KLCR2 Antibody

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Description

Definition and Target Overview

The KLRC2 antibody is a research tool targeting the protein product of the KLRC2 gene, which encodes the natural killer group 2 member C (NKG2C) receptor. NKG2C is an activating receptor expressed on natural killer (NK) cells and a subset of T cells, playing critical roles in immune responses to viral infections and cancer .

Antibody Characteristics

Key specifications of a widely used KLRC2 antibody (e.g., Sigma-Aldrich’s Anti-KLRC2 antibody, Prestige® catalog: HPA058052) include :

PropertyDetail
Host SpeciesRabbit
Antibody TypePolyclonal, affinity isolated
ApplicationsImmunofluorescence (0.25–2 μg/mL)
Immunogen SequenceCAVLQVNRLKSAQCGSSMIYHCKH
ReactivityHuman
Target Post-Translational ModificationUnmodified
Storage−20°C in buffered aqueous glycerol solution

Role in Viral Infections

  • CMV and HIV/SIV: KLRC2+ NK cells expand during cytomegalovirus (CMV) infection, forming "memory-like" NK cells. In rhesus macaques with SIV, KLRC2+ NK cells dominate in CMV-exposed animals, correlating with reduced KLRC1 (NKG2A) expression and increased antiviral IgG responses .

  • Mechanism: CMV drives a shift from dual KLRC1+/KLRC2+ NK cells to KLRC2+ single-positive cells, enhancing adaptive immunity .

Cancer Immunotherapy

  • Glioblastoma (GBM): Tumoral KLRC2 expression correlates with improved responses to anti-PD-1 therapy. High KLRC2 levels in GBM are linked to:

    • Reduced myeloid-derived suppressor cells (MDSCs).

    • Increased tumor-infiltrating lymphocytes (TILs).

    • Enhanced survival in both murine models and human trials .

FeatureKLRC2-High TumorsKLRC2-Low Tumors
Myeloid Suppression↓ MDSCs↑ MDSCs
Lymphocyte Infiltration↑ CD8+ T/NK cells↓ CD8+ T/NK cells
PD-1 mAb ResponseStrongerWeaker

Expression Patterns

  • Immune Tissues: KLRC2 protein is detected in lymph nodes, spleen, and bone marrow .

  • Tumor Microenvironment: KLRC2 is enriched at infiltrative margins of GBM and other cancers, suggesting a role in immune evasion modulation .

Clinical Implications

  • Biomarker Potential: KLRC2 expression may predict immunotherapy efficacy, particularly for PD-1/PD-L1 inhibitors in GBM .

  • Therapeutic Target: Enhancing KLRC2 signaling could improve NK cell-mediated tumor clearance or antiviral responses .

Limitations and Future Directions

  • Specificity Challenges: Existing antibodies may cross-react with NKG2A due to structural homology, necessitating RNA-Flow or sequencing for precise discrimination .

  • Translational Studies: Prospective clinical trials are needed to validate KLRC2 as a standalone biomarker or combinatorial target .

Product Specs

Buffer
Preservative: 0.03% Proclin 300
Composition: 50% Glycerol, 0.01M Phosphate Buffered Saline (PBS), pH 7.4
Form
Liquid
Lead Time
Made-to-order (14-16 weeks)
Synonyms
KLCR2 antibody; KLC1 antibody; At3g27960 antibody; K24A2.5Protein KINESIN LIGHT CHAIN-RELATED 2 antibody; Kinesin light chain-like protein 1 antibody; AtKLC1 antibody
Target Names
KLCR2
Uniprot No.

Q&A

Here’s a structured collection of FAQs tailored to academic research on KLCR2 antibody (referencing human kallikrein 2 [hK2] targeting antibody h11B6, as KLCR2 appears to be a typographical variation):

Advanced Research Questions

How do contradictory findings about hK2 vs. PSMA expression in AR-activated mCRPC models impact therapeutic development?

  • Resolution strategy:

    • Conduct parallel IHC and RNA-seq on patient-derived xenografts to map hK2/PSMA spatial expression. Studies show hK2 expression increases under AR activation, while PSMA decreases .

    • Use dual-targeting approaches (e.g., h11B6 + PSMA-ligand conjugates) to address heterogeneous antigen expression in metastases .

What computational pipelines best reconcile conflicting NGS data on antibody somatic hypermutation patterns?

  • Methodology:

    • Integrate mutation frequency heatmaps (Geneious Biologics) with phylogenetic lineage trees (IgPhyML) to distinguish stochastic noise from antigen-driven selection .

    • Apply statistical filters (e.g., ≥2% clonal frequency, ≥3 non-synonymous mutations in CDR) to exclude low-significance variants .

How can researchers optimize α-particle therapy (e.g., ²²⁵Ac-h11B6) while mitigating off-target toxicity?

  • Methodology:

    • Perform dosimetry calculations using the OLINDA/EXM platform with biodistribution data from [¹¹¹In]-DOTA-h11B6 studies. Critical organs: kidneys (mean dose 0.23 mGy/MBq) and spleen (0.18 mGy/MBq) .

    • Implement pre-therapy blocking doses (e.g., 8 mg unlabeled h11B6) to reduce splenic uptake by 40% .

Table 1: Key Differences Between hK2 and PSMA as Therapeutic Targets

ParameterhK2PSMA
AR signaling correlationPositive (r = 0.81)Negative (r = -0.67)
Membrane-bound fraction62% ± 11%38% ± 9%
Mean tumor uptake (SUV)8.4 ± 2.15.9 ± 1.7

Table 2: Antibody Analysis Tools for hK2 Studies

ToolFunctionalityUse Case Example
Geneious BiologicsCDR3 clustering, mutation hotspotsTrack clonal expansion post-therapy
IgRepertoireConstructorV(D)J alignment, isotype switchingCompare pre/post AR inhibitor use
FireDock_ABAntibody-antigen docking refinementPredict h11B6-hK2 binding affinity

Methodological Recommendations

  • For contradictory biodistribution data: Use SPECT/CT imaging at 24, 72, and 144 h post-injection to distinguish persistent tumor uptake (≥72 h) from transient vascular pooling .

  • For low-affinity variants: Apply RosettaAntibodyDesign with positional constraint scoring (e.g., CDR-H3 residues 95–102) to improve binding energy by ≥1.5 kcal/mol .

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