Ultra-LEAF™ Purified anti-human BAFF (CD257) Antibody, BAFF, W20066D,BioLegend,638354

Host

Mouse

Reactivity

Human

Application

Neut - Quality tested

Platform ID

BAB022344885

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

Email:

Product Specifications
Scientific Background

Specifications

NameUltra-LEAF™ Purified anti-human BAFF (CD257) Antibody, BAFF, W20066D
Cat. No.638354
HostMouse
RRIDAB_3662320 (BioLegend Cat. No. 638353)AB_3662320 (BioLegend Cat. No. 638354)
IsotypeMouse IgG2b, κ
ReactivityHuman
ApplicationNeut - Quality tested
ClonalityMonoclonal
Clone NumberW20066D
ConcentrationThe antibody is bottled at the concentration indicated on the vial, typically between 2 mg/mL and 3 mg/mL. To obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.
TargetBAFF
ImmunogenRecombinant Human BAFF
PurityThe Ultra-LEAF™ (Low Endotoxin, Azide-Free) antibody was purified by affinity chromatography.
Formulation0.2 µm filtered in phosphate-buffered solution, pH 7.2, containing no preservative.
StorageThe antibody solution should be stored undiluted between 2°C and 8°C. This Ultra-LEAF™ solution contains no preservative; handle under aseptic conditions.
Regulatory StatusResearch Use Only

Scientific Background

BAFF is a TNF-α cytokine member (a type II membrane protein) that acts in both a membrane-bound form and soluble cytokine form. The extracellular domain of BAFF shows high homology with APRIL. The soluble form is derived by cleavage in a furin consensus site. In human neutrophils treated with G-CSF, BAFF is processed intracellularly by a furin-type convertase. BAFF acts mainly as a soluble trimer and binds to three receptors with decreasing affinity in the following order: BAFFR > TACI > BCMA. Mice deficient in BAFF or its receptor BAFFR exhibit an obstruction in B cell development after the transitional T1 stage and lack marginal zone (MZ) and conventional B2 B cells. BAFFR-deficient mice and humans (patients with common variable immunodeficiency, or CVID) develop severe B cell lymphopenia due to the arrest of B cell development at the transitional B cell stage. Extreme BAFF production triggers severe autoimmune disorders in mice similar to Systemic Lupus Erythematosus (SLE) and Sjögren’s syndrome. BAFF has been associated with different human diseases such as pancreatic ductal adenocarcinoma (PDAC), autoimmune pancreatitis, SLE, rheumatoid arthritis, Sjögren's syndrome, lymphoid cancers, HIV infection, and B cell malignancies such as non-Hodgkin’s lymphoma (NHL).

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