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. Author manuscript; available in PMC: 2021 Dec 29.
Published in final edited form as: Diabetologia. 2021 Jul 17;64(10):2279–2291. doi: 10.1007/s00125-021-05501-8

Fig. 8.

Fig. 8

Schematic summary of human PrPC cellular localisation, trafficking and interacting partners in beta and alpha cells in non-diabetic, type 1 diabetic and AAb+ human pancreas. (a) A summary of all the results in non-diabetic islets, including: PrPC co-registration with beta cells; PrPC existence in two cellular pools with interaction of PrPC with NCAM1 on the plasma membrane and STI1 in the ER, along with the proposal that PrPC must traffic from the ER to the plasma membrane bypassing transit through the Golgi. For illustration, the unconventional protein trafficking mechanism is depicted using vesicle-mediated transit from the ER to the plasma membrane. (a, c, g) PrPC co-registers with beta cells in non-diabetic, type 1 diabetic INS(+) islets and AAb+ islets, with no co-registration with alpha cells (b, d, h). (e, f) PrPC co-registers with alpha cells in type 1 diabetic INS(−) islets. (g) PrPC is expressed at significantly lower levels in AAb+ beta cells compared with non-diabetic and INS(+) islets (a, c). Note: STI1 and NCAM1 were not measured in AAb+ (g, h). Graphic design created in biorender.com (https://biorender.com)