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TorsinA Expression in Budding Yeast ...

Chalfant, Madeleine Carol.

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TorsinA Expression in Budding Yeast Points to Missing LINC in DYT1 Dystonia Pathogenesis.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	TorsinA Expression in Budding Yeast Points to Missing LINC in DYT1 Dystonia Pathogenesis./
作者:	Chalfant, Madeleine Carol.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
面頁冊數:	134 p.
附註:	Source: Dissertations Abstracts International, Volume: 81-10, Section: B.
Contained By:	Dissertations Abstracts International81-10B.
標題:	Cellular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=13810091
ISBN:	9781658491723

TorsinA Expression in Budding Yeast Points to Missing LINC in DYT1 Dystonia Pathogenesis.
Chalfant, Madeleine Carol.

TorsinA Expression in Budding Yeast Points to Missing LINC in DYT1 Dystonia Pathogenesis. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 134 p.

Source: Dissertations Abstracts International, Volume: 81-10, Section: B.

Thesis (Ph.D.)--Yale University, 2019.

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

DYT1 dystonia, a debilitating neuro-muscular disorder with few treatment options, is caused by an in-frame deletion of a single amino acid in the gene encoding the AAA+ ATPase TorsinA. TorsinA localizes to the contiguous endoplasmic reticulum / nuclear envelope lumen and can only hydrolyze ATP after binding one of its two transmembrane activating partners, LAP1 or LULL1. TorsinA function is unknown, as its substrate is elusive. However, recent work suggests TorsinA likely participates in complex and poorly understood nuclear envelope remodeling events. Because the complexity of TorsinA's native cellular environment complicates experimental analysis, I assessed TorsinA function in the similar yet significantly simpler cellular environment of budding yeast. While yeast lack TorsinA, LAP1, and LULL1 homologs, yeast cellular machinery can interact with non-conserved human proteins and provide insight into cellular function. Here, I identified relationships between TorA and two yeast nuclear envelope proteins with structurally similar orthologs in mammalian cells. My results point to a putative TorsinA substrate and suggest strategies to interrogate TorA dysfunction in the future.

ISBN: 9781658491723Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Gene encoding

TorsinA Expression in Budding Yeast Points to Missing LINC in DYT1 Dystonia Pathogenesis.
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500 $a Source: Dissertations Abstracts International, Volume: 81-10, Section: B.
500 $a Advisor: Lusk, Patrick.
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506 $a This item must not be sold to any third party vendors.
506 $a This item must not be added to any third party search indexes.
520 $a DYT1 dystonia, a debilitating neuro-muscular disorder with few treatment options, is caused by an in-frame deletion of a single amino acid in the gene encoding the AAA+ ATPase TorsinA. TorsinA localizes to the contiguous endoplasmic reticulum / nuclear envelope lumen and can only hydrolyze ATP after binding one of its two transmembrane activating partners, LAP1 or LULL1. TorsinA function is unknown, as its substrate is elusive. However, recent work suggests TorsinA likely participates in complex and poorly understood nuclear envelope remodeling events. Because the complexity of TorsinA's native cellular environment complicates experimental analysis, I assessed TorsinA function in the similar yet significantly simpler cellular environment of budding yeast. While yeast lack TorsinA, LAP1, and LULL1 homologs, yeast cellular machinery can interact with non-conserved human proteins and provide insight into cellular function. Here, I identified relationships between TorA and two yeast nuclear envelope proteins with structurally similar orthologs in mammalian cells. My results point to a putative TorsinA substrate and suggest strategies to interrogate TorA dysfunction in the future.
590 $a School code: 0265.
650 4 $a Cellular biology. $3 3172791
650 4 $a Pathology. $3 643180
653 $a Gene encoding
653 $a TorsinA
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