Summary
The BNI3 antibody is specific for human CD152, commonly known as CTLA-4, a 33-37 kDa protein expressed as a homodimer on the surface of activated T and B cells, and on thymocytes. CTLA-4 is structurally similar, yet functionally disparate, to the T cell co-stimulatory molecule CD28. Both CTLA-4 and CD28 interact with the co-stimulatory molecules CD80 (B7-1) and CD86 (B7-2) on antigen-presenting cells, with CTLA-4 displaying a higher avidity than CD28. While CD28 typically delivers a potent co-stimulatory signal in support of T cell activation, CTLA-4 appears to act as a negative regulator of T cell activation and may contribute to the suppressor function of Treg cells.
Form
Liquid
Buffer
10mM NaH₂PO₄ (pH7.2), 150mM NaCl
Preservative
0.09% Sodium azide
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. Store at 4ºC.
Concentration
0.5 mg/ml
Antigen Species
Human
Immunogen
Human CTLA-4/human IgG heavy chain fusion protein.
Purification
Purified by affinity chromatography
From tissue culture supernatant
Conjugation
Unconjugated
RRID
AB_376701
Note
For laboratory use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Synonyms
cytotoxic T-lymphocyte associated protein 4 , ALPS5 , CD , CD152 , CELIAC3 , CTLA-4 , GRD4 , GSE , IDDM12
Cellular Localization
Cell membrane
Background
This gene is a member of the immunoglobulin superfamily and encodes a protein which transmits an inhibitory signal to T cells. The protein contains a V domain, a transmembrane domain, and a cytoplasmic tail. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. The membrane-bound isoform functions as a homodimer interconnected by a disulfide bond, while the soluble isoform functions as a monomer. Mutations in this gene have been associated with insulin-dependent diabetes mellitus, Graves disease, Hashimoto thyroiditis, celiac disease, systemic lupus erythematosus, thyroid-associated orbitopathy, and other autoimmune diseases. [provided by RefSeq, Jul 2008]
Database
Research Area