KLRC1 report

I. Expression across cell types

II. Expression across tissues

sc-RNAseq data

Insufficient scRNA-seq data for expression of KLRC1 at tissue level.

III. Associated gene sets

GO_0045954Biological processpositive regulation of natural killer cell mediated cytotoxicity
GO_0045087Biological processinnate immune response
GO_0002769Biological processnatural killer cell inhibitory signaling pathway
GO_0001915Biological processnegative regulation of T cell mediated cytotoxicity
GO_0002223Biological processstimulatory C-type lectin receptor signaling pathway
GO_0002250Biological processadaptive immune response
GO_0045953Biological processnegative regulation of natural killer cell mediated cytotoxicity
GO_0002305Biological processCD8-positive, gamma-delta intraepithelial T cell differentiation
GO_0032814Biological processregulation of natural killer cell activation
GO_0007166Biological processcell surface receptor signaling pathway
GO_0009897Cellular componentexternal side of plasma membrane
GO_0043235Cellular componentreceptor complex
GO_0005886Cellular componentplasma membrane
GO_0004888Molecular functiontransmembrane signaling receptor activity
GO_0062082Molecular functionHLA-E specific inhibitory MHC class Ib receptor activity
GO_0030246Molecular functioncarbohydrate binding
GO_0023024Molecular functionMHC class I protein complex binding
GO_1990405Molecular functionprotein antigen binding
GO_0062080Molecular functioninhibitory MHC class Ib receptor activity
GO_0005515Molecular functionprotein binding

IV. Literature review

[source]
Gene nameKLRC1
Protein nameNKG2-A
NKG2-A/NKG2-B type II integral membrane protein (CD159 antigen-like family member A) (NK cell receptor A) (NKG2-A/B-activating NK receptor) (CD antigen CD159a)
Killer cell lectin like receptor C1
SynonymsNKG2A
DescriptionFUNCTION: Immune inhibitory receptor involved in self-nonself discrimination. In complex with KLRD1 on cytotoxic and regulatory lymphocyte subsets, recognizes non-classical major histocompatibility (MHC) class Ib molecule HLA-E loaded with self-peptides derived from the signal sequence of classical MHC class Ia molecules. Enables cytotoxic cells to monitor the expression of MHC class I molecules in healthy cells and to tolerate self . Upon HLA-E-peptide binding, transmits intracellular signals through two immunoreceptor tyrosine-based inhibition motifs (ITIMs) by recruiting INPP5D/SHP-1 and INPPL1/SHP-2 tyrosine phosphatases to ITIMs, and ultimately opposing signals transmitted by activating receptors through dephosphorylation of proximal signaling molecules . 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 HLA-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 . .; FUNCTION: (Microbial infection) Viruses like human cytomegalovirus have evolved an escape mechanism whereby virus-induced down-regulation of host MHC class I molecules is coupled to the binding of viral peptides to HLA-E, restoring HLA-E expression and inducing HLA-E-dependent NK cell immune tolerance to infected cells. Recognizes HLA-E in complex with human cytomegalovirus UL40-derived peptide (VMAPRTLIL) and inhibits NK cell cytotoxicity. .; FUNCTION: (Microbial infection) May recognize HLA-E in complex with HIV-1 gag/Capsid protein p24-derived peptide (AISPRTLNA) on infected cells and may inhibit NK cell cytotoxicity, a mechanism that allows HIV-1 to escape immune recognition. .; FUNCTION: (Microbial infection) Upon SARS-CoV-2 infection, may contribute to functional exhaustion of cytotoxic NK cells and CD8-positive T cells . On NK cells, may recognize HLA-E in complex with SARS-CoV-2 S/Spike protein S1-derived peptide (LQPRTFLL) expressed on the surface of lung epithelial cells, inducing NK cell exhaustion and dampening antiviral immune surveillance . .

AccessionsENST00000408006.7 [P26715-2]
H0YGB7
ENST00000543893.1
ENST00000347831.9 [P26715-2]
Q8NIA5
ENST00000544822.2 [P26715-1]
F5GYZ0
P26715
ENST00000359151.8 [P26715-1]
ENST00000536188.5