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Biotinylated Human CD47 Protein, His,Avitag™ (MALS verified)

分子别名(Synonym)

CD47,MER6,IAP,OA3

表达区间及表达系统(Source)

Biotinylated Human CD47, His,Avitag (CD7-H82E9) is expressed from human 293 cells (HEK293). It contains AA Gln 19 - Pro 139 (Accession # Q08722-3).

Predicted N-terminus: Gln 19

Request for sequence

蛋白结构(Molecular Characterization)

CD47 Structure

This protein carries a polyhistidine tag at the C-terminus, followed by an Avi tag (Avitag™).

The protein has a calculated MW of 16.9 kDa. The protein migrates as 32-44 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)

>95% as determined by SDS-PAGE.

>90% as determined by SEC-MALS.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 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 24 months in lyophilized state;
  2. -70°C for 12 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)

CD47 SDS-PAGE

Biotinylated Human CD47, His,Avitag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95%.

SEC-MALS

CD47 SEC-MALS

The purity of Biotinylated Human CD47, His,Avitag (Cat. No. CD7-H82E9) is more than 90% and the molecular weight of this protein is around 28-38 kDa verified by SEC-MALS.

Report

 

活性(Bioactivity)-ELISA

CD47 ELISA

Immobilized Monoclonal Anti-Human CD47 Antibody, Human IgG4 at 2 μg/mL (100 μL/well) can bind Biotinylated Human CD47, His,Avitag (Cat. No. CD7-H82E9) with a linear range of 0.1-3 ng/mL (QC tested).

Protocol

CD47 ELISA

Immobilized Human SIRP alpha, Fc Tag (Cat. No. SIA-H5251) at 2 μg/mL (100 μL/well) can bind Biotinylated Human CD47, His,Avitag (Cat. No. CD7-H82E9) with a linear range of 2-25 ng/mL (Routinely tested).

Protocol

 

活性(Bioactivity)-FACS

CD47 FACS

FACS assay shows that Biotinylated Human CD47, His,Avitag (Cat. No. CD7-H82E9) can bind to ACHN cell expressing human SIRP-a. The concentration of CD47 used is 10 μg/mL (Routinely tested).

Protocol

CD47 FACS

FACS analysis shows that the binding of Human CD47 to ACHN expressing SIRP-a was inhibited by increasing concentration of neutralizing SIRP-a antibody. The concentration of Human CD47 used is 20 μg/mL. IC50=9.334 μg/mL

Protocol

 
评论(7)
  1. 156XXXXXXX8
  2. 1人赞
  3. 用于开展抗体对SIRP-α和CD47之间结合的阻断实验,流式上生物素标记的CD47蛋白在2微克/毫升的情况下即可以与SIRP-α具有极高的亲和力。
  4. 2021-8-19
  1. 183XXXXXXX9
  2. 0人赞
  3. 利用生物素-链霉亲和素系统的高特异性和高灵敏度的结合特性,我们将该生物素化蛋白与链霉亲和素相关产品联合应用于ELISA实验,与非生物素体系相比,检测速度更快、结合能力更强、非特异背景更低。通过分析近一年的检测结果,均未出现数据异常的情况,所有的检测也能满足检测方法设定的可接受标准。
  4. 2023-6-28
  1. 158XXXXXXX0
  2. 0人赞
  3. 抗体是实验室最常用科研试剂之一。抗体特异性不好、抗体稳定性不佳,或者应用效果不好都会影响结果的输出,最终还会导致实验延期。不好的抗体会导致实验结果缺乏可重复性,造成时间和金钱浪费。ACRO抗体稳定性好,得到了出色的结果。
  4. 2022-6-17
 
ACRO质量管理体系
 
 

背景(Background)

Leukocyte surface antigen CD47 is also known as Antigenic surface determinant protein OA3, Integrin-associated protein (IAP) and Protein MER6. CD47 contains 1 Ig-like V-type (immunoglobulin-like) domain. CD47 is very broadly distributed on normal adult tissues. CD47 has a role in both cell adhesion by acting as an adhesion receptor for THBS1 on platelets, and in the modulation of integrins and plays an important role in memory formation and synaptic plasticity in the hippocampus by similarity. CD47 is the receptor for SIRPA, binding to which prevents maturation of immature dendritic cells and inhibits cytokine production by mature dendritic cells. CD47 Interaction with SIRPG mediates cell-cell adhesion, enhances superantigen-dependent T-cell-mediated proliferation and costimulates T-cell activation.

 

