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Anti qki

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Anti-QKI is a laboratory reagent used to detect and quantify the presence of the QKI protein in biological samples. It is a primary antibody that specifically binds to the QKI protein, enabling its identification and measurement through various immunoassay techniques.

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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 myb antibody, by Abcam (2 mentions) Anti myc hrp, by Thermo Fisher Scientific (2 mentions)

Close spelling variants of this product

Rabbit anti-QKI antibody

2 protocols using anti qki

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

Retroviral Expression of MYB-QKI Fusion Constructs

Check if the same lab product or an alternative is used in the 5 most similar protocols
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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