ReviewBiomolecules2021
Breakdown of Filamentous Myofibrils by the UPS-Step by Step.
Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Combating muscle atrophy: emerging therapeutic targets that are fiber-type-specific.The FEBS journal · 2025Review
- Mitophagy is required to protect against excessive skeletal muscle atrophy following hindlimb immobilization.Journal of biomedical science · 2025Article
- Proteasome gene expression is controlled by coordinated functions of multiple transcription factors.The Journal of cell biology · 2024Article
- Murf1 alters myosin replacement rates in cultured myotubes in a myosin isoform-dependent manner.In vitro cellular & developmental biology. Animal · 2024Article
- Maximum entropy determination of mammalian proteome dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- βFrontiers in physiology · 2024Article
- The AAA-ATPase ATAD1 and its partners promote degradation of desmin intermediate filaments in muscle.EMBO reports · 2022Article
- Hidden Agenda - The Involvement of Endoplasmic Reticulum Stress and Unfolded Protein Response in Inflammation-Induced Muscle Wasting.Frontiers in immunology · 2022Review
- Calpain-mediated proteolysis of vimentin filaments is augmented in giant axonal neuropathy fibroblasts exposed to hypotonic stress.Frontiers in cell and developmental biology · 2022Article
- Integration of proteomic and genetic approaches to assess developmental muscle atrophy.The Journal of experimental biology · 2021Article
- Mechanisms That Activate 26S Proteasomes and Enhance Protein Degradation.Biomolecules · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Protein degradation maintains cellular integrity by regulating virtually all biological processes, whereas impaired proteolysis perturbs protein quality control, and often leads to human disease. Two major proteolytic systems are responsible for protein breakdown in all cells: autophagy, which facilitates the loss of organelles, protein aggregates, and cell surface proteins; and the ubiquitin-proteasome system (UPS), which promotes degradation of mainly soluble proteins. Recent findings indicate that more complex protein structures, such as filamentous assemblies, which are not accessible to the catalytic core of the proteasome in vitro, can be efficiently degraded by this proteolytic machinery in systemic catabolic states in vivo. Mechanisms that loosen the filamentous structure seem to be activated first, hence increasing the accessibility of protein constituents to the UPS. In this review, we will discuss the mechanisms underlying the disassembly and loss of the intricate insoluble filamentous myofibrils, which are responsible for muscle contraction, and whose degradation by the UPS causes weakness and disability in aging and disease. Several lines of evidence indicate that myofibril breakdown occurs in a strictly ordered and controlled manner, and the function of AAA-ATPases is crucial for their disassembly and loss.
Indexed as
Identifiers
What OpenQuestion holds
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.