SYF2
Pre-mRNA-splicing factor SYF2
Also known as: CBPIN, DKFZp564O2082, fSAP29, NTC31, p29, SYF2_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O95926
- Gene
- SYF2
- Ensembl
- ENSG00000117614
- Chromosome
- 1
- Canonical length
- 243 aa
- Protein class
- Predicted intracellular proteins
- Subcellular location
- Nuclear speckles
OverviewNCBI Gene
This gene encodes a nuclear protein that interacts with cyclin D-type binding-protein 1, which is thought to be a cell cycle regulator at the G1/S transition. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
243 residues, UniProt reviewed canonical sequence.
>O95926|SYF2
1 MAAIAASEVL VDSAEEGSLA AAAELAAQKR EQRLRKFREL HLMRNEARKL NHQEVVEEDK
61 RLKLPANWEA KKARLEWELK EEEKKKECAA RGEDYEKVKL LEISAEDAER WERKKKRKNP
121 DLGFSDYAAA QLRQYHRLTK QIKPDMETYE RLREKHGEEF FPTSNSLLHG THVPSTEEID
181 RMVIDLEKQI EKRDKYSRRR PYNDDADIDY INERNAKFNK KAERFYGKYT AEIKQNLERG
241 TAVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SYF2 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)
- 0.5
- Highest tissue expression
- 139 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 139 nTPM
- ovary: 98 nTPM
- blood vessel: 89 nTPM
- skeletal muscle: 77 nTPM
- thymus: 72 nTPM
- tonsil: 72 nTPM
Single-cell type
- syncytiotrophoblasts: 351 nCPM
- esophageal apical cells: 310 nCPM
- neutrophils: 299 nCPM
- enterocytes: 294 nCPM
- ovarian stromal cells: 289 nCPM
- epididymal efferent duct absorptive cells: 246 nCPM
Immune cell
- neutrophil: 339 nTPM
- eosinophil: 224 nTPM
- basophil: 186 nTPM
- memory B-cell: 141 nTPM
- T-reg: 130 nTPM
- naive B-cell: 126 nTPM
Brain region
- hypothalamus: 27 nTPM
- white matter: 25 nTPM
- medulla oblongata: 23 nTPM
- cerebellum: 23 nTPM
- spinal cord: 21 nTPM
- choroid plexus: 21 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
- 0.26
- DepMap mean gene effect
- -0.99
- DepMap dependency class
- common
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
- embryonic organ development
- gastrulation
- in utero embryonic development
- mitotic G2 DNA damage checkpoint signaling
- mRNA splicing, via spliceosome
- positive regulation of cell population proliferation
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- mRNA splicing factor SYF2
- SYF2 splicing factor
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of SYF2 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 SYF2 as an antibody target. Whether an autoantibody or antibody against SYF2 could matter depends on whether native SYF2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SYF2 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 SYF2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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