TSNAX
Translin-associated protein X
Also known as: C3PO, TRAX, TSNAX_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q99598
- Gene
- TSNAX
- Ensembl
- ENSG00000116918
- Chromosome
- 1
- Canonical length
- 290 aa
- Protein class
- Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Golgi apparatus,Cytosol
OverviewNCBI Gene
This gene encodes a protein which specifically interacts with translin, a DNA-binding protein that binds consensus sequences at breakpoint junctions of chromosomal translocations. The encoded protein contains bipartite nuclear targeting sequences that may provide nuclear transport for translin, which lacks any nuclear targeting motifs. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
290 residues, UniProt reviewed canonical sequence.
>Q99598|TSNAX
1 MSNKEGSGGF RKRKHDNFPH NQRREGKDVN SSSPVMLAFK SFQQELDARH DKYERLVKLS
61 RDITVESKRT IFLLHRITSA PDMEDILTES EIKLDGVRQK IFQVAQELSG EDMHQFHRAI
121 TTGLQEYVEA VSFQHFIKTR SLISMDEINK QLIFTTEDNG KENKTPSSDA QDKQFGTWRL
181 RVTPVDYLLG VADLTGELMR MCINSVGNGD IDTPFEVSQF LRQVYDGFSF IGNTGPYEVS
241 KKLYTLKQSL AKVENACYAL KVRGSEIPKH MLADVFSVKT EMIDQEEGISLocalizationUniProt · AlphaFold · HPA
Whether an antibody against TSNAX 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
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.36
- Highest tissue expression
- 49 nTPM
Expression across tissuesHPA
Tissue
- skeletal muscle: 49 nTPM
- tongue: 38 nTPM
- parathyroid gland: 38 nTPM
- adrenal gland: 30 nTPM
- kidney: 30 nTPM
- thyroid gland: 28 nTPM
Single-cell type
- microglia: 82 nCPM
- choroid plexus epithelial cells: 59 nCPM
- oligodendrocytes: 55 nCPM
- other brain neurons: 41 nCPM
- brain excitatory neurons: 39 nCPM
- bergmann glia: 37 nCPM
Immune cell
- basophil: 195 nTPM
- eosinophil: 86 nTPM
- non-classical monocyte: 56 nTPM
- NK-cell: 52 nTPM
- intermediate monocyte: 40 nTPM
- T-reg: 40 nTPM
Brain region
- choroid plexus: 31 nTPM
- hypothalamus: 25 nTPM
- spinal cord: 21 nTPM
- white matter: 21 nTPM
- cerebral cortex: 20 nTPM
- hippocampal formation: 20 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)
- 0.53
- gnomAD pLI
- 0.49
- gnomAD missense Z
- 1.3
- DepMap mean gene effect
- -0.04
- DepMap dependency class
- selective
OntologyGO
Biological processes
- cell differentiation
- regulatory ncRNA-mediated post-transcriptional gene silencing
- siRNA processing
- spermatogenesis
Molecular functions
- A2A adenosine receptor binding
- DNA binding
- metal ion binding
- protein-containing complex binding
- RNA binding
- RNA endonuclease activity
- sequence-specific DNA binding
- single-stranded DNA binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of TSNAX 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 TSNAX as an antibody target. Whether an autoantibody or antibody against TSNAX could matter depends on whether native TSNAX is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
TSNAX 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 TSNAX as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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