Disease relevance of Ect2

• Over-expression of Ect2 protein is a useful biomarker to detect exposure to nickel compounds and nickel ion-induced morphological and neoplastic cell transformation [1].

High impact information on Ect2

• Here we report a second novel transforming gene, ect2 [2].
• The ect2 oncogene was originally identified as a transforming complementary DNA (cDNA) from mouse epithelial cells in an expression cloning approach and encodes a product related to Rho-specific exchange factors and yeast cell cycle regulators [3].
• To explore the potential role of ect2 in the cell cycle, we examined the expression of the ect2 proto-oncogene in a liver regeneration model in mice after partial (two thirds) hepatectomy [3].
• We found that the expression of the ect2 transcript and protein were markedly elevated with the onset of DNA synthesis and remained elevated during G2 and M phases [3].
• Moreover, expression of a dominant negative or an oncogenic mutant of ect2 in cultured mouse hepatocytes resulted in a large increase in the number of binucleated cells [3].

Biological context of Ect2

• R2-5 had 100% sequence identity to part of the coding region of Ect2, a mouse proto-oncogene encoding a GDP-GTP exchange factor [1].
• Ect2 gene amplification and over-expression of Ect2 mRNA and protein can cause microtubule disassembly and cytokinesis, contributing to induction and maintenance of morphological, anchorage-independent, and neoplastic transformation of these cell lines [1].
• In situ hybridization analysis showed that ect2 was expressed at a high level in cells undergoing mitosis in regenerating liver [3].
• Assignment of the ect2 protooncogene to mouse chromosome band 3B by in situ hybridization [4].
• The ECT2 N domain interacted with the catalytic domain and significantly inhibited the focus formation by oncogenic ECT2 [5].

Anatomical context of Ect2

• Whereas DeltaN-Ect2 caused formation of lamellipodia, DeltaN-Ect2 DH/PH enhanced actin stress fiber formation, suggesting that C-terminal sequences influenced Ect2 Rho GTPase specificity [6].
• The 3.9-kb Ect2 transcript was expressed at 1.6- to 3.6-fold higher steady-state levels in four Ni transformed, and in two MCA-transformed, cell lines [1].
• The Ect2 gene was amplified by 3.5- to 10-fold in Ni transformed, and by 2.5- to 3-fold in MCA transformed cell lines [1].
• Amplification of the Ect2 proto-oncogene and over-expression of Ect2 mRNA and protein in nickel compound and methylcholanthrene-transformed 10T1/2 mouse fibroblast cell lines [1].
• Among the known Rho GTPases expressed in NIH 3T3 cells, RhoA was predominantly activated by oncogenic ECT2 in vivo [5].

Associations of Ect2 with chemical compounds

• Requirement for C-terminal sequences in regulation of Ect2 guanine nucleotide exchange specificity and transformation [6].

Other interactions of Ect2

• Taken together, these observations suggest that regions of Ect2 C-terminal to the DH domain alter the profile of Rho GTPases activated in vivo and consequently may contribute to the enhanced transforming activity of DeltaN-Ect2 DH/PH/C [6].

References