scholarly journals A Jekyll and Hyde Role of Cyclin E in the Genotoxic Stress Response: Switching from Cell Cycle Control to Apoptosis Regulation

Cell Cycle ◽  
2007 ◽  
Vol 6 (12) ◽  
pp. 1436-1441 ◽  
Author(s):  
Suparna Mazumder ◽  
Dragos Plesca ◽  
Alexandru Almasan
Keyword(s):  
Cell Cycle ◽  
Stress Response ◽  
Cyclin E ◽  
Cell Cycle Control ◽  
Genotoxic Stress ◽  
Response Switching ◽  
Apoptosis Regulation

scholarly journals Exploring the multiple roles of guardian of the genome: P53

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Wasim Feroz ◽  
Arwah Mohammad Ali Sheikh
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Crucial Role ◽  
Cellular Response ◽  
Genotoxic Stress ◽  
Specific Response ◽  
Main Body ◽  
Repair System ◽  
Tumour Suppression

Abstract Background Cells have evolved balanced mechanisms to protect themselves by initiating a specific response to a variety of stress. The TP53 gene, encoding P53 protein, is one of the many widely studied genes in human cells owing to its multifaceted functions and complex dynamics. The tumour-suppressing activity of P53 plays a principal role in the cellular response to stress. The majority of the human cancer cells exhibit the inactivation of the P53 pathway. In this review, we discuss the recent advancements in P53 research with particular focus on the role of P53 in DNA damage responses, apoptosis, autophagy, and cellular metabolism. We also discussed important P53-reactivation strategies that can play a crucial role in cancer therapy and the role of P53 in various diseases. Main body We used electronic databases like PubMed and Google Scholar for literature search. In response to a variety of cellular stress such as genotoxic stress, ischemic stress, oncogenic expression, P53 acts as a sensor, and suppresses tumour development by promoting cell death or permanent inhibition of cell proliferation. It controls several genes that play a role in the arrest of the cell cycle, cellular senescence, DNA repair system, and apoptosis. P53 plays a crucial role in supporting DNA repair by arresting the cell cycle to purchase time for the repair system to restore genome stability. Apoptosis is essential for maintaining tissue homeostasis and tumour suppression. P53 can induce apoptosis in a genetically unstable cell by interacting with many pro-apoptotic and anti-apoptotic factors. Furthermore, P53 can activate autophagy, which also plays a role in tumour suppression. P53 also regulates many metabolic pathways of glucose, lipid, and amino acid metabolism. Thus under mild metabolic stress, P53 contributes to the cell’s ability to adapt to and survive the stress. Conclusion These multiple levels of regulation enable P53 to perform diversified roles in many cell responses. Understanding the complete function of P53 is still a work in progress because of the inherent complexity involved in between P53 and its target proteins. Further research is required to unravel the mystery of this Guardian of the genome “TP53”.

The role of MCM proteins in the cell cycle control of genome duplication

BioEssays ◽  
1996 ◽  
Vol 18 (3) ◽  
pp. 183-190 ◽  
Author(s):  
Stephen E. Kearsey ◽  
Domenico Maiorano ◽  
Eddie C. Holmes ◽  
Ivan T. Todorov
Keyword(s):  
Cell Cycle ◽  
Genome Duplication ◽  
Cell Cycle Control ◽  
Mcm Proteins

Role of transcriptional and posttranscriptional regulation in expression of histone genes in Saccharomyces cerevisiae

1987 ◽  
Vol 7 (2) ◽  
pp. 614-621
Author(s):  
D E Lycan ◽  
M A Osley ◽  
L M Hereford
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Replication ◽  
Posttranscriptional Regulation ◽  
Cell Cycle Control ◽  
Dimensional Structure ◽  
Histone Genes ◽  
Transcriptional Regulatory Mechanisms ◽  
Rna Levels

