NLRC3
NLR family CARD domain-containing protein 3
Also known as: CLR16.2, FLJ00348, NLRC3_HUMAN, NOD3
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q7RTR2
- Gene
- NLRC3
- Ensembl
- ENSG00000167984
- Chromosome
- 16
- Canonical length
- 1065 aa
- Protein class
- Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Vesicles,Centriolar satellite,Cytosol
OverviewNCBI Gene
This gene encodes a NOD-like receptor family member. The encoded protein is a cytosolic regulator of innate immunity. This protein directly interacts with stimulator of interferon genes (STING), to prevent its proper trafficking, resulting in disruption of STING-dependent activation of the innate immune response. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2014]
Canonical amino-acid sequenceUniProt
1065 residues, UniProt reviewed canonical sequence.
>Q7RTR2|NLRC3
1 MRKQEVRTGR EAGQGHGTGS PAEQVKALMD LLAGKGSQGS QAPQALDRTP DAPLGPCSND
61 SRIQRHRKAL LSKVGGGPEL GGPWHRLASL LLVEGLTDLQ LREHDFTQVE ATRGGGHPAR
121 TVALDRLFLP LSRVSVPPRV SITIGVAGMG KTTLVRHFVR LWAHGQVGKD FSLVLPLTFR
181 DLNTHEKLCA DRLICSVFPH VGEPSLAVAV PARALLILDG LDECRTPLDF SNTVACTDPK
241 KEIPVDHLIT NIIRGNLFPE VSIWITSRPS ASGQIPGGLV DRMTEIRGFN EEEIKVCLEQ
301 MFPEDQALLG WMLSQVQADR ALYLMCTVPA FCRLTGMALG HLWRSRTGPQ DAELWPPRTL
361 CELYSWYFRM ALSGEGQEKG KASPRIEQVA HGGRKMVGTL GRLAFHGLLK KKYVFYEQDM
421 KAFGVDLALL QGAPCSCFLQ REETLASSVA YCFTHLSLQE FVAAAYYYGA SRRAIFDLFT
481 ESGVSWPRLG FLTHFRSAAQ RAMQAEDGRL DVFLRFLSGL LSPRVNALLA GSLLAQGEHQ
541 AYRTQVAELL QGCLRPDAAV CARAINVLHC LHELQHTELA RSVEEAMESG ALARLTGPAH
601 RAALAYLLQV SDACAQEANL SLSLSQGVLQ SLLPQLLYCR KLRLDTNQFQ DPVMELLGSV
661 LSGKDCRIQK ISLAENQISN KGAKALARSL LVNRSLTSLD LRGNSIGPQG AKALADALKI
721 NRTLTSLSLQ GNTVRDDGAR SMAEALASNR TLSMLHLQKN SIGPMGAQRM ADALKQNRSL
781 KELMFSSNSI GDGGAKALAE ALKVNQGLES LDLQSNSISD AGVAALMGAL CTNQTLLSLS
841 LRENSISPEG AQAIAHALCA NSTLKNLDLT ANLLHDQGAR AIAVAVRENR TLTSLHLQWN
901 FIQAGAAQAL GQALQLNRSL TSLDLQENAI GDDGACAVAR ALKVNTALTA LYLQVASIGA
961 SGAQVLGEAL AVNRTLEILD LRGNAIGVAG AKALANALKV NSSLRRLNLQ ENSLGMDGAI
1021 CIATALSGNH RLQHINLQGN HIGDSGARMI SEAIKTNAPT CTVEMLocalizationUniProt · AlphaFold · HPA
Whether an antibody against NLRC3 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)
- 0.25
- Highest tissue expression
- 13 nTPM
Expression across tissuesHPA
Tissue
- lymph node: 13 nTPM
- spleen: 11 nTPM
- thymus: 11 nTPM
- tonsil: 10 nTPM
- appendix: 7.3 nTPM
- small intestine: 6.1 nTPM
Single-cell type
- nk-cells: 108 nCPM
- cardiomyocytes: 97 nCPM
- t-cells: 74 nCPM
- epicardial cells: 61 nCPM
- innate lymphoid cells: 59 nCPM
- thymocytes: 42 nCPM
Immune cell
- basophil: 3.1 nTPM
- NK-cell: 2.6 nTPM
- gdT-cell: 2.3 nTPM
- memory CD8 T-cell: 2.2 nTPM
- MAIT T-cell: 2.1 nTPM
- total PBMC: 2.1 nTPM
Brain region
- choroid plexus: 4.2 nTPM
- cerebellum: 4 nTPM
- cerebral cortex: 3.4 nTPM
- basal ganglia: 3 nTPM
- amygdala: 2.8 nTPM
- midbrain: 2.8 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)
- 1.24
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.49
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
- canonical NF-kappaB signal transduction
- negative regulation of canonical NF-kappaB signal transduction
- negative regulation of cytokine production involved in inflammatory response
- negative regulation of epithelial cell proliferation
- negative regulation of fibroblast proliferation
- negative regulation of inflammatory response
- negative regulation of innate immune response
- negative regulation of interferon-alpha production
- negative regulation of interferon-beta production
- negative regulation of interleukin-6 production
- negative regulation of NF-kappaB transcription factor activity
- negative regulation of NLRP3 inflammasome complex assembly
- negative regulation of non-canonical NF-kappaB signal transduction
- negative regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction
- negative regulation of tumor necrosis factor production
- T cell activation
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Leucine-rich repeat
- NACHT nucleoside triphosphatase
- P-loop containing nucleoside triphosphate hydrolase
- Leucine-rich repeat domain superfamily
- NOD1/2, winged helix domain
- NACHT, LRR and PYD domains-containing protein, helical domain HD2
- NOD-like receptor
- NACHT domain
- Leucine Rich repeat
- NLRC4 helical domain HD2
- NOD2 winged helix domain
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of NLRC3 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 NLRC3 as an antibody target. Whether an autoantibody or antibody against NLRC3 could matter depends on whether native NLRC3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
NLRC3 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 NLRC3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
Loading the interactive Seroatlas protein explorer...