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SAB4200479

Sigma-Aldrich

Anti-SET antibody, Mouse monoclonal

clone SET51, purified from hybridoma cell culture

Synonym(s):

Monoclonal Anti-2PP2A, Monoclonal Anti-I2PP2A, Monoclonal Anti-IGAAD, Monoclonal Anti-IPP2A2, Monoclonal Anti-PHAPII, Monoclonal Anti-SET antibody produced in mouse, Monoclonal Anti-SET nuclear oncogene, Monoclonal Anti-TAF-I, Monoclonal Anti-TAF-IBETA

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

SET51, monoclonal

form

buffered aqueous solution

mol wt

antigen ~37 kDa

species reactivity

rat, human, mouse

concentration

~1.0 mg/mL

technique(s)

western blot: 0.5-1.0 μg/mL using K562 total cell extracts.

isotype

IgG2b

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... SET(6418)
mouse ... Set(56086)
rat ... Set(307947)

General description

Monoclonal Anti-SET (mouse IgG2b isotype) is derived from the hybridoma SET51 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a peptide. The SET (Suvar3-9, enhancer of zeste, trithorax) protein is localized to the nucleus and cytoplasm. It is characterized with a N-terminal domain with inhibitory activity and a highly acidic C-terminal domain that is involved in chromatin remodeling.

Immunogen

peptide corresponding to a sequence within the internal region of human SET, conjugated to KLH. The isotype is determined by ELISA using Mouse Monoclonal Antibody Isotyping Reagents (Sigma ISO-2).

Application

Monoclonal Anti-SET antibody produced in mouse has been used in immunoblotting and immunofluorescence.

Biochem/physiol Actions

Suvar3-9, enhancer of zeste, trithorax (SET) acts as a potential inhibitor of protein phosphatase 2A (PP2A) activity. It plays a key role in the regulation of normal and cancer signal transduction. In addition, it also regulates human natural killed-cell cytotoxicity by regulating natural killer cell IFN-γ production granzyme B gene expression through PP2A inactivation. SET has an ability to inhibit the tumor suppressor NM23-H1, a granzyme A DNAse-activated factor. It is also involved in negative regulation of histone acetylation. SET- nucleoporin 214 (Nup214)/CAN fusion protein might affect the normal regulation of PP2A and leads to the development of leukemogenesis.

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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wgk_germany

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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SET/I2 PP 2A overexpression induces phenotypic, molecular, and metabolic alterations in an oral keratinocyte cell line
Sobral LM, et al.
FEBS Journal, 284(17), 2774-2785 (2017)
The PP2A inhibitor SET regulates granzyme B expression in human natural killer cells
Trotta R, et al.
Blood, 117(8), 2378-2384 (2011)
Protein phosphatase 2A: a highly regulated family of serine/threonine phosphatases implicated in cell growth and signalling
Janssens V and Goris J
The Biochemical Journal, 353(3), 417-439 (2001)
Zusen Fan et al.
Cell, 112(5), 659-672 (2003-03-12)
Granzyme A (GzmA) induces a caspase-independent cell death pathway characterized by single-stranded DNA nicks and other features of apoptosis. A GzmA-activated DNase (GAAD) is in an ER associated complex containing pp32 and the GzmA substrates SET, HMG-2, and Ape1. We

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