• Western blot analysis of extracts of various cell lines, using KLRC1 antibody (STJ24337) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (STJS000856) at 1:10000 dilution. Lysates/proteins: 25 Mu g per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Enhanced Kit. Exposure time: 5min.

Anti-KLRC1 antibody (96-215) (STJ24337)

SKU:
STJ24337

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Host: Rabbit
Applications: WB
Reactivity: Mouse
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Rabbit polyclonal antibody anti-KLRC1 (96-215) is suitable for use in Western Blot research applications.
Clonality: Polyclonal
Conjugation: Unconjugated
Isotype: IgG
Formulation: PBS with 0.02% Sodium Azide, 50% Glycerol, pH7.3.
Purification: Affinity purification
Dilution Range: WB 1:500-1:2000
Storage Instruction: Store at-20°C for up to 1 year from the date of receipt, and avoid repeat freeze-thaw cycles.
Gene Symbol: KLRC1
Gene ID: 3821
Uniprot ID: NKG2A_HUMAN
Immunogen Region: 96-215
Immunogen: Recombinant fusion protein containing a sequence corresponding to amino acids 96-215 of human KLRC1 (NP_015567.1).
Immunogen Sequence: RHCGHCPEEWITYSNSCYYI GKERRTWEESLLACTSKNSS LLSIDNEEEMKFLSIISPSS WIGVFRNSSHHPWVTMNGLA FKHEIKDSDNAELNCAVLQV NRLKSAQCGSSIIYHCKHKL
Tissue Specificity Predominantly expressed in NK cells (at protein level). Expressed in intraepithelial CD8-positive T cell subsets with higher frequency in gamma-delta T cells than alpha-beta T cells (at protein level). Expressed in memory gamma-delta T cells (at protein level). Restricted to a subset of memory/effector CD8-positive alpha-beta T cells (at protein level). Expressed in intratumoral NK and CD8-positive T cells. Expressed in melanoma-specific cytotoxic T cell clones (at protein level). KLRD1-KLRC1 and KLRD1-KLRC2 are differentially expressed in NK and T cell populations, with only minor subsets expressing both receptor complexes (at protein level).
Post Translational Modifications Phosphorylated.
Function 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. (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 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
Database Links Reactome: R-HSA-198933
Cellular Localisation Cell Membrane
Single-Pass Type Ii Membrane Protein
Alternative Antibody Names Anti-Nkg2-A/Nkg2-B Type Ii Integral Membrane Protein antibody
Anti-Cd159 Antigen-Like Family Member A antibody
Anti-Nk Cell Receptor A antibody
Anti-Nkg2-A/B-Activating Nk Receptor antibody
Anti-Cd Antigen Cd159a antibody
Anti-KLRC1 antibody
Anti-NKG2A antibody

Information sourced from Uniprot.org

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