Movatterモバイル変換


[0]ホーム

URL:


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

NIH NLM Logo
Log inShow account info
Access keysNCBI HomepageMyNCBI HomepageMain ContentMain Navigation
pubmed logo
Advanced Clipboard
User Guide

Full text links

Elsevier Science full text link Elsevier Science
Full text links

Actions

.1997 Jun 27;235(3):474-8.
doi: 10.1006/bbrc.1997.6810.

Expression of ST2, an interleukin-1 receptor homologue, is induced by proinflammatory stimuli

Affiliations

Expression of ST2, an interleukin-1 receptor homologue, is induced by proinflammatory stimuli

S Kumar et al. Biochem Biophys Res Commun..

Abstract

ST2/T1 is an orphan receptor highly homologous to the IL-1 receptor. Using ST2 cDNA, ST2 specific primers, and a polyclonal antibody generated against ST2, the expression of mRNA and protein corresponding to both the soluble and membrane anchored forms of ST2 was studied. ST2 mRNAs were ubiquitously expressed in all the human tissues examined and were induced by cytokines and phorbol esters. Three different species of mRNAs were observed in different human cells and tissues. In contrast, only two species of ST2 mRNAs were observed in murine Balb/c-3T3 cells and no ST2 mRNA was seen in most tissues of normal mice. However, in a murine model where mouse ears are exposed to UVB irradiation leading to inflammation, ST2 mRNA was expressed 48 h post UV exposure. Similarly, in Balb/c-3T3 cells, the expression of soluble ST2 mRNA and protein was induced by pro-inflammatory stimuli such as TNF, IL-1alpha, IL-1beta and PMA in both exponentially growing and quiescent cells. The expression of the membrane ST2, however, remained constant. These data suggest a role for ST2 in inflammation.

PubMed Disclaimer

MeSH terms

Substances

Associated data

LinkOut - more resources

Full text links
Elsevier Science full text link Elsevier Science
Cite
Send To

NCBI Literature Resources

MeSHPMCBookshelfDisclaimer

The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Unauthorized use of these marks is strictly prohibited.


[8]ページ先頭

©2009-2025 Movatter.jp