We analyzed the role of posttranscriptional mechanisms in the regulation of histone gene expression in Saccharomyces cerevisiae. The rapid drop in histone RNA levels associated with the inhibition of ongoing DNA replication was postulated to be due to posttranscriptional degradation of histone transcripts. However, in analyzing the sequences required for this response, we showed that the coupling of histone RNA levels to DNA replication was due mostly, if not entirely, to transcriptional regulatory mechanisms. Furthermore, deletions which removed the negative, cell cycle control sequences from the histone promoter also uncoupled histone transcription from DNA replication. We propose that the arrest of DNA synthesis prematurely activates the regulatory pathway used in the normal cell cycle to repress transcription. Although posttranscriptional regulation did not appear to play a significant role in coupling histone RNA levels to DNA replication, it did affect the levels of histone RNA in the cell cycle. Posttranscriptional regulation could apparently restore much of the periodicity of histone RNA accumulation in cells which constitutively transcribed the histone genes. Unlike transcriptional regulation, periodic posttranscriptional regulation appears to operate on a clock which is independent of events in the mitotic DNA cycle. Posttranscriptional recognition of histone RNA must require either sequences in the 3' end of the RNA or an intact three-dimensional structure since H2A- and H2B-lacZ fusion transcripts, containing only 5' histone sequences, were insensitive to posttranscriptional controls.

scholarly journals Role of D-GADD45 in JNK-Dependent Apoptosis and Regeneration in Drosophila

Genes ◽  
2019 ◽  
Vol 10 (5) ◽  
pp. 378 ◽  
Author(s):  
Carlos Camilleri-Robles ◽  
Florenci Serras ◽  
Montserrat Corominas
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Control ◽  
Imaginal Discs ◽  
Cellular Functions ◽  
Correct Function ◽  
Response To Stress ◽  
Wing Imaginal Discs ◽  
Harmful Effects

The GADD45 proteins are induced in response to stress and have been implicated in the regulation of several cellular functions, including DNA repair, cell cycle control, senescence, and apoptosis. In this study, we investigate the role of D-GADD45 during Drosophila development and regeneration of the wing imaginal discs. We find that higher expression of D-GADD45 results in JNK-dependent apoptosis, while its temporary expression does not have harmful effects. Moreover, D-GADD45 is required for proper regeneration of wing imaginal discs. Our findings demonstrate that a tight regulation of D-GADD45 levels is required for its correct function both, in development and during the stress response after cell death.

Abnormalities in Cell Cycle Control in Cancer and Their Clinical Implications

1998 ◽  
Vol 84 (4) ◽  
pp. 421-433 ◽  
Author(s):  
Alessandro Sgambato ◽  
Giovanna Flamini ◽  
Achille Cittadini ◽  
I. Bernard Weinstein
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Transformation ◽  
Cell Cycle Control ◽  
Genomic Stability ◽  
Clinical Implications ◽  
Mammalian Cell Cycle ◽  
Carcinogenic Process ◽  
Review Current

Recent studies indicate that the functions of several genes that control the cell cycle are altered during the carcinogenic process and that these changes perturb both cell proliferation and genomic stability, thus promoting cell transformation and enhancing the process of tumor progression. The purpose of this paper is to review current information on the role of cyclins and related genes in the control of the mammalian cell cycle, the types of abnormalities in these genes found in human tumors and the possible clinical implications of these findings.

Role of cell cycle control in radiosensitization of mouse spermatogonial stem cells

2001 ◽  
Vol 77 (3) ◽  
pp. 357-363 ◽  
Author(s):  
P. P. W. Van Buul ◽  
A. Van Duyn-Goedhart ◽  
T. Beumer ◽  
A. L. Bootsma
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Cell Cycle Control ◽  
Spermatogonial Stem Cells

scholarly journals Cell Cycle Control of Schwann Cell Proliferation: Role of Cyclin-Dependent Kinase-2

2000 ◽  
Vol 20 (12) ◽  
pp. 4627-4634 ◽  
Author(s):  
Ravi Tikoo ◽  
George Zanazzi ◽  
Dov Shiffman ◽  
James Salzer ◽  
Moses V. Chao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Schwann Cell ◽  
Cell Cycle Control ◽  
Cyclin Dependent Kinase
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