CTDSPL
CTD small phosphatase-like protein
Also known as: C3orf8, CTDSL_HUMAN, HYA22, PSR1, RBSP3, SCP3
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O15194
- Gene
- CTDSPL
- Ensembl
- ENSG00000144677
- Chromosome
- 3
- Canonical length
- 276 aa
- Protein class
- Enzymes, Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Vesicles
OverviewNCBI Gene
Predicted to enable RNA polymerase II CTD heptapeptide repeat phosphatase activity. Predicted to be involved in chromatin remodeling and regulation of transcription by RNA polymerase II. Predicted to act upstream of or within negative regulation of G1/S transition of mitotic cell cycle and negative regulation of protein phosphorylation. Located in extracellular exosome. Biomarker of lung non-small cell carcinoma. [provided by Alliance of Genome Resources, Apr 2025]
Canonical amino-acid sequenceUniProt
276 residues, UniProt reviewed canonical sequence.
>O15194|CTDSPL
1 MDGPAIITQV TNPKEDEGRL PGAGEKASQC NVSLKKQRSR SILSSFFCCF RDYNVEAPPP
61 SSPSVLPPLV EENGGLQKGD QRQVIPIPSP PAKYLLPEVT VLDYGKKCVV IDLDETLVHS
121 SFKPISNADF IVPVEIDGTI HQVYVLKRPH VDEFLQRMGQ LFECVLFTAS LAKYADPVAD
181 LLDRWGVFRA RLFRESCVFH RGNYVKDLSR LGRELSKVII VDNSPASYIF HPENAVPVQS
241 WFDDMTDTEL LDLIPFFEGL SREDDVYSML HRLCNRLocalizationUniProt · AlphaFold · HPA
Whether an antibody against CTDSPL 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)
- 0.4
- Highest tissue expression
- 50 nTPM
Expression across tissuesHPA
Tissue
- skin: 50 nTPM
- kidney: 39 nTPM
- blood vessel: 38 nTPM
- colon: 31 nTPM
- placenta: 30 nTPM
- seminal vesicle: 30 nTPM
Single-cell type
- podocytes: 1,302 nCPM
- platelets: 580 nCPM
- distal convoluted tubule cells: 545 nCPM
- pituicytes/fscs: 425 nCPM
- megakaryocyte progenitors: 391 nCPM
- renal collecting duct intercalated cells: 352 nCPM
Immune cell
- total PBMC: 2.1 nTPM
- neutrophil: 0.4 nTPM
- classical monocyte: 0.2 nTPM
- naive CD4 T-cell: 0.2 nTPM
- basophil: 0 nTPM
- eosinophil: 0 nTPM
Brain region
- cerebellum: 35 nTPM
- cerebral cortex: 29 nTPM
- basal ganglia: 27 nTPM
- thalamus: 25 nTPM
- amygdala: 25 nTPM
- medulla oblongata: 24 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)
- 0.96
- gnomAD pLI
- 0
- gnomAD missense Z
- 2.08
- DepMap mean gene effect
- 0.07
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of CTDSPL 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 CTDSPL as an antibody target. Whether an autoantibody or antibody against CTDSPL could matter depends on whether native CTDSPL is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CTDSPL 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 CTDSPL as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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