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Key Documents

SAB2702287

Sigma-Aldrich

Monoclonal Anti-Ubiquitin antibody produced in mouse

clone GT751, affinity isolated antibody

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

GT751, monoclonal

form

buffered aqueous solution

concentration

1mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:100-1:1,000
western blot: 1:500-1:20,000

isotype

IgG2a

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Immunogen

The immunogen used to generate this antibody corresponds to Ubiquitin

Application

Suggested starting dilutions are as follows: WB: 1:500-1:20000. Not yet tested in other applications. Optimal working dilutions should be determined experimentally by the end user.

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.

Other Notes

Purification: Affinity purified by Protein G

Physical form

Phosphate-buffered saline, no preservative added.

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 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Hong Peng et al.
Autophagy, 16(4), 698-708 (2019-06-27)
SQSTM1/p62 (sequestosome 1) is a critical macroautophagy/autophagy receptor that promotes the formation and degradation of ubiquitinated aggregates. SQSTM1 can be modified by ubiquitination, and this modification modulates its autophagic activity. However, the molecular mechanisms underpinning its reversible deubiquitination have never

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