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Hnrnpab Regulates Neural Cell Motili...

Lampasona, Alexa Ariel.

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Hnrnpab Regulates Neural Cell Motility through Transcription of Eps8.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Hnrnpab Regulates Neural Cell Motility through Transcription of Eps8./
作者:	Lampasona, Alexa Ariel.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	157 p.
附註:	Source: Dissertations Abstracts International, Volume: 80-06, Section: B.
Contained By:	Dissertations Abstracts International80-06B.
標題:	Molecular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10844934
ISBN:	9780438751972

Hnrnpab Regulates Neural Cell Motility through Transcription of Eps8.
Lampasona, Alexa Ariel.

Hnrnpab Regulates Neural Cell Motility through Transcription of Eps8. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 157 p.

Source: Dissertations Abstracts International, Volume: 80-06, Section: B.

Thesis (Ph.D.)--State University of New York at Stony Brook, 2018.

This item is not available from ProQuest Dissertations & Theses.

Cell migration requires a complicated network of structural and regulatory proteins. Changes in cellular motility can impact migration as a result of cell-type or developmental stage regulated expression of critical motility genes. Hnrnpab is a conserved RNA binding protein found as two isoforms produced by alternative splicing. Its expression is enriched in the subventricular zone (SVZ) and the rostral migratory stream within the brain, suggesting possible support of the migration of neural progenitor cells in this region. Here I show the migration of cells from the SVZ of developing Hnrnpab-/- mouse brains is impaired. An RNA-seq analysis to identify Hnrnpab dependent cell motility genes led me to Eps8, and in agreement with the change in cell motility, I demonstrate that Eps8 is decreased in Hnrnpab-/- SVZ tissue. I scrutinized the motility of Hnrnpab-/- cells and confirmed that the decreases in both cell motility and Eps8 are restored by ectopically co-expressing both alternatively spliced Hnrnpab isoforms, therefore these variants are surprisingly non-redundant for cell motility. My results support a model where both Hnrnpab isoforms work in concert to regulate Eps8 transcription in the mouse SVZ to promote the normal migration of neural cells during CNS development.

ISBN: 9780438751972Subjects--Topical Terms:

517296
Molecular biology.
Subjects--Index Terms:

Cell motility

Hnrnpab Regulates Neural Cell Motility through Transcription of Eps8.
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500 $a Publisher info.: Dissertation/Thesis.
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506 $a This item is not available from ProQuest Dissertations & Theses.
506 $a This item must not be sold to any third party vendors.
520 $a Cell migration requires a complicated network of structural and regulatory proteins. Changes in cellular motility can impact migration as a result of cell-type or developmental stage regulated expression of critical motility genes. Hnrnpab is a conserved RNA binding protein found as two isoforms produced by alternative splicing. Its expression is enriched in the subventricular zone (SVZ) and the rostral migratory stream within the brain, suggesting possible support of the migration of neural progenitor cells in this region. Here I show the migration of cells from the SVZ of developing Hnrnpab-/- mouse brains is impaired. An RNA-seq analysis to identify Hnrnpab dependent cell motility genes led me to Eps8, and in agreement with the change in cell motility, I demonstrate that Eps8 is decreased in Hnrnpab-/- SVZ tissue. I scrutinized the motility of Hnrnpab-/- cells and confirmed that the decreases in both cell motility and Eps8 are restored by ectopically co-expressing both alternatively spliced Hnrnpab isoforms, therefore these variants are surprisingly non-redundant for cell motility. My results support a model where both Hnrnpab isoforms work in concert to regulate Eps8 transcription in the mouse SVZ to promote the normal migration of neural cells during CNS development.
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