Delayed liver regeneration and increased susceptibility to chemical hepatocarcinogenesis in transgenic mice expressing a dominant-negative mutant of connexin32 only in the liver.

Abstract excerpt

A growing body of evidence from in vitro studies indicates that gap junction proteins connexins may have a tumor-suppressor function. Our previous double transfection experiments on HeLa cells have shown that a dominant-negative mutant V139 M of connexin32 (Cx32) can abolish gap junctional intercellular communication (GJIC). To examine whether the same dominant-negative mutant of Cx32 inhibits GJIC between...

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