| http://purl.uniprot.org/citations/29669813 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29669813 | http://www.w3.org/2000/01/rdf-schema#comment | "The acceleration of myocardial relaxation produced by β-adrenoreceptor stimulation is mediated in part by protein kinase A (PKA)-mediated phosphorylation of cardiac troponin-I (cTnI), which decreases myofibrillar Ca2+ sensitivity. Previous evidence suggests that phosphorylation of both Ser-23 and Ser-24 in cTnI is required for this Ca2+ desensitization. PKA-mediated phosphorylation also partially protects cTnI from proteolysis by calpain. Here we report that protein kinase D (PKD) phosphorylates only one serine of cTnI Ser-23/24. To explore the functional consequences of this monophosphorylation, we examined the Ca2+ sensitivity of force production and susceptibility of cTnI to calpain-mediated proteolysis when Ser-23/24 of cTnI in mouse cardiac myofibrils was nonphosphorylated, mono-phosphorylated, or bisphosphorylated (using sequential incubations in λ-phosphatase, PKD, and PKA, respectively). Phos-tag gels, Western blotting, and high-resolution MS revealed that PKD produced >90% monophosphorylation of cTnI, primarily at Ser-24, whereas PKA led to cTnI bisphosphorylation exclusively. PKD markedly decreased the Ca2+ sensitivity of force production in detergent-permeabilized ventricular trabeculae, whereas subsequent incubation with PKA produced only a small further fall of Ca2+ sensitivity. Unlike PKD, PKA also substantially phosphorylated myosin-binding protein-C and significantly accelerated cross-bridge kinetics (ktr). After phosphorylation by PKD or PKA, cTnI in isolated myofibrils was partially protected from calpain-mediated degradation. We conclude that cTnI monophosphorylation at Ser-23/24 decreases myofibrillar Ca2+ sensitivity and partially protects cTnI from calpain-induced proteolysis. In healthy cardiomyocytes, the basal monophosphorylation of cTnI may help tonically regulate myofibrillar Ca2+ sensitivity."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.ra117.001292"xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Ge Y."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Cai W."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Salhi H.E."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Dos Remedios C.G."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Avkiran M."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Kentish J.C."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Biesiadecki B.J."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Shaifta Y."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Martin-Garrido A."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/author | "Ayaz-Guner S."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/pages | "8588-8599"xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/title | "Monophosphorylation of cardiac troponin-I at Ser-23/24 is sufficient to regulate cardiac myofibrillar Ca2+ sensitivity and calpain-induced proteolysis."xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://purl.uniprot.org/core/volume | "293"xsd:string |
| http://purl.uniprot.org/citations/29669813 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29669813 |
| http://purl.uniprot.org/citations/29669813 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/29669813 |
| http://purl.uniprot.org/uniprot/#_D3Z160-mappedCitation-29669813 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29669813 |
| http://purl.uniprot.org/uniprot/#_D3YXP5-mappedCitation-29669813 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29669813 |
| http://purl.uniprot.org/uniprot/#_A0A140LIV0-mappedCitation-29669813 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29669813 |
| http://purl.uniprot.org/uniprot/#_P48787-mappedCitation-29669813 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29669813 |
| http://purl.uniprot.org/uniprot/#_Q62101-mappedCitation-29669813 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29669813 |