Fig. 4: Overexpression of a SEPT9_i1-containing set of septins stimulates the recruitment of CLIP-170 and MCAK to microtubules, which is amplified by long-chain tubulin polyglutamylation. | Cell Death & Disease

Fig. 4: Overexpression of a SEPT9_i1-containing set of septins stimulates the recruitment of CLIP-170 and MCAK to microtubules, which is amplified by long-chain tubulin polyglutamylation.

From: Septin filament coalignment with microtubules depends on SEPT9_i1 and tubulin polyglutamylation, and is an early feature of acquired cell resistance to paclitaxel

Fig. 4

MT fractions from Ts (a) or RPE-1 (b) cells subjected to TTLL and/or septin overexpression as indicated were analyzed for the recruitment of various +TIPs (EB1, CLIP-170, and MCAK). The polyE antibody recognizes glutamate chains composed of at least three glutamic acids. The polyE signal is therefore a reflection of elongating TTLL activity. Tubulin was used as a loading control. The quantitative data are the ratio of the intensity of the protein of interest to that of α-tubulin for the blot shown

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