Retracted: MyoD-dependent regulation of NF-κB activity couples cell-cycle withdrawal to myogenic differentiation
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A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
Post-publication record
- Nature
- Retraction
- Reason
- Falsification/Fabrication of Image;
- Date
- 7/18/2013 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Abstract
BACKGROUND: Mice lacking MyoD exhibit delayed skeletal muscle regeneration and markedly enhanced numbers of satellite cells. Myoblasts isolated from MyoD-/- myoblasts proliferate more rapidly than wild type myoblasts, display a dramatic delay in differentiation, and continue to incorporate BrdU after serum withdrawal. METHODS: Primary myoblasts isolated from wild type and MyoD-/- mutant mice were examined by microarray analysis and further characterized by cell and molecular experiments in cell culture. RESULTS: We found that NF-κB, a key regulator of cell-cycle withdrawal and differentiation, aberrantly maintains nuclear localization and transcriptional activity in MyoD-/- myoblasts. As a result, expression of cyclin D is maintained during serum withdrawal, inhibiting expression of muscle-specific genes and progression through the differentiation program. Sustained nuclear localization of cyclin E, and a concomitant increase in cdk2 activity maintains S-phase entry in MyoD-/- myoblasts even in the absence of mitogens. Importantly, this deficit was rescued by forced expression of IκBαSR, a non-degradable mutant of IκBα, indicating that inhibition of NF-κB is sufficient to induce terminal myogenic differentiation in the absence of MyoD. CONCLUSION: MyoD-induced cytoplasmic relocalization of NF-κB is an essential step in linking cell-cycle withdrawal to the terminal differentiation of skeletal myoblasts. These results provide important insight into the unique functions of MyoD in regulating the switch from progenitor proliferation to terminal differentiation.
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The record
- Venue
- Skeletal Muscle
- Topic
- Muscle Physiology and Disorders
- Field
- Biochemistry, Genetics and Molecular Biology
- Canadian institutions
- McMaster UniversityOttawa Hospital
- Funders
- Canadian Institutes of Health ResearchNational Institutes of HealthMuscular Dystrophy AssociationHoward Hughes Medical Institute
- Keywords
- MyoDCell biologyNeuroscienceBiologyMyogenesisMyocyte
- Has abstract in OpenAlex
- yes