Anti-Bruton's tyrosine kinase (Btk), clone 10D11

Anti-Bruton's tyrosine kinase (Btk), clone 10D11

Recognizes human Btk, MW ~77 kDa.
A higher molecular weight protein may be detected, which is thought to be a phosphorylated species of Btk or a related protein.

~77 kDa

Intracellular

GST-tagged recombinant protein corres-ponding to human Btk.

IgG1κ

Btk (Bruton’s tyrosine kinase also known as BPK or ATK) is a member of the TEC family of non-receptor protein tyrosine kinase which includes Bmx, Itk and TEC. BTK plays a crucial role in B cell activation and development. Similar to Etk-TNFR2 interaction, Btk interacts with Fas, a member of the TNFR family involved in apoptosis in a ligand-independent manner. Mutations in the Btk gene have been linked to severe developmental blocks in human B-cell ontogeny leading to X-linked agammaglobulinemia (XLA).

• Human
• Rat

Proven to react with human and rat.

Immunoprecipitation Analysis: A previous lot of this antibody has been reported by an independent laboratory to immunoprecipitate Btk in the presence of 0.5% SDS. Not recommended for IP/kinase assays.

Raji cell lysate

Evaluated by Western Blot in Raji cell lysate.

Western Blot Analysis: 0.05- 1 µg/mL of this antibody detected Btk on 10 µg of Raji cell lysate.

Protein G purfied

Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Stable for 1 year at 2-8°C from date of receipt.

Q06187

NP_000052.1

• AGMX1
• AT
• ATK
• BPK
• EC 2.7.10.2
• IMD1
• MGC126261
• MGC126262
• OTTHUMP00000023676
• OTTHUMP00000063593
• PSCTK1
• XLA

• Agammaglobulinaemia tyrosine kinase
• B-cell progenitor kinase
• Bruton agammaglobulinemia tyrosine kinase
• Bruton tyrosine kinase
• dominant-negative kinase-deficient Brutons tyrosine kinase
• tyrosine-protein kinase BTK

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• Western Blotting
• Immunoprecipitation

Summary: The protein encoded by this gene plays a crucial role in B-cell development. Mutations in this gene cause X-linked agammaglobulinemia type 1, which is an immunodeficiency
characterized by the failure to produce mature B lymphocytes, and associated with a failure of Ig heavy chain rearrangement.

FUNCTION: Plays a crucial role in B-cell ontogeny. Transiently phosphorylates GTF2I on tyrosine residues in response to B-cell receptor cross-linking. Required for the formation of functional ARID3A DNA-binding complexes. Ref.12 Ref.15
CATALYTIC ACTIVITY:ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate.
COFACTOR: Binds 1 zinc ion per subunit.
ENZYME REGULATION: Inhibited by IBTK. Activated by phosphorylation.
SUBUNIT STRUCTURE: Binds GTF2I through the PH domain. Interacts with SH3BP5 via the SH3 domain. Interacts with IBTK via its PH domain. Interacts with GTF2I and ARID3A. Ref.15 Ref.13
SUBCELLULAR LOCATION: Cytoplasm By similarity. Membrane; Peripheral membrane protein By similarity. Nucleus By similarity.
PTM: Autophosphorylated on Tyr-223 and Tyr-551. Phosphorylation of Tyr-223 may create a docking site for a SH2 containing protein By similarity.
INVOLVEMENT IN DISEASE: Defects in BTK are the cause of X-linked agammaglobulinemia (XLA) [MIM:300755]; also called X-linked agammaglobulinemia type 1 (AGMX1) or immunodeficiency type 1 (IMD1). XLA is a humoral immunodeficiency disease which results in developmental defects in the maturation pathway of B-cells. Affected boys have normal levels of pre-B-cells in their bone marrow but virtually no circulating mature B-lymphocytes. This results in a lack of immunoglobulins of all classes and leads to recurrent bacterial infections like otitis, conjunctivitis, dermatitis, sinusitis in the first few years of life, or even some patients present overwhelming sepsis or meningitis, resulting in death in a few hours. Treatment in most cases is by infusion of intravenous immunoglobulin.
Defects in BTK may be the cause of X-linked hypogammaglobulinemia and isolated growth hormone deficiency (XLA-IGHD) [MIM:307200]; also known as agammaglobulinemia and isolated growth hormone deficiency or Fleisher syndrome or isolated growth hormone deficiency type 3 (IGHD3). In rare cases XLA is inherited together with isolated growth hormone deficiency (IGHD).
SEQUENCE SIMILARITIES:Belongs to the protein kinase superfamily. Tyr protein kinase family. TEC subfamily.
Contains 1 Btk-type zinc finger.
Contains 1 PH domain.
Contains 1 protein kinase domain.
Contains 1 SH2 domain.
Contains 1 SH3 domain.

Bruton's Tyrosine Kinase (BTK) is a cytoplasmic non-receptor tyrosine kinase of the Tec family, that is expressed in most hematopoietic tissues. Like the Src family, BTK has SH2 and SH3 domains, but also possesses a Pleckstrin Homology domain. BTK becomes activated in response to ligation of the B-cell Receptor; activation involves phosphorylation on Tyr551 by Lyn and Syk, followed by autophosphorylation on Tyr223 within the SH3 domain. BTK is critical for B-cell development and function, and is the defective gene in human X-linked a-γ-globulinemia and mouse X-linked immunodeficiency.

Anti-Bruton's tyrosine kinase (Btk), clone 10D11

1 mg/mL

Monoclonal Antibody

100 μg

Purified

Mouse