MOESM5 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C
Additional file 5: Figure S5. Loss of APP function results in the exacerbation of DEGs functionally related to antiviral response in Npc1-/-/App-/- mouse cerebella. All differentially expressed genes (DEGs) are localized to their sub-cellular location. All plotted DEGs meet the significance cutoff o...
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creator | Shin, Samuel Shin, Alexandra Mayagoitia, Karina Siebold, Lorraine Rubini, Marsilio Wilson, Christopher Bellinger, Denise Soriano, Salvador |
description | Additional file 5: Figure S5. Loss of APP function results in the exacerbation of DEGs functionally related to antiviral response in Npc1-/-/App-/- mouse cerebella. All differentially expressed genes (DEGs) are localized to their sub-cellular location. All plotted DEGs meet the significance cutoff of fold-change (absolute FC > 1.5) and p-value (p < 0.05). *Duplicate identifiers used for the same gene. A detailed key for IPA molecular shape, color, and interaction is provided in Fig. 2. |
doi_str_mv | 10.6084/m9.figshare.11393514 |
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Loss of APP function results in the exacerbation of DEGs functionally related to antiviral response in Npc1-/-/App-/- mouse cerebella. All differentially expressed genes (DEGs) are localized to their sub-cellular location. All plotted DEGs meet the significance cutoff of fold-change (absolute FC > 1.5) and p-value (p < 0.05). *Duplicate identifiers used for the same gene. A detailed key for IPA molecular shape, color, and interaction is provided in Fig. 2.</description><identifier>DOI: 10.6084/m9.figshare.11393514</identifier><language>eng</language><publisher>figshare</publisher><subject>Biochemistry ; Biophysics ; Cell Biology ; Developmental Biology ; FOS: Biological sciences ; FOS: Health sciences ; Genetics ; Infectious Diseases ; Medicine ; Mental Health ; Molecular Biology ; Neuroscience ; Physiology</subject><creationdate>2019</creationdate><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>780,1894</link.rule.ids><linktorsrc>$$Uhttps://commons.datacite.org/doi.org/10.6084/m9.figshare.11393514$$EView_record_in_DataCite.org$$FView_record_in_$$GDataCite.org$$Hfree_for_read</linktorsrc></links><search><creatorcontrib>Shin, Samuel</creatorcontrib><creatorcontrib>Shin, Alexandra</creatorcontrib><creatorcontrib>Mayagoitia, Karina</creatorcontrib><creatorcontrib>Siebold, Lorraine</creatorcontrib><creatorcontrib>Rubini, Marsilio</creatorcontrib><creatorcontrib>Wilson, Christopher</creatorcontrib><creatorcontrib>Bellinger, Denise</creatorcontrib><creatorcontrib>Soriano, Salvador</creatorcontrib><title>MOESM5 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C</title><description>Additional file 5: Figure S5. Loss of APP function results in the exacerbation of DEGs functionally related to antiviral response in Npc1-/-/App-/- mouse cerebella. All differentially expressed genes (DEGs) are localized to their sub-cellular location. All plotted DEGs meet the significance cutoff of fold-change (absolute FC > 1.5) and p-value (p < 0.05). *Duplicate identifiers used for the same gene. A detailed key for IPA molecular shape, color, and interaction is provided in Fig. 2.</description><subject>Biochemistry</subject><subject>Biophysics</subject><subject>Cell Biology</subject><subject>Developmental Biology</subject><subject>FOS: Biological sciences</subject><subject>FOS: Health sciences</subject><subject>Genetics</subject><subject>Infectious Diseases</subject><subject>Medicine</subject><subject>Mental Health</subject><subject>Molecular Biology</subject><subject>Neuroscience</subject><subject>Physiology</subject><fulltext>true</fulltext><rsrctype>image</rsrctype><creationdate>2019</creationdate><recordtype>image</recordtype><sourceid>PQ8</sourceid><recordid>eNqdjk0KwjAQRrNxIeoNXMwFWhvail2L4sI_0H0Y26kONklJItjba8FewNX7vsWDJ8RcJvEyWWULXcQ13_0DHcVSpkWay2ws-HDaXA452Br21vueqLvGcgWto_LlvHXfZQOxAXpjSe6GgTwQuqYDNnWDWmNga74HjkwajYnOXD6hYk_oCULXEqynYlRj42n240Rk2811vYsqDFhyINU61ug6JRPVFytdqKFYDcXpn9oHAT1VMQ</recordid><startdate>20191218</startdate><enddate>20191218</enddate><creator>Shin, Samuel</creator><creator>Shin, Alexandra</creator><creator>Mayagoitia, Karina</creator><creator>Siebold, Lorraine</creator><creator>Rubini, Marsilio</creator><creator>Wilson, Christopher</creator><creator>Bellinger, Denise</creator><creator>Soriano, Salvador</creator><general>figshare</general><scope>DYCCY</scope><scope>PQ8</scope></search><sort><creationdate>20191218</creationdate><title>MOESM5 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C</title><author>Shin, Samuel ; Shin, Alexandra ; Mayagoitia, Karina ; Siebold, Lorraine ; Rubini, Marsilio ; Wilson, Christopher ; Bellinger, Denise ; Soriano, Salvador</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-datacite_primary_10_6084_m9_figshare_113935143</frbrgroupid><rsrctype>images</rsrctype><prefilter>images</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Biochemistry</topic><topic>Biophysics</topic><topic>Cell Biology</topic><topic>Developmental Biology</topic><topic>FOS: Biological sciences</topic><topic>FOS: Health sciences</topic><topic>Genetics</topic><topic>Infectious Diseases</topic><topic>Medicine</topic><topic>Mental Health</topic><topic>Molecular Biology</topic><topic>Neuroscience</topic><topic>Physiology</topic><toplevel>online_resources</toplevel><creatorcontrib>Shin, Samuel</creatorcontrib><creatorcontrib>Shin, Alexandra</creatorcontrib><creatorcontrib>Mayagoitia, Karina</creatorcontrib><creatorcontrib>Siebold, Lorraine</creatorcontrib><creatorcontrib>Rubini, Marsilio</creatorcontrib><creatorcontrib>Wilson, Christopher</creatorcontrib><creatorcontrib>Bellinger, Denise</creatorcontrib><creatorcontrib>Soriano, Salvador</creatorcontrib><collection>DataCite (Open Access)</collection><collection>DataCite</collection></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Shin, