ArticleJournal of molecular biology2008
Structural evidence for co-evolution of the regulation of contraction and energy production in skeletal muscle.
Article in Journal of molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Generation of musculoskeletal cells from human urine epithelium-derived presomitic mesoderm cells.Cell & bioscience · 2024Article
- Architecture and activation of human muscle phosphorylase kinase.Nature communications · 2024Article
- Skeletal-Muscle-Specific Overexpression of Chrono Leads to Disruption of Glucose Metabolism and Exercise Capacity.Life (Basel, Switzerland) · 2022Article
- The regulation of glycogenolysis in the brain.The Journal of biological chemistry · 2018Review
- Structural characterization of the catalytic γ and regulatory β subunits of phosphorylase kinase in the context of the hexadecameric enzyme complex.Protein science : a publication of the Protein Society · 2018Article
- A model for activation of the hexadecameric phosphorylase kinase complex deduced from zero-length oxidative crosslinking.Protein science : a publication of the Protein Society · 2015Article
- Mass Spectrometric Analysis of Surface-Exposed Regions in the Hexadecameric Phosphorylase Kinase Complex.Biochemistry · 2015Article
- Mass spectrometry reveals differences in stability and subunit interactions between activated and nonactivated conformers of the (αβγδ)4 phosphorylase kinase complex.Molecular & cellular proteomics : MCP · 2012Article
- Structure and location of the regulatory β subunits in the (αβγδ)4 phosphorylase kinase complex.The Journal of biological chemistry · 2012Article
- A review of methods used for identifying structural changes in a large protein complex.Methods in molecular biology (Clifton, N.J.) · 2012Review
- Transcriptional adaptations following exercise in thoroughbred horse skeletal muscle highlights molecular mechanisms that lead to muscle hypertrophy.BMC genomics · 2009Article
- Expressed phosphorylase b kinase and its alphagammadelta subcomplex as regulatory models for the rabbit skeletal muscle holoenzyme.Biochemistry · 2009Article
- Physicochemical changes in phosphorylase kinase associated with its activation.Protein science : a publication of the Protein Society · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Skeletal muscle phosphorylase kinase (PhK) is a Ca(2+)-dependent enzyme complex, (alpha beta gamma delta)(4), with the delta subunit being tightly bound endogenous calmodulin (CaM). The Ca(2+)-dependent activation of glycogen phosphorylase by PhK couples muscle contraction with glycogen breakdown in the "excitation-contraction-energy production triad." Although the Ca(2+)-dependent protein-protein interactions among the relevant contractile components of muscle are well characterized, such interactions have not been previously examined in the intact PhK complex. Here we show that zero-length cross-linking of the PhK complex produces a covalent dimer of its catalytic gamma and CaM subunits. Utilizing mass spectrometry, we determined the residues cross-linked to be in an EF hand of CaM and in a region of the gamma subunit sharing high sequence similarity with the Ca(2+)-sensitive molecular switch of troponin I that is known to bind actin and troponin C, a homolog of CaM. Our findings represent an unusual binding of CaM to a target protein and supply an explanation for the low Ca(2+) stoichiometry of PhK that has been reported. They also provide direct structural evidence supporting co-evolution of the coordinate regulation by Ca(2+) of contraction and energy production in muscle through the sharing of a common structural motif in troponin I and the catalytic subunit of PhK for their respective interactions with the homologous Ca(2+)-binding proteins troponin C and CaM.
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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.