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MilliporeSigma

C6612

Sigma-Aldrich

Anti-CTLA-4 antibody produced in goat

affinity isolated antibody, lyophilized powder

Sinónimos:

Anti-CD152, Anti-Cytotoxic T-lymphocyte-associated Molecule-4

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

goat

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

lyophilized powder

species reactivity

mouse

technique(s)

indirect ELISA: 0.1-0.4 μg/mL
western blot: 0.1-0.2 μg/mL

UniProt accession no.

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

mouse ... Ctla4(12477)

General description

CTLA4 (cytotoxic T-lymphocyte associated protein 4) or CD152 (cluster of differentiation) is a T cell receptor which belongs to the immunoglobulin (Ig) superfamily or CD28 family. It is expressed on the surface of Th (T helper) cells. This gene is localized to human chromosome 2q33. This protein is composed of a cytosolic domain, a transmembrane region and a V domain of 116 amino acids. Alternative splicing results in membrane and soluble forms, where membrane forms work as homodimers and soluble isoforms as monomers.

Immunogen

purified recombinant mouse cytotoxic T-lymphocyte-associated molecule 4 extracellualr domain, expressed in mouse NSO cells.

Biochem/physiol Actions

CTLA4 (cytotoxic T-lymphocyte associated protein 4) is responsible for inhibiting T-cell proliferation and facilitates T cell apoptosis. This protein is expressed post-antigen presentation, and thus, is involved in immune and autoimmune disorders. Therefore, it is also implicated in the pathogenesis of various T cell mediated autoimmune disorders.

Physical form

Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline, pH 7.4 with 5% trehalose.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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Aileen Weiwei Li et al.
Nature materials, 17(6), 528-534 (2018-03-07)
Existing strategies to enhance peptide immunogenicity for cancer vaccination generally require direct peptide alteration, which, beyond practical issues, may impact peptide presentation and result in vaccine variability. Here, we report a simple adsorption approach using polyethyleneimine (PEI) in a mesoporous
Daniele Saverino et al.
PloS one, 9(11), e112509-e112509 (2014-11-11)
Primary biliary cirrhosis (PBC) is a chronic autoimmune cholestatic liver disease frequently characterized by anti-mitochondrial autoantibodies (AMA). A minority of patients are AMA-negative. Cytotoxic-T-Lymphocyte-Antigen-4 (CTLA-4) is a surface molecule expressed on activated T-cells delivering a critical negative immunoregulatory signal. A
Sigrid Regauer et al.
Histology and histopathology, 29(8), 1017-1025 (2014-01-10)
Introduction. Lichen planus (LP) is a chronic cytokine-mediated disease of possible auto-immune etiology. 25% of men have anogenital manifestations. Erosive penile LP causes a scarring phimosis of the foreskin in uncircumcised men. Mast cells as potent immune modulators have been
Jonas Pick et al.
European journal of immunology, 44(7), 2139-2152 (2014-04-12)
Although CD8(+) T cells that produce IL-17 (Tc17 cells) have been linked to host defense, Tc17 cells show reduced cytotoxic activity, which is the characteristic function of CD8(+) T cells. Here, we show that CTLA-4 enhances the frequency of IL-17 in
Chindu Govindaraj et al.
American journal of hematology, 89(8), 795-802 (2014-04-24)
A major limitation to improved outcomes in acute myelogenous leukemia (AML) is relapse resulting from leukemic cells that persist at clinical remission. Regulatory T cells (Tregs), which are increased in AML patients, can contribute to immune evasion by residual leukemic

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