Cellular Ras partly mediates gap junction closure by the polyoma virus middle tumor antigen.
Endogenous, cellular Ras proteins (c-Ras) mediate the transforming action of the polyoma virus middle Tumor antigen (mT), which is accompanied by elimination of gap junctional, intercellular communication (GJIC). In this report we show that reducing the c-Ras content of murine C3H10T1/2 fibroblasts (10T1/2) through the expression of an anti-sense ras gene, increased GJIC by 60-80% mT totally eliminated GJIC in normal 10T1/2 cells but it reduced GJIC no more than 50% in the c-Ras deficient lines. These results indicate that endogenous c-Ras is at least partly responsible for the mT-induced gap junction closure.
Brownell
H L
HL
Department of Microbiology, Queen's University, Kingston, Ontario, Canada.
Whitfield
J F
JF
Raptis
L
L
D000818:Animals; D000952:Antigens, Polyomavirus Transforming / Q000096:biosynthesis / Q000378:metabolism*; D002450:Cell Communication / Q000187:drug effects; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D003907:Dexamethasone / Q000494:pharmacology; D004558:Electric Stimulation; D018274:Electroporation; D017629:Gap Junctions / Q000187:drug effects / Q000502:physiology*; D011905:Genes, ras; D007544:Isopropyl Thiogalactoside / Q000494:pharmacology; D051379:Mice; D016283:Proto-Oncogene Proteins p21(ras) / Q000378:metabolism*; D016372:RNA, Antisense / Q000096:biosynthesis; D015032:Zinc / Q000494:pharmacology
D000952:Antigens, Polyomavirus Transforming; D016372:RNA, Antisense; D007544:Isopropyl Thiogalactoside; D003907:Dexamethasone; D016283:Proto-Oncogene Proteins p21(ras); D015032:Zinc