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Merck
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Key Documents

SAB2500664

Sigma-Aldrich

Anti-MYD88 antibody produced in goat

affinity isolated antibody, buffered aqueous solution

Sinónimos:

Anti-Myeloid differentiation primary response gene (88)

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About This Item

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

biological source

goat

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

rat, canine, mouse, chimpanzee, human

technique(s)

flow cytometry: suitable
immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... MYD88(4615)

Categorías relacionadas

Immunogen

Peptide with sequence C-IKYKAMKKEFP from the internal region of the protein sequence according to NP_002459.1.

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.

Physical form

Supplied at 0.5 mg/mL in Tris saline with 0.02% sodium azide and 0.5% bovine serum albumin.

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

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

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Jingjing Cai et al.
Molecular medicine (Cambridge, Mass.), 23 (2016-01-01)
The inflammatory pathways that drive the development of intimal hyperplasia (IH) following arterial injury are not fully understood. We hypothesized that the lysosomal cysteine protease cathepsin L activates processes leading to IH after arterial injury. Using a mouse model of

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