前沿进展

RASON promotes KRASG12C-driven tumor progression and immune evasion in non-small cell lung cancer
Wu, Xie, Zhang et al
J Exp Clin Cancer Res (2025) 44 (1), 106
Abstract: KRAS is the most frequently mutated oncogene in human cancers, with KRASG12C being a prevalent driver mutation in 12-13% non-small cell lung cancer (NSCLC) cases. Despite breakthroughs in KRASG12C inhibitors such as sotorasib (AMG-510) and adagrasib (MRTX-849), clinical resistance remains a challenging issue, highlighting the need for deeper understanding of the molecular mechanisms underlying KRASG12C-driven oncogenic signaling in NSCLC. Previously, we identified RASON as a novel regulator of KRASG12D/V signaling in pancreatic cancer. Herein, we aim to explore the role of RASON in KRASG12C-driven NSCLC and its therapeutic potential.Immunohistochemistry analysis of NSCLC patient cohorts was performed to demonstrate the correlation between RASON expression and NSCLC progression. Immunoblotting was performed to evaluate the effects of RASON on KRASG12C downstream signaling. In vitro and in vivo assays including cell proliferation, sphere formation, tumor implantation and genetic mouse models were performed to determine the oncogenic role of RASON. RNA-seq analysis was utilized to identify the key signaling pathway regulated by RASON. Immunofluorescence, immunoprecipitation, nuclear magnetic resonance and biochemistry assays were used to validate the interaction between KRASG12C and RASON. Phagocytosis assay and flow cytometry were conducted to explore the effects of RASON on the tumor immune microenvironment. Pharmacological inhibition in subcutaneous xenograft model was used to determine the therapeutical potential of RASON.RASON is overexpressed in NSCLC with KRASG12C mutation and correlates with poor patient prognosis. Genetic knockout of RASON significantly reduced lung tumor burden in LSL-KRASG12D; Trp53R172H/+ mice. In KRASG12C-mutant lung cancer cell lines, RASON overexpression enhanced, while CRISPR-mediated knockout suppressed, both in vitro proliferation and in vivo tumor growth. Mechanistically, RASON directly binds KRASG12C, stabilizes it in the GTP-bound hyperactive state and promotes downstream signaling. RASON knockout significantly reduced CD47 expression, enhancing macrophage-mediated phagocytosis and anti-tumor immunity. Therapeutically, antisense oligonucleotides targeting RASON not only exhibited tumor-suppressive effects, but also synergized with the KRASG12C inhibitor AMG-510 to significantly enhance anti-tumor efficacy.This study reveals RASON as a key oncogenic regulator of KRASG12C signaling, driving lung tumorigenesis and progression, and identifies RASON as a promising therapeutic target for KRASG12C mutant non-small cell lung cancer.© 2025. The Author(s).
Cartilage Intermediate Layer Protein-1 Promotes Extracellular Matrix Degeneration via Interacting With CD47
Deng, Yang, Xiang et al
J Cell Mol Med (2025) 29 (6), e70506
Abstract: Intervertebral Disc Degeneration (IDD) is a multifactorial result contributing to Low Back Pain (LBP) while Cartilage Intermediate Layer Protein-1 (CILP-1) is gradually up-regulated along with IDD. Whether CILP-1 acts in a direct role promoting IDD via regulating matrix metabolism remains to be elucidated. Herein, we firstly detected the expression level of matrix-related phenotypes in nucleus pulposus (NP) cells treated with CILP-1, including ADAMTS, MMPs, IL-6, Collagens, Aggrecan (ACAN) and SOX9. Meanwhile, the phosphorylation levels of MAPKs and NF-κB were detected to explore the involved signalling pathways, which were further validated by inhibition experiments. Furthermore, molecular docking analysis was employed to evaluate the possibility of CD47 acting as the direct receptor mediating CILP's regulation above, which was further validated by immunoprecipitation and inhibition experiment. Our findings have made a comprehensive investigation into the regulatory effect of CILP-1 on the matrix metabolism of NP cells and explored the underlying mechanism.© 2025 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
Radiotherapy-derived engineered stem cell exosomes improve anti-glioma immunotherapy by promoting the formation of tertiary lymphoid structure and improve the release of type I interferon
Li, Lu, Bao et al
J Nanobiotechnology (2025) 23 (1), 239
Abstract: The absence of signaling pathways related to intrinsic immune activation in tumor cells and the immunosuppressive microenvironment limit lymphocyte infiltration, constitutes an "immune-desert" tumor displaying insensitivity to various immunotherapies. This study investigates strategies to activate intrinsic immune pathways in glioma cells, reverse immunosuppression, and induce tertiary lymphoid structures (TLS) within the glioma microenvironment (GME) to enhance natural and adaptive immune responses. We successfully induced antigen-presenting cell activation, macrophage/microglia polarization, and TLS formation in GME by intracranial delivery of BafA1@Rexo-SC, which comprises exosomes from irradiated bone marrow-derived stem cells overexpressing CD47 nanobodies and STING, loaded with the autophagy inhibitor BafA1. These exosomes efficiently activated the cGAS-STING pathway, leading to the formation of "lymphoid tissue organizer cells (Lto)" cells, VEGFA release for high endothelial microvessel formation, and chemokine release for T and B cell recruitment. BafA1@Rexo-SC also promoted macrophage phagocytosis of tumor cells and enhanced effector T cell function by blocking CD47, while releasing type I interferon. Our findings suggest novel therapeutic approaches for glioma treatment.© 2025. The Author(s).
A combined "eat me/don't eat me" strategy based on exosome for acute liver injury treatment
Du, Chen, Liu et al
Cell Rep Med (2025)
Abstract: Drug-induced liver injury (DILI) involves multifaceted pathogenesis, necessitating effective therapeutic strategies. Wnt2, secreted by liver sinusoidal endothelial cell (LSEC), activates the Wnt/β-catenin signaling pathway to promote hepatocyte proliferation after injury. To address the dual challenges of targeted delivery and phagocytosis evasion, we develop a combined "eat me/don't eat me" strategy. RLTRKRGLK (RLTR) peptide-functionalized exosomes are engineered by inserting DMPE-PEG2000-CRLTRKRGLK into the lipid membrane of exosome derived from bEnd.3 cell. Surface-displayed RLTR mediates exosomal enrichment in LSEC, while CD47 engineering reduces macrophage clearance via "don't eat me" signaling. Then, lentiviral transfection enables stable encapsulation of functional Wnt2 mRNA into ExoCD47 (designated Wnt2@ExoCD47). In both acetaminophen (APAP) and dimethylnitrosamine (DMN)-induced murine liver injury models, RLTR-Wnt2@ExoCD47 demonstrates LSEC-specific targeting and significant hepatoprotection. This engineered exosome platform provides a therapeutic strategy for DILI.Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.
Showing 1-4 of 3052 papers.
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CD47靶点信息
英文全称:Cluster of differentiation 47
中文全称:分化群47
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:57详情
最高研发阶段:临床三期
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