Malinin et al. 10.1073/pnas.0408237102.

Supporting Information

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Supporting Figure 5
Supporting Figure 6
Supporting Figure 7
Supporting Figure 8




Fig. 5. p165 characterization and isolation. (A) Neurotoxicity of different amyloid-b(Ab ) forms (2 days of treatment): control, untreated cortical culture; tox, Ab(1–40) treatment by consequent application of seed and soluble as described in Materials and Methods; tox1, alternative treatment with Ab(1–40) (see Materials and Methods); tox42, Ab(1–42) treatment; seed, treatment with "seed" only; soluble, treatment with "soluble" only. (B) Whole-cell lysate pY845EGFR Western blot of cortical cultures treated for 6 h with different preparations of Ab as described in A. (C) Schematic presentation of the purification procedure. (D) pY845EGFR Western blot of aliquots from the purification steps.





Fig. 6. ADAM12 expression is not protective against FISH348–1105 toxicity. Inverted images of GFP-positive cells expressing FISH348–1105 (all images) and ADAM12 or ADAM12D MP deletion mutant as shown.





Fig. 7. Adenovirus-mediated expression of full-length, but not metalloprotease-deficient, ADAM12, causes neurotoxicity. Inverted image of GFP-positive cells expressing ADAM12 and ADAM12D MP is shown. Images were taken at the indicated postinfection times.





Fig. 8. ADAM12 cleavage is induced by FISH348-1105 expression. ADAM12D MP blocks this cleavage. Shown is an ADAM12 (N-terminal) Western blot of conditioned medium from cortical cultures expressing FISH348-1105 and ADAM12D MP mutants as indicated. Arrow indicates p32 fragment.