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96-Well Plate
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48-602MAG
Buffer Detection Kit for Magnetic Beads
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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).
References
Product Information
Format
Purified
Control
Raji cell lysate
Presentation
Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Detect Bruton's tyrosine kinase (Btk) using this Anti-Bruton's tyrosine kinase (Btk) Antibody, clone 10D11 validated for use in WB & IP.
Key Applications
Western Blotting
Immunoprecipitation
Application Notes
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.
Biological Information
Immunogen
GST-tagged recombinant protein corres-ponding to human Btk.
Epitope
Intracellular
Clone
clone 10D11
Concentration
Please refer to the Certificate of Analysis for the lot-specific concentration.
Host
Mouse
Specificity
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.
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.
Molecular Weight
~77 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
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.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
X-linked agammaglobulinemia (XLA) is a congenital humoral immunodeficiency caused by a defect in a B-cell-specific signaling molecule, Btk. There has been little concordance of phenotype with genotype in this disorder, and defects in Btk cause immunodeficiencies that range from mild impairment to complete inability to produce antibodies. The factors modifying the phenotype of XLA are not understood. The current study is the first description of two male siblings with identical T134 --> C mutations in the translation initiation ATG of Btk who have different clinical phenotypes. The proband lacks immunoglobulins and B cells and has recurrent infections, while the elder, affected brother has normal levels of IgG and IgM and very few infections. Both have undetectable levels of Btk kinase activity in circulating mononuclear cells. Complete sequencing of Btk gene transcripts in both brothers revealed no additional mutations to account for the discordant phenotypes. This description provides unequivocal evidence that the phenotype of XLA is influenced by factors additional to the Btk gene.
