C6612
Anti-CTLA-4 antibody produced in goat
affinity isolated antibody, lyophilized powder
Synonyme(s) :
Anti-CD152, Anti-Cytotoxic T-lymphocyte-associated Molecule-4
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About This Item
Source biologique
goat
Niveau de qualité
Conjugué
unconjugated
Forme d'anticorps
affinity isolated antibody
Type de produit anticorps
primary antibodies
Clone
polyclonal
Forme
lyophilized powder
Espèces réactives
mouse
Technique(s)
indirect ELISA: 0.1-0.4 μg/mL
western blot: 0.1-0.2 μg/mL
Numéro d'accès UniProt
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
mouse ... Ctla4(12477)
Description générale
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.
Immunogène
purified recombinant mouse cytotoxic T-lymphocyte-associated molecule 4 extracellualr domain, expressed in mouse NSO cells.
Actions biochimiques/physiologiques
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.
Forme physique
Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline, pH 7.4 with 5% trehalose.
Clause de non-responsabilité
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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Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 3
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
Équipement de protection individuelle
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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