Accession Number : ADA439227


Title :   Endothelial Genes


Descriptive Note : Annual summary


Corporate Author : CALIFORNIA UNIV LOS ANGELES


Personal Author(s) : Nguyen Brooks, Mai H.


Full Text : http://www.dtic.mil/get-tr-doc/pdf?AD=ADA439227


Report Date : JUN 2005


Pagination or Media Count : 19


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 fi%ther clari?y 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.


Descriptors :   *GENES , *ANGIOGENESIS , ACTIVATION , STIMULATION(GENERAL) , MOLECULES , HYPOTHESES , IMMUNOASSAY , ENDOTHELIUM , MITOSIS , TRANSFECTION , PHOSPHORUS TRANSFERASES , ANATOMICAL MODELS , CHEMICAL PRECIPITATION , PROTEINS , COMPARISON , SIGNALS.


Subject Categories : MEDICINE AND MEDICAL RESEARCH


Distribution Statement : APPROVED FOR PUBLIC RELEASE