Publication

Rapid iPSC inclusionopathy models shed light on formation, consequence, and molecular subtype of ?-synuclein inclusions.

Lam I, Ndayisaba A, Lewis AJ, Fu Y, Sagredo GT, Kuzkina A, Zaccagnini L, Celikag M, Sandoe J, Sanz RL, Vahdatshoar A, Martin TD, Morshed N, Ichihashi T, Tripathi A, Ramalingam N, Oettgen-Suazo C, Bartels T, Boussouf M, Schaebinger M, Hallacli E, Jiang X, Verma A, Tea C, Wang Z, Hakozaki H, Yu X, Hyles K, Park C, Wang X, Theunissen TW, Wang H, Jaenisch R, Lindquist S, Stevens B, Stefanova N, Wenning G, van de Berg WDJ, Luk KC, Sanchez-Pernaute R, Gomez-Esteban JC, Felsky D, Kiyota Y, Sahni N, Yi SS, Chung CY, Stahlberg H, Ferrer I, Schoeneberg J, Elledge SJ, Dettmer U, Halliday GM, Bartels T, Khurana V

The heterogeneity of protein-rich inclusions and its significance in neurodegeneration is poorly understood. Standard patient-derived iPSC models develop inclusions neither reproducibly nor in a reasonable time frame. Here, we developed screenable iPSC "inclusionopathy" models utilizing piggyBac or targeted transgenes to rapidly induce CNS cells that express aggregation-prone proteins at brain-like levels. Inclusions and their effects on cell survival were trackable ... [more]

Quantitative Score

• 2.0 [Confidence Score]

Throughput

• High Throughput

Additional Notes

• Scores from replicates: [MYTH run 1 repeat 1 ][ MYTH run 1 repeat 2 ][ MYTH run 1 repeat 3 ][ MYTH run 2 repeat 1 ][ MYTH run 2 repeat 2] = [2][3][1][NA][NA]
• Scores from technical replicates (2 rounds of MYTH, 3 technical replicates in first round, 2 technical replicates in second round)

Curated By

• BioGRID