Accession Number:

ADA439227

Title:

Endothelial Genes

Descriptive Note:

Annual summary

Corporate Author:

CALIFORNIA UNIV LOS ANGELES

Personal Author(s):

Report Date:

2005-06-01

Pagination or Media Count:

19.0

Abstract:

We report that EG-l can stimulate cellular proliferation. Transfection experiments which overexpressed the full length EG-l gene in human embryonic kidney HEK-293 cells or human breast cancer cell lines resulted in significantly increased in vitro proliferation, in comparison to transfection with empty vectors. On the other hand, siRNA co-transfection resulted in inhibition of proliferation. A subcutaneous xenograft assay was carried out in a SCID severe combined immunodeficient mouse model. We found that injection of high EG-l expressing llEK-293 clones resulted in significantly larger tumors, in comparison with clones carrying the enipty vectors. To fither clariy the function of this gene, we investigated its interaction with Src and members of the MAPK mitogen activated protein kinase family. Immunoprecipitation with anti-Src antibody, followed by immunoblotting with anti-EG- 1 antibody demonstrated an association between these two molecules. Over- expression fEG-l was correlajed with activation of the following kinases ERK-l and -2 extracellular signal- regulated, JNK Uun-terminal, and p38. These observations collectively support the hypothesis that the novel gene EG-I is a positive stimulator of cellular proliferation, and may possibly be involved in signaling pathways involving Src and MAPK activation.

Subject Categories:

  • Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE