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Biotinylated Human KIR3DL3 / CD158z Protein, Fc,Avitag™

分子别名(Synonym)

Killer cell immunoglobulin-like receptor 3DL3,CD158 antigen-like family member Z,Killer cell inhibitory receptor 1,CD158z,KIR3DL3,KIR3DL7,KIRC1

表达区间及表达系统(Source)

Biotinylated Human KIR3DL3 / CD158z Protein, Fc,Avitag (KI3-H82F3) is expressed from human 293 cells (HEK293). It contains AA Gln 26 - Leu 322 (Accession # Q8N743-1).

Predicted N-terminus: Gln 26

Request for sequence

蛋白结构(Molecular Characterization)

KIR3DL3 Structure

This protein carries a human IgG1 Fc tag at the C-terminus, followed by an Avi tag (Avitag™)

The protein has a calculated MW of 60.4 kDa. The protein migrates as 66-80 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

标记(Labeling)

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

蛋白标记度(Protein Ratio)

Passed as determined by the HABA assay / binding ELISA.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4, 25mM Arginine with trehalose as protectant.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

KIR3DL3 SDS-PAGE

Biotinylated Human KIR3DL3 / CD158z Protein, Fc,Avitag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90%.

 

活性(Bioactivity)-ELISA

KIR3DL3 ELISA

Immobilized Biotinylated Human KIR3DL3 / CD158z Protein, Fc,Avitag (Cat. No. KI3-H82F3) at 2 μg/mL (100 μL/well) on streptavidin (Cat. No. STN-N5116) precoated (0.5 μg/well) plate can bind Human B7-H7, His Tag (Cat. No. B77-H52H6) with a linear range of 0.02-5 μg/mL (QC tested).

Protocol

 
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背景(Background)

KIR3DL3 (Killer Cell Immunoglobulin Like Receptor) is the inhibitory KIR surface receptors possessing three extracellular immunoglobin (Ig) domains (3D) and only one inhibitory motif within the long cytoplasmic domain (L) due to a premature stop codon. Moreover, exon 6 of KIR3DL3 encoding the stem part of the receptor is also absent, which differs from other inhibitory KIRs. Understanding the function of KIR3DL3 is further complicated by the unknown identity of the specific ligand, but its importance is highlighted by its presence in all human KIR haplotypes with
120 distinct polymorphic alleles of the coding sequence.

 

前沿进展

Optimal injection sites for therapeutic angiogenesis: HGF-mediated regulation of HIF-1α via MAPK/PI3K pathways in hypoxic endothelial cells
Wang, Rong, Li et al
Tissue Cell (2025) 95, 102871
Abstract: Therapeutic angiogenesis offers a promising strategy for patients with critical limb-threatening ischemia (CLTI) who are unsuitable candidates for revascularization. However, the optimal administration sites for gene therapy agents, such as pCK-HGF-X7, remains undefined. Clinical trials commonly employ multiple intramuscular injections at sites of arterial occlusion; yet the necessity and efficacy of such extensive and repetitive protocols remains unclear. Targeted injections into ischemic tissues or their margins may improve therapeutic outcomes. Moreover, the molecular mechanisms by which hepatocyte growth factor (HGF)/c-Met signaling regulates hypoxia-inducible factor-1α (HIF-1α) expression under hypoxic conditions are not fully understood. This study aims to elucidate these molecular mechanisms in endothelial cells under hypoxic conditions and to identify the most effective injection sites for therapeutic angiogenesis agents. The effects of various HGF isoforms/complexes on human aortic endothelial cells (HAECs) were evaluated under normoxic and hypoxic conditions, focusing on proliferation, migration, and tube formation. Pathway inhibitors were used to explore the underlying mechanisms in hypoxic HAECs, and the findings were validated in a rat hindlimb ischemia model. Results demonstrated that HGF723 and HGF728 activated the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways, regulating HIF expression and significantly enhanced endothelial cell proliferation, migration, and tube formation, particularly under hypoxia. Despite these cellular effects, HGF treatment did not significantly improve tissue perfusion or neovascularization in normal rat hindlimbs. However, in ischemic rat hindlimbs, it markedly promoted angiogenesis and improved tissue perfusion in the gastrocnemius muscle. These findings indicate that therapeutic angiogenesis agents should primarily target hypoxic tissues, extending to the interface between normoxic and hypoxic regions, to optimize treatment efficacy.Copyright © 2025 Elsevier Ltd. All rights reserved.
Effects of Chlorella protothecoides-derived polydeoxyribonucleotides on skin regeneration and wound healing
Park, Nam, Lee et al
Arch Dermatol Res (2025) 317 (1), 483
Abstract: The skin acts as a crucial barrier and, upon injury, initiates complex wound-healing processes involving various cell types. Polydeoxyribonucleotides (PDRNs) are well-known for their efficacy in enhancing skin regeneration and wound healing. This study sought to investigate the effectiveness of PDRNs derived from Chlorella protothecoides, a sustainable and scalable microalgal source, in promoting skin regeneration and wound healing. Keratinocytes and fibroblasts were used for assessing the impact of PDRNs on cell proliferation, migration, collagen synthesis, and angiogenesis. Gene expression and associated signaling pathways were also examined using RT-qPCR and Western blot analyses. Our findings demonstrated that PDRNs significantly enhanced the proliferation and migration of skin cells, upregulated growth arrest specific 6 (GAS6) and hepatocyte growth factor (HGF) expression, and increased collagen synthesis by modulating collagen type I alpha 1 (COLIA1) expression. Additionally, PDRNs enhanced angiogenesis by promoting vascular endothelial growth factor (VEGF) expression and activation of ERK, AKT, β-catenin and STAT3 pathways via an adenosine A2A receptor (A2AR)-dependent mechanism. These findings suggest that microalgal-derived PDRNs have significant potential as sustainable and effective agents for clinical and cosmetic applications aimed at improving skin health and wound healing.© 2025. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Genetic insights into avian influenza resistance in Jeju Island chickens: the roles of Mx1 and oligoadenylate synthetase-like single nucleotide polymorphisms
Kim, Jeong, Yang et al
J Anim Sci Technol (2025) 67 (1), 69-85
Abstract: Influenza A virus (FLUAV) causes serious diseases in both poultry and humans. Various host proteins, including Mx1, are considered candidates for avian influenza (AI) resistance. After infecting Jeju Native chicken embryo fibroblasts (CEFs) with three types of AI viruses, we performed gene expression profiling, identified single nucleotide polymorphisms (SNPs) through RNA-sequencing, and confirmed phenotypes showing antiviral activity in vitro. Highly pathogenic AI viruses upregulated FGF2, LYN, and FLT4 and downregulated HGF, ANGPT1, and ROR2, while a low pathogenicity AI upregulated PARK7, RACK1, and DTX3L and downregulated SIRT1, LRRK2, and WAC. However, no virus affected Mx1 expression. Although SNPs in Mx1 could not discriminate antiviral activity alone, the only CEF resistant to H5N6, strain AN4, contained the Mx1 631 R/R genotype and strongly expressed an oligoadenylate synthetase-like (OASL) variant with a unique SNP: c.G880A (p.E294K). Using transfected cell lines, H5N6-infected cells expressing OASL with the c.G880A SNP showed minimal cytopathic effects and the lowest M gene expression. This study confirms that Jeju Native chickens with specific SNP combinations in both Mx1 and OASL showed H5N6 resistance and demonstrates the interplay of genetic factors in host-pathogen dynamics, suggesting a need for integrated analyses of multiple resistance genes to inform AI prevention strategies.© Copyright 2025 Korean Society of Animal Science and Technology.
Super-Resolution Fluorescence Imaging Reveals the Mechanism of NRP1 Clustering on Non-Small-Cell Lung Cancer Membranes
Li, Gao, Qi et al
Anal Chem (2025) 97 (4), 2326-2334
Abstract: Neuropilin 1 (NRP1) is upregulated in various types of malignant tumors, especially non-small-cell lung cancer (NSCLC). However, the precise mechanisms for membrane localization and regulation are not fully understood. Observations from super-resolution microscopy have revealed that NRP1 tends to form nanoscale clusters on the cell membrane, with these clusters varying significantly in size and density across different regions. Further research has shown that stimulation by hepatocyte growth factor (HGF) can reorganize the distribution of NRP1, reducing the number of small clusters while promoting the formation of larger ones. This suggests a propensity for internalization after activation. Additionally, dual-color dSTORM imaging has demonstrated a certain degree of colocalization between NRP1 and c-MET, indicating that c-MET plays an important role in stabilizing NRP1 clusters. This study provides new insights into the mechanism behind NRP1's clustered distribution on cell membranes and paves the way for developing more effective therapeutic strategies targeting NRP1 within tumors.
Showing 1-4 of 810 papers.
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KIR3DL3靶点信息
英文全称:Killer cell immunoglobulin-like receptor 3DL3
中文全称:杀伤细胞免疫球蛋白样受体3DL3
种类:
上市药物数量:0详情
临床药物数量:1详情
最高研发阶段:临床一期
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