产品详情

  • 产品名称：Human CD94 protein (Recombinant) (N-His-Avi) {Biotin} (STJP001683)

  • 产品型号：STJP001683
  • 产品厂商：ST john's laboratory
  • 产品文档：
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简单介绍：
Human CD94 protein (Recombinant) (N-His-Avi) {Biotin} (STJP001683)
详情介绍：
Host: HEK293
Note: STRICTLY FOR FURTHER RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Recombinant-Human CD94-N-His-Avi protein was developed from hek293 and has a target region of N-His-Avi. For use in research applications.
Conjugation: Biotin
Formulation: Lyophilised from 0.2 µm filtered PBS solution pH7.4.
Dilution Range: Upon receipt centrifuge vial to ensure maximal product extraction, recommended: 20sec, 5K RPM
Storage Instruction: The lyophilized protein is stable for at least 1 year from date of receipt at-20°C.
Endotoxin: Endotoxin content was assayed using a LAL gel clot method. Endotoxin level was found to be less than 0.1 ng/µg (1EU/µg).
Gene Symbol: KLRD1
Gene ID: 3824
Uniprot ID: KLRD1_HUMAN
Immunogen Region: Ser34-Ile179
Immunogen: DNA sequence encoding Human CD94 including a N-His-Avi tag was expressed in HEK293 Cells. The recombinant protein was then biotinylated site specific using the AVItag biotinylation technology.
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 HLA-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. 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 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. Upon HLA-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. KLRD1-KLRC2 acts as an immune activating receptor. On cytotoxic lymphocyte subsets recognizes HLA-E loaded with signal sequence-derived peptides from non-classical MHC class Ib HLA-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 HLA-E-peptide binding, transmits intracellular signals via the adapter protein TYROBP/DAP12, triggering the phosphorylation of proximal signaling molecules and cell activation. (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. (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. (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.
Protein Name Natural Killer Cells Antigen Cd94
Kp43
Killer Cell Lectin-Like Receptor Subfamily D Member 1
Nk Cell Receptor
Cd Antigen Cd94
Database Links Reactome: R-HSA-198933
Reactome: R-HSA-2172127
Reactome: R-HSA-2424491
Cellular Localisation Cell Membrane
Single-Pass Type Ii Membrane Protein
Alternative Protein Names Natural Killer Cells Antigen Cd94 protein
Kp43 protein
Killer Cell Lectin-Like Receptor Subfamily D Member 1 protein
Nk Cell Receptor protein
Cd Antigen Cd94 protein
KLRD1 protein
CD94 protein

Information sourced from Uniprot.org

12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance
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