SLC25A33
Solute carrier family 25 member 33
Also known as: BMSC-MCP, MGC4399, PNC1, S2533_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9BSK2
- Gene
- SLC25A33
- Ensembl
- ENSG00000171612
- Chromosome
- 1
- Canonical length
- 321 aa
- Protein class
- Predicted membrane proteins, Transporters
OverviewNCBI Gene
SLC25A33 belongs to the SLC25 family of mitochondrial carrier proteins (Haitina et al., 2006 [PubMed 16949250]).[supplied by OMIM, Mar 2008]
Canonical amino-acid sequenceUniProt
321 residues, UniProt reviewed canonical sequence.
>Q9BSK2|SLC25A33
1 MATGGQQKEN TLLHLFAGGC GGTVGAIFTC PLEVIKTRLQ SSRLALRTVY YPQVHLGTIS
61 GAGMVRPTSV TPGLFQVLKS ILEKEGPKSL FRGLGPNLVG VAPSRAVYFA CYSKAKEQFN
121 GIFVPNSNIV HIFSAGSAAF ITNSLMNPIW MVKTRMQLEQ KVRGSKQMNT LQCARYVYQT
181 EGIRGFYRGL TASYAGISET IICFAIYESL KKYLKEAPLA SSANGTEKNS TSFFGLMAAA
241 ALSKGCASCI AYPHEVIRTR LREEGTKYKS FVQTARLVFR EEGYLAFYRG LFAQLIRQIP
301 NTAIVLSTYE LIVYLLEDRT QLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SLC25A33 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
- 6
- Mean surface accessibility (rSASA)
- 0.33
- Highest tissue expression
- 26 nTPM
Expression across tissuesHPA
Tissue
- tongue: 26 nTPM
- skeletal muscle: 17 nTPM
- basal ganglia: 15 nTPM
- midbrain: 15 nTPM
- cerebral cortex: 13 nTPM
- testis: 13 nTPM
Single-cell type
- late spermatids: 333 nCPM
- müller glia: 331 nCPM
- late primary spermatocytes: 271 nCPM
- epididymal principal cells: 235 nCPM
- early primary spermatocytes: 224 nCPM
- rod photoreceptor cells: 194 nCPM
Immune cell
- basophil: 2.8 nTPM
- memory B-cell: 0.8 nTPM
- naive CD4 T-cell: 0.6 nTPM
- naive CD8 T-cell: 0.6 nTPM
- gdT-cell: 0.5 nTPM
- myeloid DC: 0.5 nTPM
Brain region
- thalamus: 21 nTPM
- cerebellum: 19 nTPM
- midbrain: 18 nTPM
- hypothalamus: 18 nTPM
- spinal cord: 17 nTPM
- white matter: 17 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)
- 0.83
- gnomAD pLI
- 0.01
- gnomAD missense Z
- 0.84
- DepMap mean gene effect
- -0.09
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cellular response to insulin stimulus
- cellular response to insulin-like growth factor stimulus
- mitochondrial respiratory chain complex III assembly
- mitochondrial transcription
- mitochondrion organization
- positive regulation of cell growth
- positive regulation of cell population proliferation
- pyrimidine nucleotide import into mitochondrion
- regulation of oxidative phosphorylation
- regulation of reactive oxygen species biosynthetic process
- mitochondria-nucleus signaling pathway
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads SLC25A33 as an antibody target. Whether an autoantibody or antibody against SLC25A33 could matter depends on whether native SLC25A33 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SLC25A33 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 SLC25A33 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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