Loss of Tsc1/Tsc2 activates mTOR and disrupts PI3K-Akt signaling through downregulation of PDGFR
J. Clin. Invest. Hongbing Zhang, et al. 112:1223 doi:10.1172/JCI17222 [Go to this article.]

Figure 1
Premature senescence of Tsc2^–/– MEF cultures. (a) Growth curves of cultured Tsc2^–/– (open squares), Tsc2^+/– (filled circles), and wild-type (filled triangles) MEFs. PDL, population doubling. (b) Phase-contrast view of senescent P8 Tsc2^–/– (left) and P8 control (right) MEFs. (c) Immunoblot analysis of extracts from primary MEF cultures of the indicated genotypes. Note the increased expression of p21^CIP1/WAF1 by the Tsc2^–/– MEFs. (d) Immunoblot analysis similar to that shown in c of TP53^–/– MEF lines with various Tsc2 genotypes. (e) Left, immunoblot analysis of tuberin, hamartin, and ERK expression by MEFs with various genotypes. Note reduced expression of tuberin in the Tsc1-null MEFs. Right, tuberin immunoprecipitation (IP) from starved and stimulated (30 minutes) TP53^–/– cells shows no change in tuberin or hamartin expression levels or association.