Anti-Tyk 2 Monoclonal Antibody

Product Name

Anti-Tyk 2 Monoclonal Antibody

View all TYK2 Antibodies

SKU/Catalog Number

M01642

Size

100ul

Form

Liquid

Description

Boster Bio Anti-Tyk 2 Monoclonal Antibody catalog # M01642. Tested in ELISA, WB applications. This antibody reacts with Human.

Storage & Handling

Store at -20°C for one year. For short term storage and frequent use, store at 4°C for up to one month. Avoid repeated freeze-thaw cycles.

Cite This Product

Anti-Tyk 2 Monoclonal Antibody (Boster Biological Technology, Pleasanton CA, USA, Catalog # M01642)

Host

Mouse

Contents

Ascitic fluid containing 0.03% sodium azide.

Clonality

Monoclonal

Clone Number

8G8E9 / 8G9H5 / 8G8B3

Isotype

IgG

Immunogen

Purified recombinant fragment of Tyk 2 expressed in E. Coli.

*Blocking peptide can be purchased. Costs vary based on immunogen length. Contact us for pricing.

Reactive Species

M01642 is reactive to TYK2 in Human

Applications

M01642 is guaranteed for ELISA, WB Boster Guarantee

Observed Molecular Weight

Calculated molecular weight

133.65kDa

Background of TYK2

Bin1 is a conserved member of the BAR family of genes that have been implicated in diverse cellular processes including endocytosis, actin organization, programmed cell death, stress responses, and transcriptional control. The first mammalian BAR protein to be discovered, Amphiphysin I (AmphI), was identified in an immunoscreen for proteins associated with the plasma membranes of synaptic neurons, functions in the control of clathrin-dependent synaptic vesicle endocytosis. The mammalian Bin1 gene was first identified in a two hybrid screen for polypeptides that bind to the N-terminal Myc box 1 (MB1) portion of the c-Myc oncoprotein. Bin1 is similar to AmphI in overall structure, with an N-terminal BAR domain and a C-terminal SH3 domain. However, the Bin1 gene is more complex than the AmphI gene, encoding at least seven different splice variants that differ widely in subcellular localization, tissue distribution, and ascribed functions. Alternate splicing of the Bin1 gene results in ten transcript variants encoding different isoform. Bin1 is expressed ubiquitously in mammalian cells. Certain splice variants of Bin1 are expressed in the neurons, muscle cells or tumor cells. Bin1 may act as a cancer suppressor and inhibits malignant cell transformation. Studies in mouse suggest that this gene plays an important role in cardiac muscle development. Bin1 has also been implicated in Alzheimer disease and cardiac disease. Defects in Bin1 are the cause of centronuclear myopathy autosomal recessive; also known as autosomal recessive myotubular myopathy.

Antibody Validation

Boster validates all antibodies on WB, IHC, ICC, Immunofluorescence, and ELISA with known positive control and negative samples to ensure specificity and high affinity, including thorough antibody incubations.

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Assay Dilutions Recommendation

The recommendations below provide a starting point for assay optimization. The actual working concentration varies and should be decided by the user.

WB 1:500-1:2000
ELISA 1:10000

Validation Images & Assay Conditions

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Figure 1. Western blotting validation for Anti-Tyk 2 Monoclonal Antibody M01642

Western Blot (WB) analysis using Tyk 2 Monoclonal Antibody against truncated TYK2 recombinant protein (1) and Jurkat cell lysate(2).
Electrophoresis was performed on a SDS-PAGE gel. To determine SDS-PAGE gel concentration

Gene/Protein Information For TYK2 (Source: Uniprot.org, NCBI)

Alternative Names

EC 2.7.10; EC 2.7.10.2; JTK1; non-receptor tyrosine-protein kinase TYK2; Tyk2; tyrosine kinase 2 TYK2 IMD35, JTK1 tyrosine kinase 2 non-receptor tyrosine-protein kinase TYK2

For more info on TYK2, check out the TYK2 Infographic

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In this infographic, you will see the following information for TYK2: database IDs, superfamily, protein function, synonyms, molecular weight, chromosomal locations, tissues of expression, subcellular locations, post-translational modifications, and related diseases, research areas & pathways. If you want to see more information included, or would like to contribute to it and be acknowledged, please contact [email protected].

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