The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Suppression of the tumorigenicity of mutant p53-transformed rat embryo fibroblasts through expression of a newly cloned rat nonmuscle myosin heavy chain-B.

In our previous study, a rat homolog of human nonmuscle myosin heavy chain-B ( nmMHC-B) was identified by mRNA differential display comparing of transformed against nontransformed Rat 6 cells overexpressing mutant p53val135 gene. The nmMHC-B was found to be expressed in normal Rat 6 embryo fibroblast cell line, but markedly suppressed in the mutant p53val135-transformed Rat 6 cells. To examine the possible involvement of nmMHC-B in cell transformation, we first cloned and sequenced the full length cDNA of rat nmMHC-B, which was then cloned into an ecdysone-expression vector. The resulting construct was introduced into the T2 cell line, a mutant p53val135-transformed Rat 6 cells lacking the expression of the endogenous nmMHC-B. The clonal transfectants, expressing muristerone A-induced nmMHC-B, displayed a slightly flatter morphology and reached to a lower saturation density compared to the parental transformed cells. Reconstitution of actin filamental bundles was also clearly seen in cells overexpressing the nmMHC-B. In soft agar assays, nmMHC-B transfectants formed fewer and substantially smaller colonies than the parental cells in response to muristerone A induction. Moreover, it was strikingly effective in suppressing the tumorigenicity of the T2 cells when tested in nude mice. Thus, the nmMHC-B, known as a component of the cytoskeletal network, may act as a tumor suppressor gene. Our current finding may reveal a novel role of nmMHC-B in regulating cell growth and cell signaling in nonmuscle cells. Oncogene (2001) 20, 58 - 68.[1]

References

 
WikiGenes - Universities