Klrd1
entrez
25110
canonical
uniprot
O35778
canonical
ensembl
ENSRNOG00000060246
resolver
ensembl
ENSRNOG00055024701
resolver
ensembl
ENSRNOG00060016054
resolver
ensembl
ENSRNOG00065033801
resolver
ensp
ENSRNOP00000074715
resolver
ensp
ENSRNOP00055034771
resolver
ensp
ENSRNOP00060022106
resolver
ensp
ENSRNOP00065047793
resolver
enst
ENSRNOT00000082064
resolver
enst
ENSRNOT00055042576
resolver
enst
ENSRNOT00060027518
resolver
enst
ENSRNOT00065058045
resolver
genesymbol
Klrd1
resolver
genesymbol_syn
Cd94
resolver
uniprot_entry
KLRD1_RAT
resolver
amino_acid_sequence
MAVSRITRWRLMSMFFGIKCLFLIVALGVLVKNSFTIQNIQSTPSSTPIVEFQKVSKCCACLEKWIGHQCSCYFISKEEKSWKGSREFCASQNSSLLQLQTRNELSFMSSSQAFFWIGIHYNEERSAWLWEDGTFPSKDLFPEFSKFRQDHCIGYSISREISSESCENKNRFICKQLPT
uniprot
proteins
function
FUNCTION: Immune receptor involved in self-nonself discrimination. In complex with KLRC1 or KLRC2 on cytotoxic and regulatory lymphocyte subsets, recognizes non-classical major histocompatibility (MHC) class Ib molecule MHC-E loaded with self-peptides derived from the signal sequence of classical MHC class Ia and non-classical MHC class Ib molecules. Enables cytotoxic cells to monitor the expression of MHC class I molecules in healthy cells and to tolerate self. Primarily functions as a ligand binding subunit as it lacks the capacity to signal. {ECO:0000250|UniProtKB:Q13241}.; FUNCTION: KLRD1-KLRC1 acts as an immune inhibitory receptor. Key inhibitory receptor on natural killer (NK) cells that regulates their activation and effector functions. Dominantly counteracts T cell receptor signaling on a subset of memory/effector CD8-positive T cells as part of an antigen-driven response to avoid autoimmunity. On intraepithelial CD8-positive gamma-delta regulatory T cells triggers TGFB1 secretion, which in turn limits the cytotoxic programming of intraepithelial CD8-positive alpha-beta T cells, distinguishing harmless from pathogenic antigens. In MHC-E-rich tumor microenvironment, acts as an immune inhibitory checkpoint and may contribute to progressive loss of effector functions of NK cells and tumor-specific T cells, a state known as cell exhaustion. Upon MHC-E-peptide binding, transmits intracellular signals through KLRC1 immunoreceptor tyrosine-based inhibition motifs (ITIMs) by recruiting INPP5D/SHIP-1 and INPPL1/SHIP-2 tyrosine phosphatases to ITIMs, and ultimately opposing signals transmitted by activating receptors through dephosphorylation of proximal signaling molecules. {ECO:0000250|UniProtKB:Q13241}.; FUNCTION: KLRD1-KLRC2 acts as an immune activating receptor. On cytotoxic lymphocyte subsets recognizes MHC-E loaded with signal sequence-derived peptides from non-classical MHC class Ib MHC-G molecules, likely playing a role in the generation and effector functions of adaptive NK cells and in maternal-fetal tolerance during pregnancy. Regulates the effector functions of terminally differentiated cytotoxic lymphocyte subsets, and in particular may play a role in adaptive NK cell response to viral infection. Upon MHC-E-peptide binding, transmits intracellular signals via the adapter protein TYROBP/DAP12, triggering the phosphorylation of proximal signaling molecules and cell activation. {ECO:0000250|UniProtKB:Q13241}.
uniprot
proteins
mass_dalton
20781
uniprot
proteins
pubmed
15489334
uniprot
proteins
pubmed
9295048
uniprot
proteins
sequence_length
179
uniprot
proteins
subcellular_location
SUBCELLULAR LOCATION: Cell membrane {ECO:0000250|UniProtKB:Q13241}; Single-pass type II membrane protein {ECO:0000255}.
uniprot
proteins
transmembrane_region
TRANSMEM 11..31; /note="Helical; Signal-anchor for type II membrane protein"; /evidence="ECO:0000255
uniprot
proteins