scholarly journals Repurposing the Damage Repair Protein Methyl Guanine Methyl Transferase as a Ligand Inducible Fusion Degron

Author(s):  
Gosia M. Murawska ◽  
Caspar Vogel ◽  
Max Jan ◽  
Xinyan Lu ◽  
Matthias Schild ◽  
...  
Biochemistry ◽  
2018 ◽  
Vol 57 (47) ◽  
pp. 6581-6591 ◽  
Author(s):  
Fei Song ◽  
Minxing Li ◽  
Gaohua Liu ◽  
G.V.T. Swapna ◽  
Nourhan S. Daigham ◽  
...  

2016 ◽  
Vol 212 (3) ◽  
pp. 153-161 ◽  
Author(s):  
Tingting Zhang ◽  
Xiubing Zhang ◽  
Weidong Shi ◽  
Jian Xu ◽  
Hui Fan ◽  
...  

2017 ◽  
Vol 39 ◽  
pp. 18-31 ◽  
Author(s):  
Somsubhra Nath ◽  
Shrabasti Roychoudhury ◽  
Matthew J. Kling ◽  
Heyu Song ◽  
Pranjal Biswas ◽  
...  

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Sha Jin ◽  
Nils Cordes

Abstract Intercellular communication is essential for multicellular tissue vitality and homeostasis. We show that healthy cells message protective signals through direct cell–cell connections to adjacent DNA–damaged cells in a microtubule–dependent manner. In DNA–damaged cells, mitochondria restoration is facilitated by fusion with undamaged mitochondria from healthy cells and their DNA damage repair is optimized in presence of healthy cells. Both, mitochondria transfer and intercellular signaling for an enhanced DNA damage response are critically regulated by the activity of the DNA repair protein ataxia telangiectasia mutated (ATM). These healthy–to–damaged prosurvival processes sustain normal tissue integrity and may be exploitable for overcoming resistance to therapy in diseases such as cancer.


2019 ◽  
Vol 18 (7) ◽  
pp. 1428-1436 ◽  
Author(s):  
Manal Alsulami ◽  
Nayla Munawar ◽  
Eugene Dillon ◽  
Giorgio Oliviero ◽  
Kieran Wynne ◽  
...  

2017 ◽  
Vol 114 (35) ◽  
pp. E7245-E7254 ◽  
Author(s):  
Shuai Zhao ◽  
Mo Yang ◽  
Wenfei Zhou ◽  
Baichao Zhang ◽  
Zhiqiang Cheng ◽  
...  

Chemical modifications on histones and DNA/RNA constitute a fundamental mechanism for epigenetic regulation. These modifications often function as docking marks to recruit or stabilize cognate “reader” proteins. So far, a platform for quantitative and high-throughput profiling of the epigenetic interactome is urgently needed but still lacking. Here, we report a 3D-carbene chip-based surface plasmon resonance imaging (SPRi) technology for this purpose. The 3D-carbene chip is suitable for immobilizing versatile biomolecules (e.g., peptides, antibody, DNA/RNA) and features low nonspecific binding, random yet function-retaining immobilization, and robustness for reuses. We systematically profiled binding kinetics of 1,000 histone “reader–mark” pairs on a single 3D-carbene chip and validated two recognition events by calorimetric and structural studies. Notably, a discovery on H3K4me3 recognition by the DNA mismatch repair protein MSH6 in Capsella rubella suggests a mechanism of H3K4me3-mediated DNA damage repair in plant.


2013 ◽  
Vol 139 (2) ◽  
pp. 301-310 ◽  
Author(s):  
Alaa T. Alshareeda ◽  
Ola H. Negm ◽  
Nada Albarakati ◽  
Andrew R. Green ◽  
Christopher Nolan ◽  
...  

2014 ◽  
Vol 337 (5) ◽  
pp. 302-310 ◽  
Author(s):  
Vimlendu Bhushan Sinha ◽  
Atul Grover ◽  
Zakwan Ahmed ◽  
Veena Pande

2021 ◽  
Vol 10 (1) ◽  
pp. 165-173 ◽  
Author(s):  
Tamara Maiuri ◽  
Claudia L.K. Hung ◽  
Celeste Suart ◽  
Nola Begeja ◽  
Carlos Barba-Bazan ◽  
...  

The use of genome wide association studies (GWAS) in Huntington’s disease (HD) research, driven by unbiased human data analysis, has transformed the focus of new targets that could affect age at onset. While there is a significant depth of information on DNA damage repair, with many drugs and drug targets, most of this development has taken place in the context of cancer therapy. DNA damage repair in neurons does not rely on DNA replication correction mechanisms. However, there is a strong connection between DNA repair and neuronal metabolism, mediated by nucleotide salvaging and the poly ADP-ribose (PAR) response, and this connection has been implicated in other age-onset neurodegenerative diseases. Validation of leads including the mismatch repair protein MSH3, and interstrand cross-link repair protein FAN1, suggest the mechanism is driven by somatic CAG instability, which is supported by the protective effect of CAA substitutions in the CAG tract. We currently do not understand: how somatic instability is triggered; the state of DNA damage within expanding alleles in the brain; whether this damage induces mismatch repair and interstrand cross-link pathways; whether instability mediates toxicity, and how this relates to human ageing. We discuss DNA damage pathways uncovered by HD GWAS, known roles of other polyglutamine disease proteins in DNA damage repair, and a panel of hypotheses for pathogenic mechanisms.


2001 ◽  
Vol 2 ◽  
pp. spotlight-20010810-01
Author(s):  
David Bruce

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