PE anti-BTK Phospho Tyr 223 Antibody anti-BTK Phospho - A16128B,BioLegend,601704

A16128B was generated in the same immunization that produced clone A16128C (anti-BTK Phospho (Tyr223)/ITK Phospho (Tyr180)). Both clones bind BTK Phospho Tyr223 with similar affinity, but in comparison to clone A16128C, clone A16128B has weaker recognition of phosphorylated Tyrosine 180 of ITK by intracellular staining and flow cytometric analysis.

Host

Mouse

Reactivity

Human, Mouse

Application

ICFC -Quality tested

Platform ID

BAB548893400

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Contact

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Product Specifications
Scientific Background

Specifications

NamePE anti-BTK Phospho Tyr 223 Antibody anti-BTK Phospho - A16128B
Cat. No.601704
HostMouse
RRIDAB_2721620 (BioLegend Cat. No. 601703)AB_2721621 (BioLegend Cat. No. 601704)
IsotypeMouse IgG2a, κ
ReactivityHuman, Mouse
ApplicationICFC -Quality tested
ClonalityMonoclonal
Clone NumberA16128B
ConcentrationLot-specific (to obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.)
TargetBTK Phospho Tyr223
ImmunogenHuman BTK peptide phosphorylated at Tyr 223, Complete Freund's adjuvant.
PurityThe antibody was purified by affinity chromatography and conjugated with PE under optimal conditions.
FormulationPhosphate-buffered solution, pH 7.2, containing 0.09% sodium azide and BSA (origin USA)
StorageThe antibody solution should be stored undiluted between 2°C and 8°C, and protected from prolonged exposure to light.Do not freeze.
Regulatory StatusResearch Use Only

Scientific Background

Bruton’s tyrosine kinase (BTK) is a Tec family kinase that plays a critical role in B cell development. Upon B cell receptor engagement, BTK translocates to the plasma membrane, where it is transphosphorylated by LYN and SYK kinases at Tyr 551. This initial phosphorylation event is followed by autophosphorylation at Tyr 223. Phosphorylated Tyr 223 is proposed to serve as a docking site for other proteins containing an SH2 domain. Downregulation of BTK activity is achieved through phosphorylation at Ser 180 by PKCβ, which results in reduced membrane recruitment and concomitant transphosphorylation. BTK-mediated B cell receptor signaling is required for B cell survival in the bone marrow and is a therapeutic target for certain B cell malignancies. Mutations in theBTKgene results in X-linked agammaglobulinemia (XLA), a primary immunodeficiency disease characterized by a failure in B cell maturation. Additionally, BTK plays a role in Toll-like receptor signaling in innate immune cells, and has been shown to play a direct role in NLRP3 inflammasome activation, thus contributing to ischaemic brain injury.

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