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. Author manuscript; available in PMC: 2018 Jul 11.
Published in final edited form as: Oncogene. 2018 Jan 11;37(11):1457–1471. doi: 10.1038/s41388-017-0049-3

Fig. 1. Loss of primary cilia promotes astrocyte proliferation in a growth factor-dependent manner.

Fig. 1

(A) Representative image of the cilium formed by primary human astrocyte (HA), stained for acetylated α-tubulin (AcTub, cilium marker) and γ-tubulin (γTub, basal body marker); scale bar – 10μm. (B) Quantification of primary astrocytes forming cilium, as in (A), in regular serum-supplemented media (SSM) or upon 48h of serum starvation (SFM); 300 cells, 100 cells in each of 3 independent experiments; Student’s t-test, p<0.05. (C) Western blot of IFT88 and KIF3B in primary and immortalized astrocytes (HA-LTA) stably expressing non-targeting shRNA (Con) or shRNA against IFT88 or KIF3B. (D, E) Quantification of primary astrocytes (D) and immortalized astrocytes (E) forming primary cilium, as in (B) upon depletion of IFT88 or KIF3B, as in (C); 300 cells, 100 cells in each of 3 independent experiments; one-way ANOVA with Dunnett’s post hoc test, p<0.05. (F, G) Growth rates of primary astrocytes (F) and immortalized astrocytes (G) upon depletion of IFT88 or KIF3B in full media or in serum-free conditions (SFM); 3 independent experiments; one-way ANOVA with Dunnett’s post hoc test, p<0.05.