scholarly journals Lessons From the First Comprehensive Molecular Characterization of Cell Cycle Control in Rodent Insulinoma Cell Lines

Diabetes ◽  
2008 ◽  
Vol 57 (11) ◽  
pp. 3056-3068 ◽  
Author(s):  
I. Cozar-Castellano ◽  
G. Harb ◽  
K. Selk ◽  
K. Takane ◽  
R. Vasavada ◽  
...  
1991 ◽  
Vol 11 (10) ◽  
pp. 4846-4853
Author(s):  
D A Withers ◽  
R C Harvey ◽  
J B Faust ◽  
O Melnyk ◽  
K Carey ◽  
...  

The t(11;14)(q13;q32) translocation has been associated with human B-lymphocytic malignancy. Several examples of this translocation have been cloned, documenting that this abnormality joins the immunoglobulin heavy-chain gene to the bcl-1 locus on chromosome 11. However, the identification of the bcl-1 gene, a putative dominant oncogene, has been elusive. In this work, we have isolated genomic clones covering 120 kb of the bcl-1 locus. Probes from the region of an HpaII-tiny-fragment island identified a candidate bcl-1 gene. cDNAs representing the bcl-1 mRNA were cloned from three cell lines, two with the translocation. The deduced amino acid sequence from these clones showed bcl-1 to be a member of the cyclin gene family. In addition, our analysis of expression of bcl-1 in an extensive panel of human cell lines showed it to be widely expressed except in lymphoid or myeloid lineages. This observation may provide a molecular basis for distinct modes of cell cycle control in different mammalian tissues. Activation of the bcl-1 gene may be oncogenic by directly altering progression through the cell cycle.


1991 ◽  
Vol 11 (10) ◽  
pp. 4846-4853 ◽  
Author(s):  
D A Withers ◽  
R C Harvey ◽  
J B Faust ◽  
O Melnyk ◽  
K Carey ◽  
...  

The t(11;14)(q13;q32) translocation has been associated with human B-lymphocytic malignancy. Several examples of this translocation have been cloned, documenting that this abnormality joins the immunoglobulin heavy-chain gene to the bcl-1 locus on chromosome 11. However, the identification of the bcl-1 gene, a putative dominant oncogene, has been elusive. In this work, we have isolated genomic clones covering 120 kb of the bcl-1 locus. Probes from the region of an HpaII-tiny-fragment island identified a candidate bcl-1 gene. cDNAs representing the bcl-1 mRNA were cloned from three cell lines, two with the translocation. The deduced amino acid sequence from these clones showed bcl-1 to be a member of the cyclin gene family. In addition, our analysis of expression of bcl-1 in an extensive panel of human cell lines showed it to be widely expressed except in lymphoid or myeloid lineages. This observation may provide a molecular basis for distinct modes of cell cycle control in different mammalian tissues. Activation of the bcl-1 gene may be oncogenic by directly altering progression through the cell cycle.


Diabetes ◽  
1997 ◽  
Vol 46 (6) ◽  
pp. 958-967 ◽  
Author(s):  
S. A. Clark ◽  
C. Quaade ◽  
H. Constandy ◽  
P. Hansen ◽  
P. Halban ◽  
...  

Diabetes ◽  
1997 ◽  
Vol 46 (6) ◽  
pp. 958-967 ◽  
Author(s):  
S. A. Clark ◽  
C. Quaade ◽  
H. Constantly ◽  
P. Hansen ◽  
P. Halban ◽  
...  

2005 ◽  
Vol 16 (5) ◽  
pp. 2129-2138 ◽  
Author(s):  
Frederick R. Cross ◽  
Lea Schroeder ◽  
Martin Kruse ◽  
Katherine C. Chen

Regulation of cyclin abundance is central to eukaryotic cell cycle control. Strong overexpression of mitotic cyclins is known to lock the system in mitosis, but the quantitative behavior of the control system as this threshold is approached has only been characterized in the in vitro Xenopus extract system. Here, we quantitate the threshold for mitotic block in budding yeast caused by constitutive overexpression of the mitotic cyclin Clb2. Near this threshold, the system displays marked loss of robustness, in that loss or even heterozygosity for some regulators becomes deleterious or lethal, even though complete loss of these regulators is tolerated at normal cyclin expression levels. Recently, we presented a quantitative kinetic model of the budding yeast cell cycle. Here, we use this model to generate biochemical predictions for Clb2 levels, asynchronous as well as through the cell cycle, as the Clb2 overexpression threshold is approached. The model predictions compare well with biochemical data, even though no data of this type were available during model generation. The loss of robustness of the Clb2 overexpressing system is also predicted by the model. These results provide strong confirmation of the model's predictive ability.


1995 ◽  
Vol 270 (31) ◽  
pp. 18216-18218 ◽  
Author(s):  
Robert S. Boyd ◽  
Michael J. Duggan ◽  
Clifford C. Shone ◽  
Keith A. Foster

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