KLRG1 (Ulviprubart Biosimilar) Recombinant Monoclonal Antibody

Code CSB-RA846610MB1HU
Size US$9799
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Product Details

Uniprot No.
Target Names
Alternative Names
ABC008 research-grade biosimilar; ABC 008 research-grade biosimilar; ABC-008 research-grade biosimilar ;KLRG1 antibody; CLEC15A antibody; MAFA antibody; MAFAL antibody; Killer cell lectin-like receptor subfamily G member 1 antibody; C-type lectin domain family 15 member A antibody; ITIM-containing receptor MAFA-L antibody; MAFA-like receptor antibody; Mast cell function-associated antigen antibody
Species Reactivity
Human
Immunogen
Recombinant Human KLRG1 protein
Immunogen Species
Homo sapiens (Human)
Conjugate
Non-conjugated
Clonality
Monoclonal
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
0.01M PBS,pH7.4
Form
Liquid
Troubleshooting and FAQs
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
Description

This recombinant monoclonal antibody is developed as a research-grade biosimilar to Ulviprubart, targeting KLRG1 (Killer cell Lectin-like Receptor subfamily G member 1), an inhibitory receptor expressed on senescent and terminally differentiated immune cells. KLRG1 functions as a negative regulator of T cell and NK cell activation, binding to E-cadherin and N-cadherin on target cells to deliver inhibitory signals that limit immune responses. This receptor plays a critical role in immune senescence, chronic inflammation, and tumor immune evasion, as KLRG1-expressing cells exhibit reduced proliferative capacity and effector functions. Elevated KLRG1 expression has been associated with aging, chronic viral infections, autoimmune disorders, and cancer, where it contributes to immune exhaustion and impaired anti-tumor immunity.

Ulviprubart represents a therapeutic antibody designed to block KLRG1 signaling, thereby reinvigorating exhausted immune cells and enhancing anti-tumor responses. This biosimilar provides researchers with a valuable tool for investigating KLRG1-mediated immune regulation, studying mechanisms of immune senescence, and exploring potential therapeutic strategies for cancer immunotherapy and age-related immune dysfunction. The antibody enables detailed examination of KLRG1 blockade effects in preclinical models and cellular systems.

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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Target Background

Function
Plays an inhibitory role on natural killer (NK) cells and T-cell functions upon binding to their non-MHC ligands. May mediate missing self recognition by binding to a highly conserved site on classical cadherins, enabling it to monitor expression of E-cadherin/CDH1, N-cadherin/CDH2 and R-cadherin/CDH4 on target cells.
Gene References into Functions
  1. KLRG1 might contribute to the impaired antitumor immunity of memory T cells in tumor microenvironment PMID: 27557510
  2. Killer Cell Lectin-like Receptor G1 Inhibits NK Cell Function through Activation of Adenosine 5'-Monophosphate-Activated Protein Kinase PMID: 27566818
  3. The results suggest that a disease-associated SNP located within the 3'UTR of KLRG1 directly interferes with miR-584-5p binding, allowing for KLRG1 mRNA differential accumulation, which in turn may contribute to pathogenesis of pemphigus. PMID: 27424220
  4. Demonstrate the presence of increased KLRG1-expressing T-cells in tuberculosis-treated individuals, and present KLRG1 as a marker of decreased human T-cell proliferation following BCG-vaccination. PMID: 26750180
  5. This finding provides a rationale for the reciprocal expression of KLRG1 and CD103 in different CD8(+) T-cell subsets. PMID: 26014037
  6. high levels of TfRs such as those found on activated lymphocytes were found to be associated with decreased KLRG1 inhibitory function, indicating that TfRs may sequester KLRG1 from interacting with cadherins. PMID: 24752778
  7. More T cells were KLRG1+ in the synovial fluid of patients with spondylarthritis/rheumatoid arthritis than crystal arthritis or controls. Those T cells were more functionally active, and migrated towards the synovial fluid of SpA/RA patients. PMID: 23740233
  8. KLRG1 was overexpressed on CD4(+) T cells. PMID: 24337749
  9. Data indicate that increments of CD8 + effector memory T cells in human and mouse chronic lymphocytic leukemia (CLL)(Emu-TCL1 model) were due to an expansion of the inhibitory killer cell lectin-like receptor G1 (KLRG1) expressing cellular subset. PMID: 24022692
  10. These results indicate that KLRG1 negatively regulates natural killer cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for hepatitis C virus infection. PMID: 23966413
  11. The lower inhibitory capacity of mKLRG1 compared with hKLRG1 can thus be rationalized by a decreased proportion of dimeric entities, which can be pinpointed to a single amino acid. PMID: 22684915
  12. cytomegalovirus positive had lower proportions of NK-cells expressing inhibitory receptors (KLRG1 and CD158a) PMID: 21933704
  13. trastuzumab-mediated antibody-dependent cellular cytotoxicity was markedly enhanced by KLRG1-negative peripheral blood mononuclear cells PMID: 21387286
  14. Results demonstrated a substantial reduction in both CD94- and KLRG1- expressing CD3(-)CD56(+) NK cells with increased age. PMID: 20394788
  15. Expression of MafA analyzed in conditional knockout mice during embryonic development is the first specific marker of a subpopulation of "early c-ret" positive sensory neurons. PMID: 20213756
  16. human effector and memory T cells expressing KLRG1 lack proliferative capacity PMID: 12393723
  17. KLRG1 expression discriminated between cord blood T cells that differed in their post-thymic expansion rate PMID: 15368283
  18. KLRG1 is expressed in the overwhelming majority of CD8-positive T cells specific for epitopes of cytomegalovirus or Epstein- Barr virus during the latent stage; a slightly lower KLRG1 expression level is observed in HIV-specific T8 cells. PMID: 15879103
  19. virus-specific CD8+ T cells are mostly KLRG1+ in chronic viral infections (human immunodeficiency virus, cytomegalovirus, and Epstein-Barr virus) but not in resolved infection (influenza virus) PMID: 16140789
  20. peripheral HCV-specific CD8+ T cells were CD127+ and KLRG1-; Intrahepatic virus-specific CD8+ T cells displayed significantly reduced levels of CD127 expression but similar levels of KLRG1 expression compared to the peripheral blood. PMID: 17079288
  21. study demonstrates that E-cadherin represents a ligand for KLRG1 and that ligation of KLRG1 by E-cadherin inhibited effector cell functions of polyclonal NK cells PMID: 17617594
  22. Certain aspects of the dysfunction seen in highly differentiated CD8+ T cells are maintained actively by KLRG1 signaling. KLRG1 blockade enhances Akt (ser(473)) phosphorylation & T-cell-receptor-induced proliferation of CD8+CD28-CD27- T cells. PMID: 19406987
  23. E-cadherin may coengage KLRG1 and alpha(E)beta(7) and that KLRG1 overcomes its exceptionally weak affinity for cadherins through multipoint attachment to target cells, resulting in inhibitory signaling. PMID: 19604491

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Subcellular Location
Cell membrane; Single-pass type II membrane protein.
Tissue Specificity
Expressed specifically on natural killer (NK) cells and T-cells, mainly CD8 T-cells.
Database Links

HGNC: 6380

OMIM: 604874

KEGG: hsa:10219

STRING: 9606.ENSP00000349477

UniGene: Hs.558446

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