SYNCRIP
Heterogeneous nuclear ribonucleoprotein Q
Also known as: dJ3J17.2, GRY-RBP, hnRNP-Q, HNRNPQ, HNRPQ_HUMAN, HNRPQ1, NSAP1
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O60506
- Gene
- SYNCRIP
- Ensembl
- ENSG00000135316
- Chromosome
- 6
- Canonical length
- 623 aa
- Protein class
- Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Cytosol
OverviewNCBI Gene
This gene encodes a member of the cellular heterogeneous nuclear ribonucleoprotein (hnRNP) family. hnRNPs are RNA binding proteins that complex with heterogeneous nuclear RNA (hnRNA) and regulate alternative splicing, polyadenylation, and other aspects of mRNA metabolism and transport. The encoded protein plays a role in multiple aspects of mRNA maturation and is associated with several multiprotein complexes including the apoB RNA editing-complex and survival of motor neurons (SMN) complex. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene, and a pseudogene of this gene is located on the short arm of chromosome 20. [provided by RefSeq, Dec 2011]
Canonical amino-acid sequenceUniProt
623 residues, UniProt reviewed canonical sequence.
>O60506|SYNCRIP
1 MATEHVNGNG TEEPMDTTSA VIHSENFQTL LDAGLPQKVA EKLDEIYVAG LVAHSDLDER
61 AIEALKEFNE DGALAVLQQF KDSDLSHVQN KSAFLCGVMK TYRQREKQGT KVADSSKGPD
121 EAKIKALLER TGYTLDVTTG QRKYGGPPPD SVYSGQQPSV GTEIFVGKIP RDLFEDELVP
181 LFEKAGPIWD LRLMMDPLTG LNRGYAFVTF CTKEAAQEAV KLYNNHEIRS GKHIGVCISV
241 ANNRLFVGSI PKSKTKEQIL EEFSKVTEGL TDVILYHQPD DKKKNRGFCF LEYEDHKTAA
301 QARRRLMSGK VKVWGNVGTV EWADPIEDPD PEVMAKVKVL FVRNLANTVT EEILEKAFSQ
361 FGKLERVKKL KDYAFIHFDE RDGAVKAMEE MNGKDLEGEN IEIVFAKPPD QKRKERKAQR
421 QAAKNQMYDD YYYYGPPHMP PPTRGRGRGG RGGYGYPPDY YGYEDYYDYY GYDYHNYRGG
481 YEDPYYGYED FQVGARGRGG RGARGAAPSR GRGAAPPRGR AGYSQRGGPG SARGVRGARG
541 GAQQQRGRGV RGARGGRGGN VGGKRKADGY NQPDSKRRQT NNQNWGSQPI AQQPLQGGDH
601 SGNYGYKSEN QEFYQDTFGQ QWKLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SYNCRIP 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)
- 0.45
- Highest tissue expression
- 65 nTPM
Expression across tissuesHPA
Tissue
- esophagus: 65 nTPM
- tonsil: 64 nTPM
- appendix: 55 nTPM
- thymus: 55 nTPM
- lymph node: 54 nTPM
- thyroid gland: 54 nTPM
Single-cell type
- microglia: 74 nCPM
- proximal tubule cells: 54 nCPM
- distal convoluted tubule cells: 51 nCPM
- oligodendrocytes: 50 nCPM
- choroid plexus epithelial cells: 50 nCPM
- renal connecting tubule cells: 50 nCPM
Immune cell
- non-classical monocyte: 21 nTPM
- intermediate monocyte: 19 nTPM
- NK-cell: 17 nTPM
- myeloid DC: 14 nTPM
- gdT-cell: 14 nTPM
- T-reg: 14 nTPM
Brain region
- medulla oblongata: 47 nTPM
- hypothalamus: 46 nTPM
- cerebellum: 44 nTPM
- spinal cord: 41 nTPM
- thalamus: 41 nTPM
- pons: 41 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about SYNCRIP.
Disease | GeneticClinVar
5 pathogenic / likely-pathogenic of 142 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- SYNCRIP-associated neurodevelopmental disorder
- SYNCRIP-related neurodevelopmental disorder
Disease | ImmuneIEDB
Conditions an epitope on SYNCRIP was assayed in.
- skin melanoma T cell
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)
- 0.21
- gnomAD pLI
- 1
- gnomAD missense Z
- 3.54
- DepMap mean gene effect
- -0.31
- 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 type II interferon
- chromosomal 5-methylcytosine DNA demethylation pathway
- CRD-mediated mRNA stabilization
- mRNA modification
- mRNA splicing, via spliceosome
- negative regulation of nuclear-transcribed mRNA catabolic process, deadenylation-dependent decay
- negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay
- negative regulation of translation
- osteoblast differentiation
- positive regulation of cytoplasmic translation
- RNA processing
- RNA splicing
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- RNA recognition motif domain
- HnRNP R/Q splicing factor
- Nucleotide-binding alpha-beta plait domain superfamily
- RNA-binding domain superfamily
- Heterogeneous nuclear ribonucleoprotein Q acidic domain
- RNA recognition motif
- Heterogeneous nuclear ribonucleoprotein Q acidic domain
- Heterogeneous nuclear ribonucleoprotein Q, RNA recognition motif 1
- Heterogeneous nuclear ribonucleoprotein Q, RNA recognition motif 2
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of SYNCRIP 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 SYNCRIP as an antibody target. Whether an autoantibody or antibody against SYNCRIP could matter depends on whether native SYNCRIP is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SYNCRIP 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 SYNCRIP as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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