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As shown in Figure 1, pERK immunoreactivity was not restricted to the cell body, but also extended to dendritic and axonal processes.
The signaling pathways of UPR have three well-defined transducers activated upon ER stress, called IRE1 (inositol requiring 1), PERK (PKR-like ER kinase), and ATF6 (activating transcription factor 6), respectively [ 13, 14].
The unfolded protein response (UPR) is induced when the protein folding capacity of the ER is surpassed, triggering the activation of three transmembrane sensors/signal transducers, IRE1 (inositol-requiring enzyme 1), PERK (protein kinase RNA (PKR -like ER kinase), and ATF6 (activating transcriPKR -liketor-6).
Each branch is regulated by a different sensor transmembrane protein, that is, IRE1 (inositol-requiring enzyme 1), PERK (double-stranded RNA-activated Protein kinase (PKR) – like ER Kinase) or ATF6 (Activating Transcription Factor 6) – which senses unfolded protein accumulation and leads to the transcriptional activation of genes involved in the UPR.
α-Solanine treatment caused an increase in the expression of endoplasmic reticulum (ER) stress proteins (BiP, activating transcription factor 6 (ATF6), X-box-binding protein 1, PERK, inositol-requiring transmembrane kinase/endonuclease 1, ATF4 and CCAAT-enhancer-binding protein (C/EBP -homologous protein) suggesting aC/EBP -homologouslded protein resuggestinghwactivation
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Three ER stress transducers can be recognized: IRE1, ATF6 and PERK [15], [18], [19].
Endoplasmic reticulum (ER) stress has been implicated in both pre-eclampsia (PE) and fetal growth restriction (FGR), and is characterised by activation of three signalling branches: 1) PERK-pEIF2α, 2) and6 and 3) splicing of XBP1(U) into XBP1(S).
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Fig. 2 pERK immunohistochemistry on the TG.
The UPR consists of three signaling arms: IRE1, PERK, and ATF6.
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