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. 2003 Jan 15;23(2):493–502. doi: 10.1523/JNEUROSCI.23-02-00493.2003

Fig. 5.

Fig. 5.

PTP-PEST binding to paxillin is required for Aβ-induced neuronal dystrophy. A, Aβ-induced neuronal dystrophy was assessed in neurons transfected with paxillin constructs bearing Cys-to-Ala point mutations, which disrupt the LIM domain tertiary structure, with FRNK, an FAK dominant negative construct, or with PESTdl, a PTP-PEST deletion construct.B, Mutations C470A, C467/470A, and C523A in paxillin, which prevent PTP-PEST binding and integrin association, significantly reduce Aβ-induced neuronal dystrophy (C470A, 62.6 ± 1.3%; C467/C470A, 21.2 ± 4.4%;C523A, 39.9 ± 18.5%). The mutationC467A, which also prevents PTP-PEST binding and integrin association, has no effect on Aβ-induced neuronal dystrophy (112.2 ± 36.1). Expression of PESTdl, which prevents PTP-PEST binding to paxillin, completely prevents neuronal dystrophy. Expression of FRNK, which contains the FAK focal adhesion targeting domain but lacks the kinase domain, has no effect on Aβ-induced neuronal dystrophy. The number of dystrophic neurons was quantified 24 hr after transfection and expressed as a percentage of the number of Aβ-induced dystrophic neurons expressing GFP (100%). Values are mean ± SEM; n = 3–7 individual experiments; 250 neurons were scored per condition in each experiment; *p < 0.05; **p < 0.01 relative to control (GFP) by ANOVA followed by the Student–Newman–Keuls post hoc test.