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SAB2702192

Sigma-Aldrich

Monoclonal Anti-Myc tag antibody produced in mouse

clone GT0002, affinity isolated antibody

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biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

GT0002, monoclonal

form

buffered aqueous solution

concentration

1mg/mL

technique(s)

immunoprecipitation (IP): suitable
indirect immunofluorescence: suitable
western blot: 5000-20000

isotype

IgG1

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

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antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

clone

GT0002, monoclonal

clone

GT134, monoclonal

clone

GT4810, monoclonal

clone

GT1071, monoclonal

isotype

IgG1

isotype

IgG2b

isotype

IgG2a

isotype

IgG1

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

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Immunogen

The immunogen used to generate this antibody corresponds to Myc tag

Application

Suggested starting dilutions are as follows: ICC/IF: 1:100-1:2000, IP: 1:100-1:500, WB: 1:5000-1:20000. 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.

Storage Class

12 - Non Combustible Liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


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Hai-Lin Dong et al.
NPJ genomic medicine, 6(1), 1-1 (2021-01-06)
Sorbitol dehydrogenase gene (SORD) has been identified as a novel causative gene of recessive forms of hereditary neuropathy, including Charcot-Marie-Tooth disease type 2 and distal hereditary motor neuropathy (dHMN). Our findings reveal two novel variants (c.404 A > G and c.908 + 1 G > C) and one
Kai He et al.
Nature communications, 9(1), 3310-3310 (2018-08-19)
Tubulin polyglutamylation is a predominant axonemal post-translational modification. However, if and how axoneme polyglutamylation is essential for primary cilia and contribute to ciliopathies are unknown. Here, we report that Joubert syndrome protein ARL13B controls axoneme polyglutamylation, which is marginally required
Mario Torrado et al.
Scientific reports, 12(1), 7284-7284 (2022-05-05)
The finding of a genotype-negative hypertrophic cardiomyopathy (HCM) pedigree with several affected members indicating a familial origin of the disease has driven this study to discover causative gene variants. Genetic testing of the proband and subsequent family screening revealed the
Mario Torrado et al.
NPJ genomic medicine, 6(1), 21-21 (2021-03-06)
Here we report an infant with clinical findings suggestive of Jervell and Lange-Nielsen syndrome (JLNS), including a prolonged QT interval (LQTS) and chronic bilateral sensorineural deafness. NGS analysis revealed one known heterozygous pathogenic missense variant, KCNQ1 p.R259L, previously associated with
Cefan Zhou et al.
Autophagy, 16(10), 1786-1806 (2019-11-08)
Macroautophagy/autophagy plays key roles in development, oncogenesis, and cardiovascular and metabolic diseases. Autophagy-specific class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) is essential for autophagosome formation. However, the regulation of this complex formation requires further investigation. Here, we discovered that STYK1

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