Journal of cell science
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Journal of cell science · Jan 1996
The carboxyl terminus of myosin binding protein C (MyBP-C, C-protein) specifies incorporation into the A-band of striated muscle.
Myosin binding protein-C (MyBP-C), also known as C-protein, is a major constituent of the thick filaments of vertebrate striated muscles. The protein, approximately 130 kDa, consists of a series of 10 globular motifs (numbered I to X) each of approximately 90-100 amino acids, bearing resemblance to the C2-set of immunoglobins (Ig C2) and to the fibronectin type III (FnIII) motifs. Using pure preparations of myosin and MyBP-C, it has been demonstrated that the major myosin binding domain of MyBP-C resides within the C-terminal Ig C2 motif (motif X). ⋯ One construct (delta 10) lacking only motif X strongly inhibited myofibril assembly. We conclude that the myosin binding domain of MyBP-C, although essential, is not sufficient for correct incorporation into the A-band and that motifs VII to IX are required for this process. The data suggest a topological model in which MyBP-C is associated with the thick filament through its C terminus.
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Journal of cell science · Jun 1994
Comparative StudyCell cycle analysis and chromosomal localization of human Plk1, a putative homologue of the mitotic kinases Drosophila polo and Saccharomyces cerevisiae Cdc5.
polo and CDC5 are two genes required for passage through mitosis in Drosophila melanogaster and Saccharomyces cerevisiae, respectively. Both genes encode structurally related protein kinases that have been implicated in regulating the function of the mitotic spindle. Here, we report the characterization of a human protein kinase that displays extensive sequence similarity to Drosophila polo and S. cerevisiae Cdc5; we refer to this kinase as Plk1 (for polo-like kinase 1). ⋯ The Plk1 gene maps to position p12 on chromosome 16, a locus for which no associations with neoplastic malignancies are known. The Plk1 protein levels and its distribution change during the cell cycle, in a manner consistent with a role of Plk1 in mitosis. Thus, like Drosophila polo and S. cerevisiae Cdc5, human Plk1 is likely to function in cell cycle progression.
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Journal of cell science · Jan 1994
Multiple mechanisms are responsible for altered expression of gap junction genes during oncogenesis in rat liver.
Although several abnormalities in gap junction (GJ) structure and/or function have been described in neoplasms, the molecular mechanisms responsible for many of the alterations remain unknown. The identification of a family of GJ proteins, termed connexins, prompted this study of connexin32 (Cx32), connexin26 (Cx26) and connexin43 (Cx43) expression during rat hepatocarcinogenesis. Using antibody, cDNA and cRNA probes, we investigated connexin mRNA and protein expression in preneoplastic and neoplastic rat livers. ⋯ Areas of bile duct proliferation and cholangiomas displayed Cx43 staining, whereas, cholangiocarcinomas were deficient in immunoreactivity. These findings show that alterations in the expression of connexins, by either downregulation or differential induction, represent common modifications during hepatocarcinogenesis. Although our results imply that connexins represent useful markers for the boundary between tumor promotion and progression, preneoplastic and neoplastic rat hepatocytes fail to use a common mechanism to modify connexin expression.
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Journal of cell science · Dec 1979
Quantitative replicon analysis of DNA synthesis in cancer-prone conditions and the defects in Bloom's syndrome.
A quantitative method of replicon analysis of DNA fibre autoradiographs has been used to study the relationship between mean rate of DNA chain growth (R) and distance between adjacent replicons (ID) in fibroblasts from cancer-prone conditions. Results are expressed in terms of the mean linear regression R = delta +(K. ID)10-2. ⋯ Pretreatment of all cultures with fluorodeoxyuridine (FUdR) produced the same differential effect on release from DNA synthesis inhibition, that is a similar increase in the activation of normally inactive replicons and a slightly slower rate of chain growth over all replicons. No evidence of a substance released by Bloom's cells in culture capable of increasing the sister-chromatid frequency in normal cells could be found. Since SCE frequencies were found to increase with fixation time after BUdR introduction it is concluded that some of the reported changes could be due to differences in cell cycle kinetics brought about by the different media conditions.