ArticleJournal of molecular and cellular cardiology2009
Threonine-5 at the N-terminus can modulate sarcolipin function in cardiac myocytes.
Article in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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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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.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
- Microprotein, macro-effect: DWORF as a therapeutic strategy in heart failure.Frontiers in cell and developmental biology · 2026Review
- Emerging roles for microproteins as critical regulators of endoplasmic reticulum function and cellular homeostasis.Seminars in cell & developmental biology · 2025Review
- Sex Differences in Cardiac Tolerance to Oxygen Deprivation - 40 Years of Cardiovascular Research.Physiological research · 2024Review
- The Meeting of Micropeptides with Major CaMembranes · 2023Review
- Heart Failure in Menopause: Treatment and New Approaches.International journal of molecular sciences · 2022Review
- Calcium cycling as a mediator of thermogenic metabolism in adipose tissue.Molecular pharmacology · 2022Article
- Structural basis for sarcolipin's regulation of muscle thermogenesis by the sarcoplasmic reticulum CaScience advances · 2021Article
- Sarcoplasmic Reticulum from Horse Gluteal Muscle Is Poised for Enhanced Calcium Transport.Veterinary sciences · 2021Article
- Nothing Regular about the Regulins: Distinct Functional Properties of SERCA Transmembrane Peptide Regulatory Subunits.International journal of molecular sciences · 2021Review
- Sarcolipin alters SERCA1a interdomain communication by impairing binding of both calcium and ATP.Scientific reports · 2021Article
- Sarcolipin Exhibits Abundant RNA Transcription and Minimal Protein Expression in Horse Gluteal Muscle.Veterinary sciences · 2020Article
- Schistosoma mansoni sarco/endoplasmic reticulum CaJournal of bioenergetics and biomembranes · 2020Review
- Conserved Luminal C-Terminal Domain Dynamically Controls Interdomain Communication in Sarcolipin.Journal of chemical information and modeling · 2020Article
- SERCA2a: a key protein in the CaHeart failure reviews · 2020Review
- Estrogen regulation of cardiac cAMP-L-type CaCell communication and signaling : CCS · 2019Article
- Non-ion channel therapeutics for heart failure and atrial fibrillation: Are CaMKII inhibitors ready for clinical use?Journal of molecular and cellular cardiology · 2018Article
- Sarcolipin Makes Heat, but Is It Adaptive Thermogenesis?Frontiers in physiology · 2018Article
- The Role of Sarcolipin in Muscle Non-shivering Thermogenesis.Frontiers in physiology · 2018Article
- Early vertebrate origin and diversification of small transmembrane regulators of cellular ion transport.The Journal of physiology · 2017Article
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Sarcolipin (SLN) has emerged as an important regulator of the atrial sarcoplasmic reticulum (SR) Ca2+ transport. The inhibitory effect of SLN on cardiac SR Ca2+ ATPase (SERCA) pump can be relieved by beta-adrenergic stimulation, which indicates that SLN is a reversible inhibitor. However, the mechanism of this reversible regulation of SERCA pump by SLN is yet to be determined. In the current study using adult rat ventricular myocytes we provide evidence that the threonine 5 (T5) residue at the N-terminus of SLN which is conserved among various species, critically regulates the SLN function. Point mutation of T5-->alanine exerts an inhibitory effect on myocyte contractility and calcium transients similar to that of wild-type SLN, whereas mutation of T5-->glutamic acid which mimics the phosphorylation abolished the inhibitory function of SLN. Our results showed that T5 can be phosphorylated in vitro by calcium-calmodulin dependent protein kinase II (CaMKII). Blocking the CaMKII activity in WT-SLN overexpressing myocytes using autocamtide inhibitory peptide completely abolished the beta-adrenergic response. Taken together, our data suggest that T5 is the key amino acid which modulates SLN function via phosphorylation/dephosphorylation mechanisms through CaMKII pathway.
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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.