SLN
Sarcolipin
Also known as: MGC12301, MGC125854, MGC125855, SARCO_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O00631
- Gene
- SLN
- Ensembl
- ENSG00000170290
- Chromosome
- 11
- Canonical length
- 31 aa
- Protein class
- Predicted membrane proteins, Transporters
- Subcellular location
- Microtubules
- Quaternary structure
- Homooligomer
OverviewNCBI Gene
Sarcoplasmic reticulum Ca(2+)-ATPases are transmembrane proteins that catalyze the ATP-dependent transport of Ca(2+) from the cytosol into the lumen of the sarcoplasmic reticulum in muscle cells. This gene encodes a small proteolipid that regulates several sarcoplasmic reticulum Ca(2+)-ATPases. The transmembrane protein interacts with Ca(2+)-ATPases and reduces the accumulation of Ca(2+) in the sarcoplasmic reticulum without affecting the rate of ATP hydrolysis. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
31 residues, UniProt reviewed canonical sequence.
>O00631|SLN
1 MGINTRELFL NFTIVLITVI LMWLLVRSYQ YLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SLN can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Other membrane
- Secreted
- No
- Transmembrane segments
- 1
- Mean surface accessibility (rSASA)
- 0.55
- Highest tissue expression
- 7,680 nTPM
Expression across tissuesHPA
Tissue
- skeletal muscle: 7,680 nTPM
- tongue: 3,171 nTPM
- heart muscle: 931 nTPM
- esophagus: 141 nTPM
- salivary gland: 58 nTPM
- retina: 56 nTPM
Single-cell type
- thymic myoid cells: 348 nCPM
- müller glia: 306 nCPM
- myonuclei: 129 nCPM
- late spermatids: 15 nCPM
- epididymal efferent duct ciliated cells: 14 nCPM
- early spermatids: 12 nCPM
Immune cell
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- eosinophil: 0 nTPM
- gdT-cell: 0 nTPM
- intermediate monocyte: 0 nTPM
- MAIT T-cell: 0 nTPM
Brain region
- cerebellum: 5.5 nTPM
- basal ganglia: 4.3 nTPM
- cerebral cortex: 3.8 nTPM
- pons: 2.4 nTPM
- midbrain: 2.3 nTPM
- white matter: 1.6 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.89
- gnomAD pLI
- 0.29
- gnomAD missense Z
- 0.19
- DepMap mean gene effect
- -0.05
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- calcium ion transport
- negative regulation of ATPase-coupled calcium transmembrane transporter activity
- negative regulation of calcium ion import
- negative regulation of calcium ion import into sarcoplasmic reticulum
- negative regulation of protein-containing complex disassembly
- positive regulation of cold-induced thermogenesis
- regulation of ATPase-coupled calcium transmembrane transporter activity
- regulation of calcium ion transport
- regulation of relaxation of muscle
- sarcoplasmic reticulum calcium ion transport
- positive regulation of protein depolymerization
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Sarcolipin
- Sarcolipin
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of SLN in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads SLN as an antibody target. Whether an autoantibody or antibody against SLN could matter depends on whether native SLN is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SLN is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label SLN as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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