Regulation of cyclin B1, cyclin B2 and cdc25C genes by the tumor suppressor protein p53 and by p73 in colorectal adenocarcinoma cells mediating G2 cell cycle arrest

2001 ◽  
Vol 120 (5) ◽  
pp. A296
Author(s):  
Kurt Engeland ◽  
Karen Krause ◽  
Sebastian Dietz ◽  
Andrea Tannapfel ◽  
Christian Wittekind ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Colorectal Adenocarcinoma ◽  
Cyclin B1 ◽  
Tumor Suppressor Protein ◽  
Tumor Suppressor Protein P53 ◽  
Cycle Arrest ◽  
Adenocarcinoma Cells ◽  
G2 Cell Cycle Arrest

scholarly journals Recent Advances in p53

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 211
Author(s):  
Gabriella D’Orazi
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Transcription Factor ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Tumor Suppressor Protein ◽  
Cellular Functions ◽  
Tumor Suppressor Protein P53 ◽  
Cycle Arrest ◽  
Stress Signals

Tumor suppressor protein p53 (TP53) is a key transcription factor that, in response to various stress signals, regulates numerous genes involved in a broad range of cellular functions including DNA repair, apoptosis, cell cycle arrest, senescence, metabolism, etc [...]

scholarly journals mdm-2 inhibits the G1 arrest and apoptosis functions of the p53 tumor suppressor protein.

1996 ◽  
Vol 16 (5) ◽  
pp. 2445-2452 ◽  
Author(s):  
J Chen ◽  
X Wu ◽  
J Lin ◽  
A J Levine
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Biological Activities ◽  
Tumor Suppressor Protein ◽  
G1 Arrest ◽  
Physical Interaction ◽  
P53 Tumor Suppressor ◽  
Cycle Arrest ◽  
P53 Tumor Suppressor Protein

The mdm-2 gene encodes a 90-kDa polypeptide that binds specifically to the p53 tumor suppressor protein. This physical interaction results in the inhibition of the transcriptional functions of p53 (J. Chen, J. Lin, and A. J. Levine, Mol. Med. 1:142-152, 1995, and J. Momand, G. P. Zambetti, D. C. Olson, D. George, and A. J. Levine, Cell 69:1237-1245, 1992). Experiments are described that demonstrate the ability of mdm-2 to abrogate both the p53-mediated cell cycle arrest and the apoptosis functions. In addition, the results presented here suggest that mdm-2 binding to p53 and the resultant inhibition of p53 transcription functions are critical for reversing p53-mediated cell cycle arrest. The N-terminal half or domain of the mdm-2 protein is sufficient to regulate these biological activities of p53, consistent with the possibility that the highly conserved central acidic region and the C-terminal putative zinc fingers of mdm-2 may encode other functions.

scholarly journals MyoD induced cell cycle arrest is associated with increased nuclear affinity of the Rb protein.

1993 ◽  
Vol 4 (7) ◽  
pp. 705-713 ◽  
Author(s):  
A M Thorburn ◽  
P A Walton ◽  
J R Feramisco
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Dna Synthesis ◽  
Cell Cycle Arrest ◽  
S Phase ◽  
Tumor Suppressor Protein ◽  
G1 Phase ◽  
Induced Expression ◽  
Rb Protein ◽  
Cycle Arrest

In studying the mechanism through which the myogenic determination protein MyoD prevents entry into the S phase of the cell cycle, we have found a relationship between MyoD and the retinoblastoma (Rb) tumor suppressor protein. By direct needle microinjection of purified recombinant MyoD protein into quiescent fibroblasts, which were then induced to proliferate by serum, we found that MyoD arrested progression of the cell cycle, in agreement with studies utilizing expression constructs for MyoD. By studying temporal changes in cells injected with MyoD protein, it was found that MyoD did not prevent serum induced expression of the protooncogene c-Fos, an event that occurs in the G0 to G1 transition of the cycle. Injection of the MyoD protein as late as 8 h after the addition of serum still caused an inhibition in DNA synthesis, suggesting that MyoD inhibits the G1 to S transition as opposed to the G0 to G1 transition. MyoD injection did not prevent the expression of cyclin A. However MyoD injection did result in a block in the increase in Rb extractibility normally seen in late G1 phase cells. As this phenomenon is associated with the hyperphosphorylation of Rb at this point in the cell cycle and is correlated with progression into S phase, this provides further evidence that MyoD blocks the cycle late in G1.

Estrogen receptor β causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2

2010 ◽  
Vol 129 (3) ◽  
pp. 777-784 ◽  
Author(s):  
Sreenivasan Paruthiyil ◽  
Aleksandra Cvoro ◽  
Mary Tagliaferri ◽  
Isaac Cohen ◽  
Emma Shtivelman ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Estrogen Receptor ◽  
Cell Cycle Arrest ◽  
Cyclin B1 ◽  
Estrogen Receptor Β ◽  
Cycle Arrest ◽  
G2 Cell Cycle Arrest

scholarly journals Cyclin A Is a Functional Target of Retinoblastoma Tumor Suppressor Protein-mediated Cell Cycle Arrest

1999 ◽  
Vol 274 (39) ◽  
pp. 27632-27641 ◽  
Author(s):  
Karen E. Knudsen ◽  
Anne F. Fribourg ◽  
Matthew W. Strobeck ◽  
Jean-Marie Blanchard ◽  
Erik S. Knudsen
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Cyclin A ◽  
Tumor Suppressor Protein ◽  
Retinoblastoma Tumor Suppressor Protein ◽  
Retinoblastoma Tumor Suppressor ◽  
Cycle Arrest ◽  
Retinoblastoma Tumor

scholarly journals Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Christophe Nicot
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Tumor Suppressors ◽  
Epigenetic Mechanisms ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Cycle Arrest

Tumor suppressor functions are essential to control cellular proliferation, to activate the apoptosis or senescence pathway to eliminate unwanted cells, to link DNA damage signals to cell cycle arrest checkpoints, to activate appropriate DNA repair pathways, and to prevent the loss of adhesion to inhibit initiation of metastases. Therefore, tumor suppressor genes are indispensable to maintaining genetic and genomic integrity. Consequently, inactivation of tumor suppressors by somatic mutations or epigenetic mechanisms is frequently associated with tumor initiation and development. In contrast, reactivation of tumor suppressor functions can effectively reverse the transformed phenotype and lead to cell cycle arrest or death of cancerous cells and be used as a therapeutic strategy. Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoproliferative disease associated with infection of CD4 T cells by the Human T-cell Leukemia Virus Type 1 (HTLV-I). HTLV-I-associated T-cell transformation is the result of a multistep oncogenic process in which the virus initially induces chronic T-cell proliferation and alters cellular pathways resulting in the accumulation of genetic defects and the deregulated growth of virally infected cells. This review will focus on the current knowledge of the genetic and epigenetic mechanisms regulating the inactivation of tumor suppressors in the pathogenesis of HTLV-I.

Sign in / Sign up

Export Citation Format

Share Document