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 >  Protein>CTLA-4 >CT4-H82F3

Biotinylated Human CTLA-4 Protein, Fc,Avitag™

分子别名(Synonym)

CTLA4,CD152

表达区间及表达系统(Source)

Biotinylated Human CTLA-4, Fc,Avitag (CT4-H82F3) is expressed from human 293 cells (HEK293). It contains AA Ala 37 - Phe 162 (Accession # P16410-1).

Predicted N-terminus: Ala 37

Request for sequence

蛋白结构(Molecular Characterization)

CTLA-4 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 41.8 kDa. The protein migrates as 48-60 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.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in Tris with Glycine, Arginine and NaCl, pH7.5 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)

CTLA-4 SDS-PAGE

Biotinylated Human CTLA-4, Fc,Avitag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95%.

 

活性(Bioactivity)-ELISA

CTLA-4 ELISA

Immobilized Human B7-2, Fc Tag (Cat. No. CD6-H5257) at 5 μg/mL (100 μL/well) can bind Biotinylated Human CTLA-4, Fc,Avitag (Cat. No. CT4-H82F3) with a linear range of 0.6-10 ng/mL (QC tested).

Protocol

CTLA-4 ELISA

Immobilized Human B7-1, Fc Tag (Cat. No. B71-H5259) at 5 μg/mL (100 μL/well) can bind Biotinylated Human CTLA-4, Fc,Avitag (Cat. No. CT4-H82F3) with a linear range of 0.6-10 ng/mL (Routinely tested).

Protocol

CTLA-4 ELISA

Immobilized Cynomolgus / Rhesus macaque B7-2, His Tag (Cat. No. CD6-C52H5) at 5 μg/mL (100 μL/well) can bind Biotinylated Human CTLA-4, Fc,Avitag (Cat. No. CT4-H82F3) with a linear range of 0.02-0.625 μg/mL (Routinely tested).

Protocol

CTLA-4 ELISA

Immobilized Biotinylated Human CTLA-4, Fc,Avitag (Cat. No. CT4-H82F3) at 1 μg/mL (100 μL/well) on Streptavidin (Cat. No. STN-N5116) precoated (0.5 μg/well) plate, can bind Ipilimumab with a linear range of 0.2-2 ng/mL (Routinely tested).

Protocol

CTLA-4 ELISA

Serial dilutions of Ipilimumab neutralizing antibody (1:2 serial dilutions, from 40 μg/mL to 0.019 μg/mL) were added into Human B7-1, Fc Tag (Cat. No. B71-H5259): Biotinylated Human CTLA-4, Fc,Avitag (Cat. No. CT4-H82F3) binding reactions. The assay was performed according to the above described protocol. Background was subtracted from data points before curve fitting.

Protocol

CTLA-4 ELISA

Serial dilutions of Ipilimumab neutralizing antibody (1:2 serial dilutions, from 40 μg/mL to 0.019 μg/mL) were added into Human B7-2, Fc Tag (Cat. No. CD6-H5257): Biotinylated Human CTLA-4, Fc,Avitag (Cat. No. CT4-H82F3) binding reactions. The assay was performed according to the above described protocol. Background was subtracted from data points before curve fitting.

Protocol

 
评论(1)
  1. 184XXXXXXX4
  2. 0人赞
  3. 主要为了筛选相应抗体,做ELISA,western blot实验。该公司抗原特异性高,纯度好,包装精致,服务态度很满意。
  4. 2020-2-26
 
ACRO质量管理体系
 
 

背景(Background)

CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) is also known as CD152 (Cluster of differentiation 152), is a protein receptor that downregulates the immune system. CTLA4 is a member of the immunoglobulin superfamily, which is expressed on the surface of Helper T cells and transmits an inhibitory signal to T cells. The protein contains an extracellular V domain, a transmembrane domain, and a cytoplasmic tail. Alternate splice variants, encoding different isoforms. CTLA4 is similar to the T-cell co-stimulatory protein, CD28, and both molecules bind to CD80 and CD86, also called B7-1 and B7-2 respectively, on antigen-presenting cells. CTLA4 transmits an inhibitory signal to T cells, whereas CD28 transmits a stimulatory signal. Intracellular CTLA4 is also found in regulatory T cells and may be important to their function. Fusion proteins of CTLA4 and antibodies (CTLA4-Ig) have been used in clinical trials for rheumatoid arthritis.

文献引用(Citations)

 

