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Iron-Sulfur Cluster Deficiency Can Be Sensed by IRP2 and Regulates Iron Homeostasis and Sensitivity to Ferroptosis Independent of IRP1 and FBXL5.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Iron-Sulfur Cluster Deficiency Can Be Sensed by IRP2 and Regulates Iron Homeostasis and Sensitivity to Ferroptosis Independent of IRP1 and FBXL5./
Author:	Terzi, Erdem M.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
Description:	123 p.
Notes:	Source: Dissertations Abstracts International, Volume: 83-06, Section: B.
Contained By:	Dissertations Abstracts International83-06B.
Subject:	Cellular biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28546573
ISBN:	9798496508414

Iron-Sulfur Cluster Deficiency Can Be Sensed by IRP2 and Regulates Iron Homeostasis and Sensitivity to Ferroptosis Independent of IRP1 and FBXL5.
Terzi, Erdem M.

Iron-Sulfur Cluster Deficiency Can Be Sensed by IRP2 and Regulates Iron Homeostasis and Sensitivity to Ferroptosis Independent of IRP1 and FBXL5. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 123 p.

Source: Dissertations Abstracts International, Volume: 83-06, Section: B.

Thesis (Ph.D.)--New York University, 2021.

This item must not be sold to any third party vendors.

Intracellular iron levels are strictly regulated to support homeostasis and avoid iron-mediated ROS production. Loss of iron-sulfur cluster (ISC) synthesis can increase iron loading and promote cell death by ferroptosis. Iron-responsive element-binding proteins IRP1 and IRP2 post-transcriptionally regulate iron homeostasis. IRP1 binding to target mRNAs is competitively regulated by ISC occupancy. However, IRP2 is principally thought to be regulated at the protein level via E3 ubiquitin ligase FBXL5 mediated degradation. Here, we show that ISC synthesis suppression can activate IRP2 and promote ferroptosis sensitivity via a novel mechanism. At tissue-level O2 concentrations, ISC deficiency enhances IRP2 binding to target mRNAs independent of IRP1, FBXL5, and changes in IRP2 protein level. Deletion of both IRP1 and IRP2 abolishes the iron starvation response and blocks its activation by ISC synthesis inhibition. These findings will inform strategies to manipulate ferroptosis sensitivity and help illuminate the mechanism underlying ISC biosynthesis disorders, such as Friedreich's Ataxia.

ISBN: 9798496508414Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Ferroptosis

Iron-Sulfur Cluster Deficiency Can Be Sensed by IRP2 and Regulates Iron Homeostasis and Sensitivity to Ferroptosis Independent of IRP1 and FBXL5.
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506 $a This item must not be sold to any third party vendors.
520 $a Intracellular iron levels are strictly regulated to support homeostasis and avoid iron-mediated ROS production. Loss of iron-sulfur cluster (ISC) synthesis can increase iron loading and promote cell death by ferroptosis. Iron-responsive element-binding proteins IRP1 and IRP2 post-transcriptionally regulate iron homeostasis. IRP1 binding to target mRNAs is competitively regulated by ISC occupancy. However, IRP2 is principally thought to be regulated at the protein level via E3 ubiquitin ligase FBXL5 mediated degradation. Here, we show that ISC synthesis suppression can activate IRP2 and promote ferroptosis sensitivity via a novel mechanism. At tissue-level O2 concentrations, ISC deficiency enhances IRP2 binding to target mRNAs independent of IRP1, FBXL5, and changes in IRP2 protein level. Deletion of both IRP1 and IRP2 abolishes the iron starvation response and blocks its activation by ISC synthesis inhibition. These findings will inform strategies to manipulate ferroptosis sensitivity and help illuminate the mechanism underlying ISC biosynthesis disorders, such as Friedreich's Ataxia.
590 $a School code: 0146.
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653 $a Ferroptosis
653 $a Iron metabolism
653 $a Iron-sulfur cluster
653 $a IRP2
690 $a 0379
710 2 $a New York University. $b Basic Medical Science. $3 1683852
773 0 $t Dissertations Abstracts International $g 83-06B.
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