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Rabbit Anti-BTK Recombinant Antibody (HL1803) (CBMAB-1230-CN)


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Summary

Host Animal
Rabbit
Specificity
Human, Mouse
Clone
HL1803
Antibody Isotype
IgG
Application
WB, IF

Basic Information

Immunogen
Recombinant protein of human BTK.
Host Species
Rabbit
Specificity
Human, Mouse
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:500-1:3,000

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4
Preservative
None
Concentration
1 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Bruton Tyrosine Kinase
Introduction
The protein encoded by this gene plays a crucial role in B-cell development. Non-receptor tyrosine kinase indispensable for B lymphocyte development, differentiation and signaling. Binding of antigen to the B-cell antigen receptor (BCR) triggers signaling that ultimately leads to B-cell activation. After BCR engagement and activation at the plasma membrane, phosphorylates PLCG2 at several sites, igniting the downstream signaling pathway through calcium mobilization, followed by activation of the protein kinase C (PKC) family members.
Entrez Gene ID
695
UniProt ID
Q06187
Alternative Names
AT; ATK; BPK; XLA; IMD1; AGMX1; PSCTK1
Function
Non-receptor tyrosine kinase indispensable for B lymphocyte development, differentiation and signaling. Binding of antigen to the B-cell antigen receptor (BCR) triggers signaling that ultimately leads to B-cell activation. After BCR engagement and activation at the plasma membrane, phosphorylates PLCG2 at several sites, igniting the downstream signaling pathway through calcium mobilization, followed by activation of the protein kinase C (PKC) family members. PLCG2 phosphorylation is performed in close cooperation with the adapter protein B-cell linker protein BLNK. BTK acts as a platform to bring together a diverse array of signaling proteins and is implicated in cytokine receptor signaling pathways. Plays an important role in the function of immune cells of innate as well as adaptive immunity, as a component of the Toll-like receptors (TLR) pathway. The TLR pathway acts as a primary surveillance system for the detection of pathogens and are crucial to the activation of host defense. Especially, is a critical molecule in regulating TLR9 activation in splenic B-cells. Within the TLR pathway, induces tyrosine phosphorylation of TIRAP which leads to TIRAP degradation. BTK plays also a critical role in transcription regulation. Induces the activity of NF-kappa-B, which is involved in regulating the expression of hundreds of genes. BTK is involved on the signaling pathway linking TLR8 and TLR9 to NF-kappa-B. Transiently phosphorylates transcription factor GTF2I on tyrosine residues in response to BCR. GTF2I then translocates to the nucleus to bind regulatory enhancer elements to modulate gene expression. ARID3A and NFAT are other transcriptional target of BTK. BTK is required for the formation of functional ARID3A DNA-binding complexes. There is however no evidence that BTK itself binds directly to DNA. BTK has a dual role in the regulation of apoptosis.
Biological Process
Adaptive immune response Source: UniProtKB
Apoptotic signaling pathway Source: ProtInc
B cell activation Source: UniProtKB
B cell affinity maturation Source: Ensembl
B cell receptor signaling pathway Source: UniProtKB
Calcium-mediated signaling Source: HGNC-UCL
Cell maturation Source: Ensembl
Cellular response to interleukin-7 Source: Ensembl
Cellular response to molecule of fungal origin Source: Ensembl
Cellular response to reactive oxygen species Source: Ensembl
Fc-epsilon receptor signaling pathway Source: Reactome
G protein-coupled receptor signaling pathway Source: Reactome
Histamine secretion by mast cell Source: Ensembl
I-kappaB kinase/NF-kappaB signaling Source: Ensembl
Innate immune response Source: UniProtKB
Intracellular signal transduction Source: ARUK-UCL
Mesoderm development Source: ProtInc
MyD88-dependent toll-like receptor signaling pathway Source: Reactome
Negative regulation of B cell proliferation Source: Ensembl
Negative regulation of cytokine production Source: Ensembl
Peptidyl-tyrosine phosphorylation Source: ARUK-UCL
Positive regulation of B cell differentiation Source: UniProtKB
Positive regulation of NF-kappaB transcription factor activity Source: UniProtKB
Positive regulation of type I hypersensitivity Source: Ensembl
Positive regulation of type III hypersensitivity Source: Ensembl
Protein autophosphorylation Source: Ensembl
Protein phosphorylation Source: HGNC-UCL
Regulation of B cell apoptotic process Source: UniProtKB
Regulation of B cell cytokine production Source: UniProtKB
Cellular Location
Nucleus; Cell membrane; Cytoplasm. In steady state, BTK is predominantly cytosolic. Following B-cell receptor (BCR) engagement by antigen, translocates to the plasma membrane through its PH domain. Plasma membrane localization is a critical step in the activation of BTK. A fraction of BTK also shuttles between the nucleus and the cytoplasm, and nuclear export is mediated by the nuclear export receptor CRM1.
Involvement in disease
X-linked agammaglobulinemia (XLA): 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.
Growth hormone deficiency, isolated, 3, with agammaglobulinemia (IGHD3): An X-linked recessive disorder characterized by growth hormone deficiency, short stature, delayed bone age, agammaglobulinemia with markedly reduced numbers of B cells, and good response to treatment with growth hormone.
PTM
Following B-cell receptor (BCR) engagement, translocates to the plasma membrane where it gets phosphorylated at Tyr-551 by LYN and SYK. Phosphorylation at Tyr-551 is followed by autophosphorylation of Tyr-223 which may create a docking site for a SH2 containing protein. Phosphorylation at Ser-180 by PRKCB, leads in translocation of BTK back to the cytoplasmic fraction. Phosphorylation at Ser-21 and Ser-115 creates a binding site for PIN1 at these Ser-Pro motifs, and promotes it's recruitment.
More Infomation

