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Key Documents

SAB3500205

Sigma-Aldrich

Anti-Daxx antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonym(s):

Anti-Daxx

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About This Item

MDL number:
MFCD01865517
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

predicted mol wt 120 kDa

species reactivity

mouse, human

technique(s)

immunocytochemistry: suitable
indirect ELISA: suitable
western blot: suitable

NCBI accession no.

CAG33366

UniProt accession no.

Q9UER7

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... DAXX(1616)

Immunogen

Daxx antibody was raised against a peptide corresponding to amino acids near the carboxy-terminus of human Daxx.

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 SBP3500205.

Physical form

Supplied in PBS with 0.02% 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)

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Tetsuya Kitamura et al.
Cancer research, 69(19), 7681-7688 (2009-10-01)
Daxx is a regulatory protein for apoptosis signal-regulating kinase 1 (ASK1) which activates c-Jun NH2-terminal kinase (JNK) and p38 pathways in response to stressors such as tumor necrosis factor-alpha (TNFalpha). Here, we show that TNFalpha treatment induces the accumulation of

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