MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.

The MID1 ubiquitin ligase activates mTOR signaling and regulates mRNA translation. Misregulation of MID1 expression is associated with various diseases including midline malformation syndromes, cancer and neurodegenerative diseases. While this indicates that MID1 expression must be tightly regulated...

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Main Authors: Kristoffer Unterbruner, Frank Matthes, Judith Schilling, Rohit Nalavade, Stephanie Weber, Jennifer Winter, Sybille Krauß
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0190437
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author Kristoffer Unterbruner
Frank Matthes
Judith Schilling
Rohit Nalavade
Stephanie Weber
Jennifer Winter
Sybille Krauß
author_facet Kristoffer Unterbruner
Frank Matthes
Judith Schilling
Rohit Nalavade
Stephanie Weber
Jennifer Winter
Sybille Krauß
author_sort Kristoffer Unterbruner
collection DOAJ
description The MID1 ubiquitin ligase activates mTOR signaling and regulates mRNA translation. Misregulation of MID1 expression is associated with various diseases including midline malformation syndromes, cancer and neurodegenerative diseases. While this indicates that MID1 expression must be tightly regulated to prevent disease states specific mechanisms involved have not been identified. We examined miRNAs to determine mechanisms that regulate MID1 expression. MicroRNAs (miRNA) are small non-coding RNAs that recognize specific sequences in their target mRNAs. Upon binding, miRNAs typically downregulate expression of these targets. Here, we identified four miRNAs, miR-19, miR-340, miR-374 and miR-542 that bind to the 3'-UTR of the MID1 mRNA. These miRNAs not only regulate MID1 expression but also mTOR signaling and translation of disease associated mRNAs and could therefore serve as potential drugs for future therapy development.
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spelling doaj.art-f14f8b1465b44cfe9d2601e0213de0852022-12-21T21:48:37ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-01131e019043710.1371/journal.pone.0190437MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.Kristoffer UnterbrunerFrank MatthesJudith SchillingRohit NalavadeStephanie WeberJennifer WinterSybille KraußThe MID1 ubiquitin ligase activates mTOR signaling and regulates mRNA translation. Misregulation of MID1 expression is associated with various diseases including midline malformation syndromes, cancer and neurodegenerative diseases. While this indicates that MID1 expression must be tightly regulated to prevent disease states specific mechanisms involved have not been identified. We examined miRNAs to determine mechanisms that regulate MID1 expression. MicroRNAs (miRNA) are small non-coding RNAs that recognize specific sequences in their target mRNAs. Upon binding, miRNAs typically downregulate expression of these targets. Here, we identified four miRNAs, miR-19, miR-340, miR-374 and miR-542 that bind to the 3'-UTR of the MID1 mRNA. These miRNAs not only regulate MID1 expression but also mTOR signaling and translation of disease associated mRNAs and could therefore serve as potential drugs for future therapy development.https://doi.org/10.1371/journal.pone.0190437
spellingShingle Kristoffer Unterbruner
Frank Matthes
Judith Schilling
Rohit Nalavade
Stephanie Weber
Jennifer Winter
Sybille Krauß
MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.
PLoS ONE
title MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.
title_full MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.
title_fullStr MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.
title_full_unstemmed MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.
title_short MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.
title_sort micrornas mir 19 mir 340 mir 374 and mir 542 regulate mid1 protein expression
url https://doi.org/10.1371/journal.pone.0190437
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