Analysis of replication profiles reveals key role of RFC-Ctf18 in yeast replication stress response

2010 ◽  
Vol 17 (11) ◽  
pp. 1391-1397 ◽  
Author(s):  
Laure Crabbé ◽  
Aubin Thomas ◽  
Véronique Pantesco ◽  
John De Vos ◽  
Philippe Pasero ◽  
...  
Keyword(s):  
Stress Response ◽  
Replication Stress

scholarly journals ATR Signaling Uncouples the Role of RAD51 Paralogs in Homologous Recombination and Replication Stress Response

Cell Reports ◽  
2019 ◽  
Vol 29 (3) ◽  
pp. 551-559.e4
Author(s):  
Sneha Saxena ◽  
Suruchi Dixit ◽  
Kumar Somyajit ◽  
Ganesh Nagaraju
Keyword(s):  
Stress Response ◽  
Homologous Recombination ◽  
Replication Stress ◽  
Rad51 Paralogs

scholarly journals Treacle and TOPBP1 control replication stress response in the nucleolus

2021 ◽  
Vol 220 (8) ◽  
Author(s):  
Artem K. Velichko ◽  
Natalia Ovsyannikova ◽  
Nadezhda V. Petrova ◽  
Artem V. Luzhin ◽  
Maria Vorobjeva ◽  
...  
Keyword(s):  
Stress Response ◽  
Genome Instability ◽  
Replication Stress ◽  
Low Complexity ◽  
Drug Induced ◽  
Response Factors ◽  
Checkpoint Activation ◽  
Stalled Replication Forks

Replication stress is one of the main sources of genome instability. Although the replication stress response in eukaryotic cells has been extensively studied, almost nothing is known about the replication stress response in nucleoli. Here, we demonstrate that initial replication stress–response factors, such as RPA, TOPBP1, and ATR, are recruited inside the nucleolus in response to drug-induced replication stress. The role of TOPBP1 goes beyond the typical replication stress response; it interacts with the low-complexity nucleolar protein Treacle (also referred to as TCOF1) and forms large Treacle–TOPBP1 foci inside the nucleolus. In response to replication stress, Treacle and TOPBP1 facilitate ATR signaling at stalled replication forks, reinforce ATR-mediated checkpoint activation inside the nucleolus, and promote the recruitment of downstream replication stress response proteins inside the nucleolus without forming nucleolar caps. Characterization of the Treacle–TOPBP1 interaction mode leads us to propose that these factors can form a molecular platform for efficient stress response in the nucleolus.

scholarly journals Role of a Candida albicans Nrm1/Whi5 homologue in cell cycle gene expression and DNA replication stress response

2012 ◽  
Vol 84 (4) ◽  
pp. 778-794 ◽  
Author(s):  
Ayala Ofir ◽  
Kay Hofmann ◽  
Esther Weindling ◽  
Tsvia Gildor ◽  
Katherine S. Barker ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Candida Albicans ◽  
Dna Replication ◽  
Stress Response ◽  
Replication Stress ◽  
Cell Cycle Gene ◽  
Dna Replication Stress ◽  
Cell Cycle Gene Expression

scholarly journals Constitutive role of the Fanconi anemia D2 gene in the replication stress response

2017 ◽  
Vol 292 (49) ◽  
pp. 20184-20195 ◽  
Author(s):  
Yanyan Tian ◽  
Xi Shen ◽  
Rui Wang ◽  
Naeh L. Klages-Mundt ◽  
Erica J. Lynn ◽  
...  
Keyword(s):  
Stress Response ◽  
Fanconi Anemia ◽  
Replication Stress

Characterizing and Targeting Replication Stress Response Defects in Breast Cancer

2014 ◽  
Author(s):  
Shiaw-Yih Lin ◽  
Chun-Jen Lin ◽  
Lili Gong ◽  
Hui Dai ◽  
Ju-Seog Lee
Keyword(s):  
Breast Cancer ◽  
Stress Response ◽  
Replication Stress

scholarly journals Flavonoids: Potential Candidates for the Treatment of Neurodegenerative Disorders

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 99
Author(s):  
Shweta Devi ◽  
Vijay Kumar ◽  
Sandeep Kumar Singh ◽  
Ashish Kant Dubey ◽  
Jong-Joo Kim
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Neurodegenerative Disorders ◽  
Cell Damage ◽  
Cellular Stress ◽  
Clinical Manifestations ◽  
Cellular Stress Response ◽  
Dramatic Rise ◽  
Cellular Stress Responses

Neurodegenerative disorders, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), are the most concerning disorders due to the lack of effective therapy and dramatic rise in affected cases. Although these disorders have diverse clinical manifestations, they all share a common cellular stress response. These cellular stress responses including neuroinflammation, oxidative stress, proteotoxicity, and endoplasmic reticulum (ER)-stress, which combats with stress conditions. Environmental stress/toxicity weakened the cellular stress response which results in cell damage. Small molecules, such as flavonoids, could reduce cellular stress and have gained much attention in recent years. Evidence has shown the potential use of flavonoids in several ways, such as antioxidants, anti-inflammatory, and anti-apoptotic, yet their mechanism is still elusive. This review provides an insight into the potential role of flavonoids against cellular stress response that prevent the pathogenesis of neurodegenerative disorders.

scholarly journals Mitochondrien unter Stress: Die Rolle der Präsequenzprotease MPP

BIOspektrum ◽  
2021 ◽  
Vol 27 (4) ◽  
pp. 390-393
Author(s):  
F.-Nora Vögtle
Keyword(s):  
Stress Response ◽  
Cellular Stress ◽  
Critical Role ◽  
Mitochondrial Protein ◽  
Nuclear Genome ◽  
Cellular Stress Response ◽  
Mitochondrial Proteins ◽  
Protein Biogenesis ◽  
Cellular Integrity

AbstractThe majority of mitochondrial proteins are encoded in the nuclear genome, so that the nearly entire proteome is assembled by post-translational preprotein import from the cytosol. Proteomic imbalances are sensed and induce cellular stress response pathways to restore proteostasis. Here, the mitochondrial presequence protease MPP serves as example to illustrate the critical role of mitochondrial protein biogenesis and proteostasis on cellular integrity.

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