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SAB3500989

Sigma-Aldrich

Anti-PRDM16 antibody produced in rabbit

affinity isolated antibody

Synonym(s):

Anti-CMD1LL, Anti-KMT8F, Anti-LVNC8, Anti-MEL1, Anti-PFM13

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

predicted mol wt 109-120 kDa

species reactivity

human, mouse

concentration

1 mg/mL

technique(s)

ELISA: suitable
immunoblotting: suitable
immunofluorescence: suitable
immunohistochemistry: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... PRDM16(63976)

Immunogen

Antibody was raised against a 17 amino acid synthetic peptide from near the carboxy terminus of human PRDM16.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Linkage

The action of this antibody can be blocked using blocking peptide SBP3500989.

Physical form

Supplied at 1 mg/mL in PBS with 0.02% sodim 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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Pricing

Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Fenfen Li et al.
Nature communications, 12(1), 6838-6838 (2021-11-27)
Brown adipocytes share the same developmental origin with skeletal muscle. Here we find that a brown adipocyte-to-myocyte remodeling also exists in mature brown adipocytes, and is induced by prolonged high fat diet (HFD) feeding, leading to brown fat dysfunction. This
Bhavin V Patel et al.
Journal of molecular biology, 432(23), 6127-6145 (2020-10-16)
Mitochondrial fatty acid oxidation (FAO) contributes to the proton motive force that drives ATP synthesis in many mammalian tissues. In eutherian (placental) mammals, brown adipose tissue (BAT) can also dissipate this proton gradient through uncoupling protein 1 (UCP1) to generate

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