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CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells.

Record Type:	Electronic resources : Monograph/item
Title/Author:	CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells./
Author:	Mutetwa, Tinaye.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
Description:	63 p.
Notes:	Source: Masters Abstracts International, Volume: 81-04.
Contained By:	Masters Abstracts International81-04.
Subject:	Virology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=22622173
ISBN:	9781687924711

CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells.
Mutetwa, Tinaye.

CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 63 p.

Source: Masters Abstracts International, Volume: 81-04.

Thesis (M.S.)--Icahn School of Medicine at Mount Sinai, 2019.

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

Type I and Type III interferon (IFN) play pivotal roles in the modulation of host innate immune response. In addition to providing direct defenses, they also prime uninfected neighboring cells for possible infection. Upon influenza A virus (IAV) infection, a multifunctional nonstructural protein (NS1) is especially adept at antagonizing host innate immune responses mediated by interferons. The determinant of viral success is therefore modulated by an interplay between interferons and viral defenses. To study the contribution of IFN to early innate immune response of epithelial cells after IAV infection, we developed CRISPR/Cas9 mediated type I or type III IFN receptor knockout cell lines from human A549 epithelial cells. Validation of successful knockouts was conducted using IFN receptor functional analysis, quantitative Sanger sequence analysis, and expression profiles of interferon stimulated genes (ISGs). Type I IFN receptor knockout cells seem to play a more prominent role in inducing type III interferon.

ISBN: 9781687924711Subjects--Topical Terms:

642304
Virology.
Subjects--Index Terms:

CRISPR/Cas9

CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells.
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245 1 0 $a CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2019
300 $a 63 p.
500 $a Source: Masters Abstracts International, Volume: 81-04.
500 $a Advisor: Fernandez-Sesma, Ana;Ramos-Lopez, Irene.
502 $a Thesis (M.S.)--Icahn School of Medicine at Mount Sinai, 2019.
506 $a This item must not be sold to any third party vendors.
520 $a Type I and Type III interferon (IFN) play pivotal roles in the modulation of host innate immune response. In addition to providing direct defenses, they also prime uninfected neighboring cells for possible infection. Upon influenza A virus (IAV) infection, a multifunctional nonstructural protein (NS1) is especially adept at antagonizing host innate immune responses mediated by interferons. The determinant of viral success is therefore modulated by an interplay between interferons and viral defenses. To study the contribution of IFN to early innate immune response of epithelial cells after IAV infection, we developed CRISPR/Cas9 mediated type I or type III IFN receptor knockout cell lines from human A549 epithelial cells. Validation of successful knockouts was conducted using IFN receptor functional analysis, quantitative Sanger sequence analysis, and expression profiles of interferon stimulated genes (ISGs). Type I IFN receptor knockout cells seem to play a more prominent role in inducing type III interferon.
590 $a School code: 1734.
650 4 $a Virology. $3 642304
650 4 $a Microbiology. $3 536250
650 4 $a Immunology. $3 611031
653 $a CRISPR/Cas9
653 $a IFNAR1
653 $a IFNLR1
653 $a Influenza A virus
653 $a Interferon
653 $a Type III interferon
690 $a 0720
690 $a 0410
690 $a 0982
710 2 $a Icahn School of Medicine at Mount Sinai. $b Microbiology. $3 3194085
773 0 $t Masters Abstracts International $g 81-04.
790 $a 1734
791 $a M.S.
792 $a 2019
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=22622173