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Ab17958

Manufactured by Abcam
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Ab17958 is a primary antibody product manufactured by Abcam. It is designed for use in various immunoassay applications.

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Lab products found in correlation

Ab10412, by Abcam (1 mentions) Jbw301, by Merck Group (1 mentions) Nb200 109, by Novus Biologicals (1 mentions) Sc 53993, by Santa Cruz Biotechnology (1 mentions) Ab1791, by Abcam (1 mentions) Anti myc tag, by Cell Signaling Technology (1 mentions) Anti actin, by Merck Group (1 mentions) Anti tubulin, by Merck Group (1 mentions)

2 protocols using ab17958

1

Antibody Detection in Cell Signaling

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The following antibodies were used: anti-MYCN monoclonal antibodies (OP13, Calbiochem and NB200-109, Novus Biologicals); anti-MYCN monoclonal antibody (B8.4.B) (sc-53993, Santa Cruz); anti-SMC2 rabbit polyclonal antibodies (GTX10411, GeneTex; and ab10412, Abcam); anti-β-ACTIN monoclonal antibody (AC-15) (A5441, Sigma); anti-SMC4 rabbit polyclonal antibody (ab17958, Abcam); anti-CAP-D2 rabbit polyclonal antibody (A300-601A, Bethyl Laboratories); and anti-phospho-histone H2A.X (Ser139) mouse monoclonal antibody (JBW301, Millipore).
Murakami-Tonami Y., Kishida S., Takeuchi I., Katou Y., Maris J.M., Ichikawa H., Kondo Y., Sekido Y., Shirahige K., Murakami H, & Kadomatsu K. (2014). Inactivation of SMC2 shows a synergistic lethal response in MYCN-amplified neuroblastoma cells. Cell Cycle, 13(7), 1115-1131.
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2

Antibody Usage for Immunoblotting and Immunofluorescence

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The following primary antibodies were used for immunoblots and immunofluorescence (IF): anti‐SMC2 (A300‐056A; Bethyl), anti‐SMC4 (ab17958; Abcam), anti‐CAPD3 (A300‐604A; Bethyl), anti‐CAPG2 (A300‐605A; Bethyl), anti‐CAPH2 (A302‐275A; Bethyl), anti‐53BP1 (ab38623; Abcam), anti‐γH2AX (05‐636; EMD Millipore), anti‐tubulin (T9026; Sigma), anti‐actin (A5441; Sigma), anti‐myc‐tag (2272; Cell Signaling), anti‐Histone H3 (ab1791; Abcam), and anti‐GFP (632381; Takara Bio).
Weyburne E, & Bosco G. (2020). Cancer‐associated mutations in the condensin II subunit CAPH2 cause genomic instability through telomere dysfunction and anaphase chromosome bridges. Journal of Cellular Physiology, 236(5), 3579-3598.
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