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FLASH GENE
Symbol SLN contributors: mct - updated : 23-10-2017
HGNC name sarcolipin
HGNC id 11089
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • low molecular weight proteolipid
  • a conserved threonine 5 at the N-terminus of SLN critically regulating SLN function and mediates beta-adrenergic responses , and deletion of SLN N-terminal residues (2)ERSTQ leads to loss of the uncoupling function even though the truncated peptide can target and constitutively bind ATP2A1
  • has a conserved C-terminal luminal tail composed of five amino acids ((27)RSYQY), which may contribute to a distinct ATP2A1 regulatory mechanism; C-terminal tail of SLN is a distinct, essential domain in the regulation of ATP2A1 and the functional properties of the SLN tail can be transferred to PLN
  • HOMOLOGY
    intraspecies homolog to phospholamban
    Homologene
    FAMILY
  • sarcolipin family
  • CATEGORY structural protein
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    text
  • sarco(endo)plasmic reticulum (SR) membrane protein
  • transmembrane protein expressed in the sarco/endoplasmic reticulum of skeletal and atrial muscles
  • basic FUNCTION
  • regulator of the sarco(endo)plasmic reticulum Ca(2+)-ATPase of fast-twitch skeletal muscle (SERCA1a)
  • inhibits polymerization of phospholamban to induce superinhibition of sarco(endo)plasmic reticulum Ca2+-ATPases (SERCAs)
  • its downregulation could play an important role in abnormal intracellular Ca2+ cycling in atrial pathology
  • is likely an important mediator of muscle thermogenesis and whole-body energy metabolism
  • effect of PLN and SLN, which becomes synergic when they are both present in the SR membrane, is expected to favor a rapid equilibration of ions on both sides of the membrane
  • SLN provides likely a novel mechanism of adaptive thermogenesis within skeletal muscle and protects against diet-induced obesity
  • important role for SLN in muscle metabolism and energy expenditure
  • SLN and its close analog phospholamban (PLN) are membrane proteins that regulate SERCA by inhibiting Ca(2+) transport in skeletal and cardiac muscl
  • small proteolipid and a regulator of sarco(endo)plasmic reticulum Ca(2+)-ATPase
  • transmembrane protein that can form a self-assembled pentamer
  • SLN, not PLN, is required for muscle-based thermogenesis
  • regulator of ATP2A1 activity in muscle, playing an important role in regulating muscle thermogenesis and metabolism
  • potential role for SLN during increased metabolic demand
  • plays an important role in adaptive muscle remodeling potentially through calcineurin stimulation, which could have important implications for other muscle diseases and conditions
  • plays crucial roles in heat production through modifying the function of sarco/endoplasmic reticulum Ca2+ ATPase, thereby being involved in thermogenesis and systemic metabolism
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • associated with the fast-twitch skeletal muscle sarcoplasmic reticulum Ca++ ATPase (ATP2A1)
  • inhibitor of cardiac sarcoplasmic reticulum Ca2+-ATPase (SERCA)
  • SLN and STIM1 act in opposing fashions to govern store operated Ca(2+) entry (SOCE) during myogenesis
  • SLN binding to ATP2A1 uncouples Ca(2+) transport from ATP hydrolysis
  • SLN and PLN inhibit ATP2A1 by using a similar mechanism
  • ANK1 interacts likely with SLN both directly and in complex with ATP2A1 and reduces SLN inhibitory effect on ATP2A1 activity
  • inhibitor of the sarco/endoplasmic reticulum (SR) Ca2+ ATPase (SERCA)
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --low  
    in tetralogy of Fallot
    constitutional     --low  
    in chronic atrial fibrillation (AF)
    constitutional     --low  
    in atria from heart failure patients
    constitutional     --over  
    in the muscle of Duchenne muscular dystrophy (DMD) patients
    constitutional     --low  
    results in cardiac hypertrophy and decreased cardiac contractility
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    neuromuscularmyopathydegenerative
    SLN reduction is a promising therapeutic approach for DMD
    ANIMAL & CELL MODELS
  • ablation of sarcolipin (Sln), a regulatory protein and uncoupler of sarco(endo)plasmic reticulum Ca2+-ATPases, leads to excessive diet-induced obesity and glucose intolerance in mice