More MS news articles for June 2002

A novel transactivating factor that regulates IFN-g dependent gene expression

http://www.jbc.org/cgi/content/abstract/M202679200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=Meng+Q&searchid=1024060586940_5056&stored_search=&FIRSTINDEX=0&sortspec=Score+desc+PUBDATE_SORTDATE+desc

J. Biol. Chem, 10.1074/jbc.M202679200
Junbo Hu, Qingjun Meng, Sanjit K. Roy, Abhijit Raha, Jiadi Hu, Jun Zhang, Katsuyuki Hashimoto, and Dhananjaya V Kalvakolanu
Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201

We have previously identified a novel Interferon stimulated cis-acting enhancer element, g-IFN activated transcriptional element (GATE).

GATE differs from the known IFN stimulated elements in its primary sequence.

Preliminary analysis has indicated that GATE dependent transcriptional response requires the binding of novel transacting factors.

A cDNA expression library derived from an IFN-g stimulated murine macrophage cell line was screened with a 32P-labeled GATE probe to identify the potential GATE binding factors.

A cDNA coding for novel transcription activating factor was identified.

Based on its discovery, we named it as GATE binding factor -1 (GBF-1).

GBF-1 homologues are present in mouse, human, monkey and Drosophila.

It activates transcription from reporter genes carrying GATE.

It possesses a strong transactivating activity but has a weak DNA binding property.

GBF-1 is expressed in most tissues with relatively higher steady state levels in heart, liver, kidney and brain.

Its expression is induced by IFN-g treatment.

GBF-1 is present in both cytosolic and nuclear compartments.

These studies thus identify a novel transactivating factor in IFN-signaling pathways.

Copyright © 2002 by the American Society for Biochemistry and Molecular Biology