Selenoprotein S protects against adipocyte death through mediation of the IRE1α-sXBP1 pathway.
Biochem Biophys Res Commun
; 503(4): 2866-2871, 2018 09 18.
Article
en En
| MEDLINE
| ID: mdl-30146262
ABSTRACT
As the most conserved branch of the unfolded protein response (UPR), the inositol-requiring enzyme 1a (IRE1a)/X-box binding protein 1 (XBP1) pathway plays crucial roles in cell survival and cell death by upregulating UPR-associated genes involved in protein entry into the endoplasmic reticulum (ER) and ER-associated degradation (ERAD). Selenoprotein S (SelS) is localized to the ER membrane and involved in ERAD. Although SelS plays an important role in restoring ER stress, the SelS-dependent protective mechanisms against cell death remain unclear. Here, using an inducible SelS knockdown (KD) 3T3-L1 cell model, we showed that SelS KD resulted adipocyte death, which was associated with imbalance of the Bcl-2 family members. Furthermore, SelS KD decreased spliced XBP1 (sXBP1), increased IRE1α and p-JNK, suggesting a role of SelS in the modulation of the IRE1α-sXBP1 pathway. Moreover, adipocyte death induced by SelS suppression can be inhibited by overexpression of sXBP1. Thus, it is proposed that SelS promotes cell survival through the IRE1α-XBP1 signaling pathway.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Muerte Celular
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Proteínas Serina-Treonina Quinasas
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Adipocitos
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Endorribonucleasas
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Selenoproteínas
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Degradación Asociada con el Retículo Endoplásmico
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Proteína 1 de Unión a la X-Box
Límite:
Animals
Idioma:
En
Año:
2018
Tipo del documento:
Article