Seroatlas · Human Serome Atlas

NOG

Noggin

Also known as: NOGG_HUMAN, SYM1, SYNS1

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
Q13253
Gene
NOG
Ensembl
ENSG00000183691
Chromosome
17
Canonical length
232 aa
Protein class
Disease related genes, Human disease related genes, Predicted secreted proteins
Secretome location
Secreted to blood
Quaternary structure
Homodimer

OverviewNCBI Gene

The secreted polypeptide, encoded by this gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, this protein may have a principal role in creating morphogenic gradients. The protein appears to have pleiotropic effect, both early in development as well as in later stages. It was originally isolated from Xenopus based on its ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by UV treatment. The results of the mouse knockout of the ortholog suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation. Recently, several dominant human NOG mutations in unrelated families with proximal symphalangism (SYM1) and multiple synostoses syndrome (SYNS1) were identified; both SYM1 and SYNS1 have multiple joint fusion as their principal feature, and map to the same region (17q22) as this gene. All of these mutations altered evolutionarily conserved amino acid residues. The amino acid sequence of this human gene is highly homologous to that of Xenopus, rat and mouse. [provided by RefSeq, Jul 2008]

Canonical amino-acid sequenceUniProt

232 residues, UniProt reviewed canonical sequence.

>Q13253|NOG
     1  MERCPSLGVT LYALVVVLGL RATPAGGQHY LHIRPAPSDN LPLVDLIEHP DPIFDPKEKD
    61  LNETLLRSLL GGHYDPGFMA TSPPEDRPGG GGGAAGGAED LAELDQLLRQ RPSGAMPSEI
   121  KGLEFSEGLA QGKKQRLSKK LRRKLQMWLW SQTFCPVLYA WNDLGSRFWP RYVKVGSCFS
   181  KRSCSVPEGM VCKPSKSVHL TVLRWRCQRR GGQRCGWIPI QYPIISECKC SC

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against NOG 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
Secreted
Secreted
Yes
Transmembrane segments
0
Mean surface accessibility (rSASA)
0.43
Highest tissue expression
10 nTPM

Expression across tissuesHPA

Tissue

  • placenta: 10 nTPM
  • basal ganglia: 5.5 nTPM
  • cerebral cortex: 3.8 nTPM
  • amygdala: 3.7 nTPM
  • cervix: 3.4 nTPM
  • hippocampal formation: 3.4 nTPM

Single-cell type

  • retinal pigment epithelial cells: 98 nCPM
  • extravillous trophoblasts: 26 nCPM
  • hematopoietic stem cells: 6.8 nCPM
  • bergmann glia: 6.5 nCPM
  • thymic myoid cells: 5.4 nCPM
  • thymocytes: 4.2 nCPM

Immune cell

  • naive CD4 T-cell: 73 nTPM
  • naive CD8 T-cell: 35 nTPM
  • memory CD4 T-cell: 4.4 nTPM
  • T-reg: 3.4 nTPM
  • total PBMC: 3.1 nTPM
  • basophil: 0.9 nTPM

Brain region

  • thalamus: 18 nTPM
  • amygdala: 14 nTPM
  • midbrain: 11 nTPM
  • basal ganglia: 11 nTPM
  • cerebral cortex: 9.5 nTPM
  • hippocampal formation: 9.3 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about NOG.

Disease | AllUniProt

Conditions NOG is implicated in, by any mechanism.

Disease | GeneticClinVar

50 pathogenic / likely-pathogenic of 249 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

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)
0.42
gnomAD pLI
0.89
gnomAD missense Z
1.32
DepMap mean gene effect
0
DepMap dependency class
none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% 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 NOG 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 NOG as an antibody target. Whether an autoantibody or antibody against NOG could matter depends on whether native NOG is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

NOG is annotated as secreted, so native NOG circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.

Annotation status

The present source text does not explicitly label NOG as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/NOG. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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