Fleming, M. R., Xiao, L., Jackson, K. D., Beckman, J. A., Barac, A., & Moslehi, J. J. (2021). Vascular impact of cancer therapies: the case of BTK (Bruton tyrosine kinase) inhibitors. Circulation Research, 128(12), 1973-1987.

Von Hundelshausen, P., Lorenz, R., Siess, W., & Weber, C. (2021). Vaccine-induced immune thrombotic thrombocytopenia (VITT): targeting pathomechanisms with Bruton tyrosine kinase inhibitors. Thrombosis and haemostasis.

Gu, D., Tang, H., Wu, J., Li, J., & Miao, Y. (2021). Targeting Bruton tyrosine kinase using non-covalent inhibitors in B cell malignancies. Journal of Hematology & Oncology, 14(1), 1-15.

Roschewski, M., Lionakis, M. S., Sharman, J. P., Roswarski, J., Goy, A., Monticelli, M. A., ... & Wilson, W. H. (2020). Inhibition of Bruton tyrosine kinase in patients with severe COVID-19. Science immunology, 5(48), eabd0110.

Kanagal‐Shamanna, R., Jain, P., Patel, K. P., Routbort, M., Bueso‐Ramos, C., Alhalouli, T., ... & Medeiros, L. J. (2019). Targeted multigene deep sequencing of Bruton tyrosine kinase inhibitor–resistant chronic lymphocytic leukemia with disease progression and Richter transformation. Cancer, 125(4), 559-574.

Tam, C. S., Opat, S., Zhu, J., Cull, G., Gottlieb, D., Li, J., ... & Trotman, J. (2019). PS1159 pooled analysis of safety data from monotherapy studies of the bruton tyrosine kinase (Btk) inhibitor, zanubrutinib (BGB-3111), in B-cell malignancies. HemaSphere, 3(S1), 526.

Tang, C. P. S., McMullen, J., & Tam, C. (2018). Cardiac side effects of bruton tyrosine kinase (BTK) inhibitors. Leukemia & lymphoma, 59(7), 1554-1564.

Wang, G., Guo, Z., Tong, L., Xue, F., Krafft, P. R., Budbazar, E., ... & Tang, J. (2018). TLR7 (Toll-Like Receptor 7) Facilitates Heme Scavenging Through the BTK (Bruton Tyrosine Kinase)–CRT (Calreticulin)–LRP1 (Low-Density Lipoprotein Receptor–Related Protein-1)–Hx (Hemopexin) Pathway in Murine Intracerebral Hemorrhage. Stroke, 49(12), 3020-3029.

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For research use only. Not intended for any clinical use.

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