ArticleCell discovery2016
Temporal activation of XRCC1-mediated DNA repair is essential for muscle differentiation.
Article in Cell discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- Caspase-Activated DNase localizes to cancer causing translocation breakpoints during cell differentiation.bioRxiv : the preprint server for biology · 2024Article
- Transient caspase-mediated activation of caspase-activated DNase causes DNA damage required for phagocytic macrophage differentiation.Cell reports · 2024Article
- Regulation of base excision repair during adipogenesis and osteogenesis of bone marrow-derived mesenchymal stem cells.Scientific reports · 2023Article
- Caspase-mediated nuclear pore complex trimming in cell differentiation and endoplasmic reticulum stress.eLife · 2023Article
- DNA-PKcs regulates myogenesis in an Akt-dependent manner independent of induced DNA damage.Cell death and differentiation · 2023Article
- Chromatin Reorganization during Myoblast Differentiation Involves the Caspase-Dependent Removal of SATB2.Cells · 2022Article
- Mutagenic Consequences of Sublethal Cell Death Signaling.International journal of molecular sciences · 2021Review
- The landscape of chromatin accessibility in skeletal muscle during embryonic development in pigs.Journal of animal science and biotechnology · 2021Article
- Uncovering the PIDDosome and caspase-2 as regulators of organogenesis and cellular differentiation.Cell death and differentiation · 2020Review
- Prospect and challenge of detecting dynamic gene copy number increases in stem cells by whole genome sequencing.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Control of DNA integrity in skeletal muscle under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2017Review
- Aberrant Compartment Formation by HSPB2 Mislocalizes Lamin A and Compromises Nuclear Integrity and Function.Cell reports · 2017Article
- Evolution of caspase-mediated cell death and differentiation: twins separated at birth.Cell death and differentiation · 2017Review
- Physiological functions of programmed DNA breaks in signal-induced transcription.Nature reviews. Molecular cell biology · 2017Review
- The beneficial role of proteolysis in skeletal muscle growth and stress adaptation.Skeletal muscle · 2016Review
- Short-term nicotinamide riboside treatment improves muscle quality and function in mice and increases cellular energetics and differentiating capacity of myogenic progenitors.Nutrition (Burbank, Los Angeles County, Calif.)Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Transient DNA strand break formation has been identified as an effective means to enhance gene expression in living cells. In the muscle lineage, cell differentiation is contingent upon the induction of caspase-mediated DNA strand breaks, which act to establish the terminal gene expression program. This coordinated DNA nicking is rapidly resolved, suggesting that myoblasts may deploy DNA repair machinery to stabilize the genome and entrench the differentiated phenotype. Here, we identify the base excision repair pathway component XRCC1 as an indispensable mediator of muscle differentiation. Caspase-triggered XRCC1 repair foci form rapidly within differentiating myonuclei, and then dissipate as the maturation program proceeds. Skeletal myoblast deletion of Xrcc1 does not have an impact on cell growth, yet leads to perinatal lethality, with sustained DNA damage and impaired myofiber development. Together, these results demonstrate that XRCC1 manages a temporally responsive DNA repair process to advance the muscle differentiation program.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.