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Genome-wide analysis of thapsigargin-induced microRNAs and their targets in NIH3T3 cells.


ABSTRACT: Disruption of the endoplasmic reticulum (ER) homeostasis is the cause of ER stress. We performed microRNA (miRNA) analysis (deep sequencing) to search for coping responses (including signaling pathways) induced by disrupted ER Ca(2 +) homeostasis. Our focus was on a specific branch of UPR namely the bi-functional protein kinase/endoribonuclease inositol-requiring element 1? (IRE1?). Activated IRE1? undergoes autophosphorylation and oligomerization, leading to the activation of the endoribonuclease domain and splicing of the mRNA encoding XBP1 specific transcription factor. This processing changes the coding reading frame, producing a potent transcription factor termed XBP1s. We utilized the XBP1 splicing luciferase reporter to screen for modulators of the IRE1? branch of the unfolded protein response (UPR). Here, we describe a detailed experimental design and bioinformatics analysis of ER Ca(2 +) depletion (thapsigargin treated)-induced microRNA (deep sequencing) profile. The data can be access at the Gene Expression Omnibus (GEO), the National Center for Biotechnology Information (NCBI), reference number GSE57138.

SUBMITTER: Groenendyk J 

PROVIDER: S-EPMC4535834 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature

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Genome-wide analysis of thapsigargin-induced microRNAs and their targets in NIH3T3 cells.

Groenendyk Jody J   Fan Xiao X   Peng Zhenling Z   Ilnytskyy Yaroslav Y   Kurgan Lukasz L   Michalak Marek M  

Genomics data 20141007


Disruption of the endoplasmic reticulum (ER) homeostasis is the cause of ER stress. We performed microRNA (miRNA) analysis (deep sequencing) to search for coping responses (including signaling pathways) induced by disrupted ER Ca(2 +) homeostasis. Our focus was on a specific branch of UPR namely the bi-functional protein kinase/endoribonuclease inositol-requiring element 1α (IRE1α). Activated IRE1α undergoes autophosphorylation and oligomerization, leading to the activation of the endoribonuclea  ...[more]

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