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CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
CRISPR/Cas9 Mediated Knockout of IFNAR1 and IFNLR1 in A549 Cells./
作者:
Mutetwa, Tinaye.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2019,
面頁冊數:
63 p.
附註:
Source: Masters Abstracts International, Volume: 81-04.
Contained By:
Masters Abstracts International81-04.
標題:
Virology. -
電子資源:
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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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.
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