前沿进展

[First line treatment of non-oncogene-addicted metastatic non-small cell lung cancer]
Gille, Pérol
Bull Cancer (2025) 112 (3S1), 3S64-3S74
Abstract: Since 2017, anti-PD-(L)1 immunotherapy has been the cornerstone of first-line treatment for stage IV non-oncogene-addicted non-small cell lung cancer. Its phase I development has established that the level of PD-L1 expression by tumor cells is predictive of response rate and progression-free survival. Above 50%, it makes chemotherapy not mandatory, with a median survival for pembrolizumab monotherapy of around 26 months and five-year survival of 32%. Large phase III studies have also validated the combination of anti-PD-(L)1 immunotherapy and platinum-based chemotherapy regardless of PD-L1 level of expression, increasing five-year survival from 10% to 18%. Dual immunotherapy combining anti-CTLA-4 and anti-PD-(L)1 might be interesting, especially in PD-L1 negative tumors, but is not available in France. Treatment personalization, particularly in the case of PD-L 1 expression >50%, should be based on response and non-response factors to immunotherapy, including patient-related factors such as performans status, age, smoking status, as well as tumor-related factors such as disease aggressiveness, tumor volume, mutational profile, along with concomitant medications. The optimal duration of immunotherapy is uncertain and arbitrarily set at two years. Many options are currently being explored to improve first-line treatment outcomes, as the majority of patients experience resistance to immunotherapy.Copyright © 2025 Elsevier Masson SAS. Tous droits réservés. All rights reserved.
Navigating established and emerging biomarkers for immune checkpoint inhibitor therapy
Wang, Chan
Cancer Cell (2025)
Abstract: Immune checkpoint inhibitors (ICIs) have improved outcomes of patients with many different cancers. These antibodies target molecules such as programmed cell death 1 (PD-1) or cytotoxic T lymphocyte associated protein 4 (CTLA-4) which normally function to limit immune activity. Treatment with ICIs reactivates T cells to destroy tumor cells in a highly specific manner, which in some patients, results in dramatic remissions and durable disease control. Over the last decade, much effort has been directed at characterizing factors that drive efficacy and resistance to ICI therapy. Food and Drug Administration (FDA)-approved biomarkers for ICI therapy have facilitated more judicious treatment of cancer patients and transformed the field of precision oncology. Yet, adaptive immunity against cancers is complex, and newer data have revealed the potential utility of other biomarkers. In this review, we discuss the utility of currently approved biomarkers and highlight how emerging biomarkers can further improve the identification of patients who benefit from ICIs.Copyright © 2025 Elsevier Inc. All rights reserved.
Identification of new immune target and signaling for cancer immunotherapy
Narote, Desai, Patel et al
Cancer Genet (2025) 294-295, 57-75
Abstract: Immunotherapy has become one of the innovative treatments in malignancy as it activates the immune system to find and eliminate malignant cells. The tumor immunology interface has become increasingly intricate, making the identification of new immune targets and signalling pathways on which to base improved therapeutic strategies an ongoing process. This review, we goal to clarify the contacts between cancer and immune system with a focus on immune surveillance as well as immune evasion mechanisms. Comprehensive immunotherapeutic therapies are overviewed with ICI (CTLA-4, PD-1, PD-L1), CAR-T cell therapy, and cancer vaccines whereas, advanced therapies targeting new immune checkpoints are also elucidated including TIM-3, LAG-3, and TIGIT. The JAK/STAT, MAPK and PI3K-AKT-mTOR pathways are reviewed with regards to cancer progression and immunotherapeutic resistance. The dysregulation of these pathways gives hope for the identification of fresh targets for therapy. Genomics, proteomics, immunopeptidomics, single cell mass spectrometry, CRISPR-based functional genomics and bioinformatics are described as essential for immune target identification and for mapping of cancer relevant signaling pathways. This review also considers some emerging issues in the subject area like the tumor heterogeneity, immune-related adverse events (irAEs), and personalized treatment. These barriers are described to facilitate the understanding of ways to overcome them and increase the efficacy of immunotherapies through combination therapies. This means that by developing new knowledge of immunological targets and pathways, immunoprecision medicine for cancer could greatly enhance outcomes.Copyright © 2025 Elsevier Inc. All rights reserved.
Targeting cTRIP12 counteracts ferroptosis resistance and augments sensitivity to immunotherapy in pancreatic cancer
Lin, Zhu, Chen et al
Drug Resist Updat (2025) 81, 101240
Abstract: Current therapeutic strategies for pancreatic ductal adenocarcinoma (PDAC) have limited efficacy in increasing patient survival rates, largely due to ferroptosis resistance and immunosuppression. The aim of this study is to identify molecular mechanisms associated with ferroptosis resistance and immunosuppression in PDAC tumour cells.Circular RNA sequencing (circRNA-seq) was performed on clinical samples to identify potential circRNAs that mediate ferroptosis resistance. C11-BODIPY staining, FerroOrange staining, the glutathione ratio, malondialdehyde quantification, and transmission electron microscopy were employed to assess ferroptosis. RNA pulldown, mass spectrometry, RNA immunoprecipitation, and coimmunoprecipitation assays were conducted to investigate the molecular mechanisms involved. A HuNSG mouse xenograft tumour model was utilized to validate therapeutic agents.A circRNA derived from TRIP12 (cTRIP12) was identified in PDAC samples resistant to ferroptosis. cTRIP12 knockdown increased the sensitivity of PDAC cells to ferroptosis and immunotherapy. Subsequent mechanistic studies revealed that cTRIP12 specifically binds to the O-linked N-acetylglucosamine transferase (OGT) protein and increases intracellular O-GlcNAcylation levels, leading to increased protein levels of ferritin heavy chain (FTH) and PD-L1 in tumour cells. Notably, high cTRIP12 expression suppressed ferroptosis sensitivity and increased immune resistance in PDAC cells by functioning as a protein scaffold through its interaction with OGT and protein kinase R-like endoplasmic reticulum kinase (PERK). cTRIP12 inhibition induced ferroptosis in PDAC cells by reducing FTH and PD-L1 expression and synergistically increased the immunotherapy efficacy. In vivo animal experiments confirmed that the triple therapy consisting of GSK2656157, erastin, and anti-CTLA-4 effectively suppressed the progression of PDAC in tumours with high cTRIP12 expression.We elucidated the molecular mechanisms underlying the simultaneous occurrence of ferroptosis resistance and immune suppression in PDAC patients. Our study provides a novel therapeutic strategy that could promote ferroptosis in tumour cells and increase immunotherapy efficacy.Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.
Showing 1-4 of 14465 papers.
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CTLA-4靶点信息
英文全称:Cytotoxic T-Lymphocyte-Associated Antigen 4
中文全称:细胞毒性T淋巴细胞相关抗原4
种类:Homo sapiens
上市药物数量:4详情
临床药物数量:64详情
最高研发阶段:临床三期
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