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10.18632/aging.100189 77 WangB.HanJ.ElisseeffJ

To elucidate which proteins are susceptible to carbonylation in -cells in T1D settings, we recently mapped over 1000 individual carbonylated proteins in islets from pre-diabetic NOD mice side by side with MIN6 -cells treated with 4-HNE or cytokines ( Table 1 ), including, Sec61 translocon subunit alpha 1 (SEC61A1), ADP ribosylation factor 1 and 3 (ARF1, 3), RAB3 GTPase activating protein catalytic subunit 1 (RAB3GAP1), N ethylmaleimide sensitive factor (NSF), RAB18, member RAS oncogene family (RAB18), Syntaxin binding protein 1 (MUNC18-1), RAB7A, member RAS oncogene family (RAB7A), Syntaxin 5 (STX5), Adaptor related protein complex 2 subunit alpha 2 (AP2A2), Endoplasmic reticulum Golgi intermediate compartment 1 (ERGIC1), Dynamin 1 like (DNM1L), Transmembrane p24 trafficking protein 10 (TMED10), Post GPI attachment to proteins 1 (PGAP1) and JNK interacting protein 4 (JIP4) (182), we observed insulin (INS2) carbonylation upon exposure to 4-HNE (183)

Metastasis mechanisms

It also reduced pro-apoptotic protein Bax and increased Bcl-2 levels, thereby limiting mucosal cell apoptosis and improving overall tissue regeneration