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.

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 p53 connects tumorigenesis and reprogramming to pluripotency

2010 ◽  
Vol 207 (10) ◽  
pp. 2045-2048 ◽  
Author(s):  
Natalia Tapia ◽  
Hans R. Schöler
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Suppressor Gene ◽  
Tumor Formation ◽  
Nuclear Reprogramming ◽  
Differentiation Process ◽  
Cycle Arrest ◽  
Tumor Suppressor Gene P53

The tumor suppressor gene p53 prevents the initiation of tumor formation by inducing cell cycle arrest, senescence, DNA repair, and apoptosis. Recently, the absence or mutation of p53 was described to facilitate nuclear reprogramming. These findings suggest an influence of p53 on the de-differentiation process, and highlight the similarities between induction of pluripotency and tumor formation.

scholarly journals Role of Mis Localization of DNA Repair Factors in Cell Cycle Arrest

2019 ◽  
Vol 116 (3) ◽  
pp. 76a
Author(s):  
Manasvita Vashisth ◽  
Sangkyun Cho ◽  
Dennis Discher
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Cell Cycle Arrest ◽  
Cycle Arrest
Sign in / Sign up

Export Citation Format

Share Document