, both a DNA-damage-causing nucleoside analog (5-hydroxymethyl-2'-deoxyuridine) and UV light alone did not induce CHOP. These results suggest that CHOP is more responsive to ER stress than to growth arrest or DNA damage and indicate a potential role for CHOP in linking stress in the ER to alterations in gene expression.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Genes Dev. 1994 Nov 1;8(21):2513-26 - PubMed
    1. Mol Cell Biol. 1993 Oct;13(10):6367-74 - PubMed
    1. Carcinogenesis. 1995 May;16(5):1173-9 - PubMed
    1. J Cell Biol. 1995 Oct;131(2):371-83 - PubMed
    1. Annu Rev Biochem. 1995;64:345-73 - PubMed

Publication types

MeSH terms