Anti-Human CD20 [Clone 2H7] — Purifiedin vivoGOLD™ Functional Grade,Leinco,C1652

Host

Mouse

Reactivity

Human

Application

FC,in vivo,WB

Platform ID

BAB133942096

Leinco

Headquarters

410 Axminister Drive St. Louis, Missouri 63026

Contact

Tel: +1 (800) 538-1145,+1 (636) 230-9477
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Product Specifications
Scientific Background

Specifications

NameAnti-Human CD20 [Clone 2H7] — Purifiedin vivoGOLD™ Functional Grade
Cat. No.C1652
HostMouse
ReactivityHuman
ApplicationFC,in vivo,WB
Clone Number2H7
Concentration≥ 5.0 mg/ml
ImmunogenHuman tonsillar B cells
Purity≥95% monomer by analytical SEC ⋅ >95% by SDS Page
Endotoxin Level< 1.0 EU/mg as determined by the LAL method
ShippingNext Day 2-8°C
FormulationThis monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.
StorageFunctional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.

Scientific Background

CD20 is a 33-37 kD transmembrane-spanning phosphoprotein that facilitates optimal B-cell immune response against T-independent antigens. It can exist in a complex with MHC class I, MHC class II, CD53, CD81, and CD82. However, CD20 can also form homo-oligomers. It has been suggested that homo-oligomerization of CD20 forms calcium ion channels in the plasma membrane of B cells. CD20 can be useful in diagnosing B-cell lymphomas and leukemias, and is the target of mAbs in the treatment of all B cell lymphomas, leukemias, and B cell-mediated autoimmune diseases. Interestingly, studies show a link between the immune system's B cells and diabetes mellitus in which anti-CD20 antibodies rendered the T cell antibodies dysfunctional and, hence, unable to cause insulin desensitivity by a B cell antibody-modulated autoimmune response.

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