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SAB4200483

Sigma-Aldrich

Anti-JAK2 antibody, Mouse monoclonal

clone 10.1.5, purified from hybridoma cell culture

Synonym(s):

Anti-JAK-2, Anti-JTK10, Anti-Janus kinase 2, Monoclonal Anti-JAK2 antibody produced in mouse

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.44

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

10.1.5, monoclonal

form

buffered aqueous solution

mol wt

antigen ~125 kDa

species reactivity

bovine, human

concentration

~1.0 mg/mL

technique(s)

indirect immunofluorescence: 2.5-5.0 μg/mL using MCF7 cells.
western blot: 2.0-4.0 μg/mL using TF1 total cell extracts.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... JAK2(3717)

General description

Monoclonal Anti-JAK2 (mouse IgG1 isotype) is derived from the hybridoma 10.1.5 produced by the fusion of mouse myeloma cells and splenocytes from immunized BALB/c mice. The Janus kinases (Jak) family of proteins includes four members: Jak1, Jak2, Jak3 and the tyrosine kinase 2 (Tyk2). Jak2 is ubiquitously expressed. It is also expressed in normal and neoplastic mammary epithelial cells.

Immunogen

synthetic peptide corresponding to an internal sequence of human JAK2 (GeneID 3717), conjugated to KLH.

Application

Monoclonal Anti-JAK2 antibody produced in mouse has been used in:
  • immunoblotting
  • immunocytochemistry
  • flow cytometry

Biochem/physiol Actions

Janus kinases engage in interactions with the intracellular tails of several cytokine receptors, which result in the activation of members of the signal transducer and activator of transcription (STAT) family of transcription factors. The latter bind specific cognate sequences at the promoter region of genes that regulate proliferation and differentiation. JAK activation plays an important role in cell proliferation, differentiation, migration and apoptosis. A member of this family, JAK2, has been found to induce signaling regulating gene expression of various pro-survival and anti-apoptotic molecules. Furthermore, inhibition of JAK2 signaling triggered cell death in human cancer cells. These findings indicate JAK2 inhibition as a potential therapeutic approach for various cancers.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

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.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Spleen deflation and beyond: The pros and cons of Janus kinase 2 inhibitor therapy for patients with myeloproliferative neoplasms
Quintas CA and Verstovsek S
Cancer, 118(4), 870-877 (2012)
Janus kinases in immune cell signaling
Ghoreschi K, et al.
Immunological Reviews, 228(1), 273-287 (2009)
Reetobrata Basu et al.
Oncotarget, 8(13), 21579-21598 (2017-02-23)
Recent reports have confirmed highest levels of growth hormone (GH) receptor (GHR) transcripts in melanoma, one of the most aggressive forms of human cancer. Yet the mechanism of GH action in melanoma remains mostly unknown. Here, using human malignant melanoma
Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial-mesenchymal transition in ovarian carcinomas
Colomiere M, et al.
British Journal of Cancer, 100(1), 134-134 (2009)
The JAK/STAT signaling pathway
Rawlings JS
Journal of Cell Science, 117(8), 1281-1283 (2004)

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