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AB210384

PE/Cy7® Anti-CTLA4 antibody [UC10-4F10-11]

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(3 Publications)

Armenian hamster Monoclonal CTLA4 antibody - conjugated to PE/Cy7®. Suitable for Flow Cyt (Intra) and reacts with Mouse samples. Cited in 3 publications.

View Alternative Names

CD152, Cd152, Ctla4, Cytotoxic T-lymphocyte protein 4, Cytotoxic T-lymphocyte-associated antigen 4, CTLA-4

1 Images
Flow Cytometry (Intracellular) - PE/Cy7® Anti-CTLA4 antibody [UC10-4F10-11] (AB210384)
  • Flow Cyt (Intra)

Supplier Data

Flow Cytometry (Intracellular) - PE/Cy7® Anti-CTLA4 antibody [UC10-4F10-11] (AB210384)

Intracellular flow cytometric analysis of C57Bl/6 splenocytes, stimulated with ConA for 3 days, labeling CTLA4 with APC Anti-Mouse CD4 followed by intracellular staining with 0.125 μg ab210384 (right) or 0.125 μg PE-Cy7 Armenian Hamster isotype control (left).

Key facts

Host species

Armenian hamster

Clonality

Monoclonal

Clone number

UC10-4F10-11

Isotype

IgG

Conjugation

PE/Cy7®

Excitation/Emission

Ex: 565nm, Em: 778nm

Carrier free

No

Reacts with

Mouse

Applications

Flow Cyt (Intra)

applications

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Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "FlowCytIntra" : {"fullname" : "Flow Cytometry (Intracellular)", "shortname":"Flow Cyt (Intra)"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Mouse": { "FlowCytIntra-species-checked": "testedAndGuaranteed", "FlowCytIntra-species-dilution-info": "", "FlowCytIntra-species-notes": "<p></p>" } } }
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Product details

The purified antibody was conjugated under optimal conditions, with unreacted dye removed from the preparation.
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Properties and storage information

Form
Liquid
Purification notes
ab210384 was purified from tissue culture supernatant via affinity chromatography.
Storage buffer
pH: 7.2 Preservative: 0.09% Sodium azide Constituents: 0.87% Sodium chloride, 0.12% Sodium dihydrogen phosphate, 0.1% Gelatin
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
+4°C
Storage information
Store in the dark
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Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

CTLA-4 also known as CD152 is an immune checkpoint receptor with a molecular weight of approximately 34 kDa. This protein is expressed on the surface of T-cells especially after activation and sometimes on regulatory T-cells (Tregs). CTLA-4 competes with CD28 for binding to the same ligands CD80 and CD86 on antigen-presenting cells. Unlike CD28 which stimulates T-cell activation CTLA-4 sends inhibitory signals to downregulate immune responses. By doing this CTLA-4 helps maintain immune system homeostasis and prevents autoimmune reactions.
Biological function summary

The CTLA-4 protein functions as a critical regulator of the immune system. It interacts with CD80/CD86 in a complex that effectively transmits inhibitory signals to T-cells. CTLA-4 controls the amplitude of the initial activation of T-cells ensuring that the body's immune responses are kept under control. In regulatory T-cells CTLA-4 engagement contributes to their immunosuppressive functions through which they maintain tolerance to self-antigens and prevent overactive immune reactions.

Pathways

CTLA-4 involves itself in the adaptive immune response pathways specifically the regulation of T-cell activity. CTLA-4's interaction with CD80/CD86 modulates pathways associated with TCR (T-cell receptor) signaling. When CTLA-4 binds its ligands it recruits phosphatases such as SHP-2 that dephosphorylate signaling proteins leading to the downregulation of T-cell interaction. This pathway interaction exemplifies how CTLA-4 acts in concert with proteins like CD28 to finely tune immune responses.

CTLA-4 plays a role in autoimmune diseases and cancer. The dysregulation of CTLA-4 function can lead to autoimmune disorders where the immune system attacks the body's own tissue. In cancer tumor cells may manipulate CTLA-4 pathways to evade immune surveillance. Targeted therapies like anti-CTLA-4 antibodies such as ipilimumab have been developed to block CTLA-4 aiming to enhance the immune system’s ability to attack cancer cells. These treatments highlight the role of CTLA-4 in balancing immune activity and the potential to alter this balance for therapeutic benefit.
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Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:
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Target data

Inhibitory receptor acting as a major negative regulator of T-cell responses. The affinity of CTLA4 for its natural B7 family ligands, CD80 and CD86, is considerably stronger than the affinity of their cognate stimulatory coreceptor CD28.
See full target information Ctla4
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Publications (3)

Recent publications for all applications. Explore the full list and refine your search

Cell death & disease 15:386 PubMed38824143

2024

A novel doxorubicin/CTLA-4 blocker co-loaded drug delivery system improves efficacy and safety in antitumor therapy.

Applications

Unspecified application

Species

Unspecified reactive species

Wenli Yang,Qinghui Sun,Xiaodian Zhang,Liping Zheng,Xiaomei Yang,Na He,Yanyang Pang,Xi Wang,Zhiheng Lai,Wuping Zheng,Shaoping Zheng,Wu Wang

Cell death & disease 14:406 PubMed37419930

2023

A novel CTLA-4 blocking strategy based on nanobody enhances the activity of dendritic cell vaccine-stimulated antitumor cytotoxic T lymphocytes.

Applications

Unspecified application

Species

Unspecified reactive species

Wenli Yang,Yanyang Pang,Xi Wang,Zhiheng Lai,Yanda Lu,Shaojiang Zheng,Wu Wang

Cellular physiology and biochemistry : internation 49:260-270 PubMed30138920

2018

Effects of Combination of Anti-CTLA-4 and Anti-PD-1 on Gastric Cancer Cells Proliferation, Apoptosis and Metastasis.

Applications

Unspecified application

Species

Unspecified reactive species

Bin Wang,Lei Qin,Mei Ren,Hao Sun
View all publications
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