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Anti myc hrp

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Anti-MYC HRP is a horseradish peroxidase (HRP) conjugated antibody that specifically recognizes the MYC protein epitope tag. It is designed for detection of MYC-tagged recombinant proteins in various applications, such as Western blotting, immunoprecipitation, and immunocytochemistry.

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Lab products found in correlation

Platinum e retroviral packaging cells, by Cell Biolabs (2 mentions) N myc tagged pmxs puro retroviral vector, by Cell Biolabs (2 mentions) Anti qki, by Fortis Life Sciences (2 mentions) Anti myb antibody, by Abcam (2 mentions) Anti gapdh, by Thermo Fisher Scientific (1 mentions) Anti drosha, by Cell Signaling Technology (1 mentions) Ecl substrate, by Merck Group (1 mentions) Quantipro bca assay kit, by Merck Group (1 mentions) Protease inhibitor cocktail, by Merck Group (1 mentions) Phosphatase inhibitor cocktail 3, by Merck Group (1 mentions)

Close spelling variants of this product

Anti-Myc-HRP antibody Mouse anti-c-Myc-HRP Anti-Myc

3 protocols using anti myc hrp

1

Retroviral Expression of MYB-QKI Fusion Constructs

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MYB-QKI5 and MYB-QKI6 constructs were synthesized as Gateway compatible entry clones. MYBtr constructs were generated via PCR mutagenesis using MYB-QKI fusions as templates. Full-length MYB and QKI constructs were purchased as gateway entry clones from PlasmID/DF/HCC DNA Resource Core. MYB-QKI5 and MYB-QKI6, MYBtr, full-length MYB and QKI constructs were sub-cloned into a Gateway-compatible N-MYC-tagged pMXs-Puro Retroviral Vector (Cell Biolabs). Platinum-E retroviral packaging cells (Cell BioLabs) were used to generate retrovirus as per manufacturer protocols. NIH3T3 cells were infected with retrovirus containing media for 6 hours and puromycin selection commenced 48 hours post infection. Stable expression of MYC-tagged proteins was confirmed via western blot analysis (anti-MYC HRP 1:5000 (Invitrogen), anti-MYB antibody 1:5000 (Abcam) and anti-QKI 1:1000 (Bethyl Lab).
Bandopadhayay P., Ramkissoon L.A., Jain P., Bergthold G., Wala J., Zeid R., Schumacher S.E., Urbanski L., O’Rourke R., Gibson W.J., Pelton K., Ramkissoon S.H., Han H.J., Zhu Y., Choudhari N., Silva A., Boucher K., Henn R.E., Kang Y.J., Knoff D., Paolella B.R., Gladden-Young A., Varlet P., Pages M., Horowitz P.M., Federation A., Malkin H., Tracy A., Seepo S., Ducar M., Hummelen P.V., Santi M., Buccoliero A.M., Scagnet M., Bowers D.C., Giannini C., Puget S., Hawkins C., Tabori U., Klekner A., Bognar L., Burger P.C., Eberhart C., Rodriguez F.J., Hill D.A., Mueller S., Haas-Kogan D.A., Phillips J.J., Santagata S., Stiles C.D., Bradner J.E., Jabado N., Goren A., Grill J., Ligon A.H., Goumnerova L., Waanders A.J., Storm P.B., Kieran M.W., Ligon K.L., Beroukhim R, & Resnick A.C. (2016). MYB-QKI rearrangements in Angiocentric Glioma drive tumorigenicity through a tripartite mechanism. Nature genetics, 48(3), 273-282.
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2

Quantitative Western Blot Analysis

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Western blotting was performed to detect the expression of transfected wild-type and
E1147K DROSHA in HEK293 and
HEK293T cell lines. Cell pellets were diluted in RIPA buffer with phosphatase inhibitor
cocktail 3 (1:100, Sigma-Aldrich) and protease inhibitor cocktail (1:100, Sigma), and
lysed by temperature change (dry ice and 37 °C repeated 10 × ). Protein
concentration was quantified using the QuantiPRO BCA assay kit (Sigma-Aldrich), loaded
onto an SDS-PAGE gel (10%) and transferred onto polyvinylidene difluoride membrane. The
blots were probed with anti-myc-HRP (1:5,000, Invitrogen), anti-Drosha (rabbit monoclonal, 1:1,000, Cell Signaling)
and anti-GAPDH (mouse polyclonal, 1:1,000, Invitrogen) at 4 °C overnight and
subsequently incubated with horseradish peroxidase-conjugated secondary antibody
(1:3,000). Signals were visualized using ECL Substrates (Millipore) and captured with
UVItec Alliance 4.7 (UVItec) (Supplementary Figs
5b, 7b and 8). For quantification of proteins bands, densitometry was performed
with ImageJ 1.4 (http://imagej.software.informer.com/1.4/).
Torrezan G.T., Ferreira E.N., Nakahata A.M., Barros B.D., Castro M.T., Correa B.R., Krepischi A.C., Olivieri E.H., Cunha I.W., Tabori U., Grundy P.E., Costa C.M., de Camargo B., Galante P.A, & Carraro D.M. (2014). Recurrent somatic mutation in DROSHA induces microRNA profile changes in Wilms tumour. Nature Communications, 5, 4039.
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3

Retroviral Expression of MYB-QKI Fusion Constructs

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MYB-QKI5 and MYB-QKI6 constructs were synthesized as Gateway compatible entry clones. MYBtr constructs were generated via PCR mutagenesis using MYB-QKI fusions as templates. Full-length MYB and QKI constructs were purchased as gateway entry clones from PlasmID/DF/HCC DNA Resource Core. MYB-QKI5 and MYB-QKI6, MYBtr, full-length MYB and QKI constructs were sub-cloned into a Gateway-compatible N-MYC-tagged pMXs-Puro Retroviral Vector (Cell Biolabs). Platinum-E retroviral packaging cells (Cell BioLabs) were used to generate retrovirus as per manufacturer protocols. NIH3T3 cells were infected with retrovirus containing media for 6 hours and puromycin selection commenced 48 hours post infection. Stable expression of MYC-tagged proteins was confirmed via western blot analysis (anti-MYC HRP 1:5000 (Invitrogen), anti-MYB antibody 1:5000 (Abcam) and anti-QKI 1:1000 (Bethyl Lab).
Bandopadhayay P., Ramkissoon L.A., Jain P., Bergthold G., Wala J., Zeid R., Schumacher S.E., Urbanski L., O’Rourke R., Gibson W.J., Pelton K., Ramkissoon S.H., Han H.J., Zhu Y., Choudhari N., Silva A., Boucher K., Henn R.E., Kang Y.J., Knoff D., Paolella B.R., Gladden-Young A., Varlet P., Pages M., Horowitz P.M., Federation A., Malkin H., Tracy A., Seepo S., Ducar M., Hummelen P.V., Santi M., Buccoliero A.M., Scagnet M., Bowers D.C., Giannini C., Puget S., Hawkins C., Tabori U., Klekner A., Bognar L., Burger P.C., Eberhart C., Rodriguez F.J., Hill D.A., Mueller S., Haas-Kogan D.A., Phillips J.J., Santagata S., Stiles C.D., Bradner J.E., Jabado N., Goren A., Grill J., Ligon A.H., Goumnerova L., Waanders A.J., Storm P.B., Kieran M.W., Ligon K.L., Beroukhim R, & Resnick A.C. (2016). MYB-QKI rearrangements in Angiocentric Glioma drive tumorigenicity through a tripartite mechanism. Nature genetics, 48(3), 273-282.
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