KLRD1 (DR-01 Biosimilar) Recombinant Monoclonal Antibody

Code: CSB-RA615672MB1HU

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100ug

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US$199

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Species Reactivity: Human

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Target Background

Product Details

Uniprot NO.

Q13241

Alternative Names

DR 01 research-grade biosimilar; DR-01 research-grade biosimilar; DR-01 program research-grade biosimilar ;KLRD1 antibody; CD94 antibody; Natural killer cells antigen CD94 antibody; KP43 antibody; Killer cell lectin-like receptor subfamily D member 1 antibody; NK cell receptor antibody; CD antigen CD94 antibody

Species Reactivity

Human

Immunogen

Recombinant Human KLRD1 protein

Conjugate

Non-conjugated

Clonality

Monoclonal

Buffer

0.01M PBS，pH7.4

Storage

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.

Notes

Validation Status
Application-specific performance (e.g., in flow cytometry, ELISA, IHC or other assay formats) has not yet been experimentally verified by CUSABIO. Users are advised to determine the optimal working conditions empirically in their own assay systems.
Guaranteed Quality
① Antibody purity > 95% tested by SDS-PAGE.
② Endotoxin level < 0.1EU/ug tested by LAL method.

Lead Time

3-4 weeks
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.

Concentration

It differs from different batches. Please contact us to confirm it.

Usage

It is a non-therapeutic biosimilar antibody, owning the same variable region from the corresponding approved therapeutic antibody. In conclusion, it is a research-grade biosimilar antibody and expressed in mammalian cell, which can be directly used as positive controls in drug discovery or used for rapid verification of the biological functions of target protein.

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Description

This recombinant monoclonal antibody is developed as a research-grade biosimilar to DR-01, targeting KLRD1 (Killer cell Lectin-like Receptor subfamily D member 1), also known as CD94. KLRD1 is a C-type lectin receptor expressed predominantly on natural killer (NK) cells and a subset of CD8+ T cells, where it forms heterodimers with NKG2 family members to regulate cytotoxic lymphocyte activity. By interacting with HLA-E molecules on target cells, KLRD1/CD94 complexes function as critical immune checkpoints that modulate NK cell-mediated cytotoxicity and immune surveillance. Dysregulation of KLRD1 expression has been implicated in various immunological disorders, viral infections, and cancer immune evasion mechanisms, making it a valuable target for immunological research.

The reference antibody DR-01 has been utilized in studies examining NK cell biology, immune checkpoint regulation, and tumor immunology. This biosimilar provides researchers with a reliable tool for investigating KLRD1-mediated immune responses, NK cell phenotyping, and the role of innate immunity in disease pathogenesis. It supports diverse experimental approaches in immunology, oncology, and infectious disease research.

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Target Background

Function(From Uniprot)

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.

Gene References into Functions

an early response by KLRD1-expressing Natural killer cells may control influenza infection. PMID:29898768
it is not clear if high expression of CD94 on peripheral blood NK cells is related to abnormal activity of endometrial NK cells. PMID:24975965
Synergistic inhibition of natural killer cells by the nonsignaling molecule CD94. PMID:24082146
Studies indicate that HLA-E interacts with CD94/NKG2 receptors expressed mainly on the surface of natural killer (NK) cells, thus confining its role to the regulation of NK-cell function. PMID:22576308
Loss of CD94 is associated with rheumatoid arthritis. PMID:22102879
increased expression on natural killer cells in women with recurrent spontaneous abortion after IVIG therapy PMID:19811464
human CD56(bright) NK cells progress through a continuum of differentiation that ends with a CD94(low)CD56(dim) phenotype. PMID:19897577
Conservation and variation in human and chimpanzee CD94 genes PMID:11751968
A critical role of CD94-dependent MHC-I recognition for the regulation of IFN-gamma production and target lysis was demonstrated. PMID:12149421
TCR specificity dictates CD94/NKG2A expression by CTL. PMID:12387742
CD94 gene expression is regulated by distal and proximal promoters that transcribe unique initial exons specific to each promoter, resulting in two species of transcripts--the previously described CD94 mRNA and a novel CD94C mRNA. PMID:14607929
Aberrant expression of natural killer (NK) receptors CD94/NKG2A may have an impact on the magnitude and direction of dendritic cell activation of T cells under pathological conditions, such as chronic hepatitis C virus infection. PMID:15528343
A CD94 alternatively spliced transcript paired with an NKG2B isoform may contribute to the plasticity of the natural killer cell immunological synapse by insuring an adequate inhibitory signal. PMID:16237464
Cytolytic activity levels of purified CD94-expressing cells from 7-day cultures with FK506 were much higher than those from 7-day cultures without FK506. PMID:16378079
results indicate that the SNPs of the inhibitory receptor CD94/NKG2A and its haplotypes, as well as its ligand HLA-E, are associated with Behcet's disease immune systems PMID:17767552
identified molecular characteristics of an aggressive subset of pediatric patients with AML through a prospective evaluation of CD56+ neural cell adhesion molecule (NCAM) and CD94 expression PMID:18323797
Uncommon endocytic and trafficking pathway of the natural killer cell CD94/NKG2A inhibitory receptor is described. PMID:18363778
Under the influence of interleukin-12 stimulation, CD94/NKG2A is transiently inducible in natural killer (NK) cells bearing the homologous CD94/NKG2C-activating receptor, providing a potential negative regulatory feedback mechanism. PMID:19124726
In this work, the glycan ligands of NKG2D and CD94 for the first time were resolved. PMID:19303396
NKG2D and CD94 bind to heparin and sulfate-containing polysaccharides. PMID:19555665

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Subcellular Location

Cell membrane; Single-pass type II membrane protein.

Tissue Specificity

Expressed in NK cell subsets (at protein level). Expressed in memory/effector CD8-positive alpha-beta T cell subsets (at protein level). Expressed in melanoma-specific cytotoxic T cell clones (at protein level). Expressed in terminally differentiated cyto

Database Links

HGNC: 6378

UNIGENE: Hs.562457

KEGG: hsa:3824

STRING: 9606.ENSP00000338130

OMIM: 602894

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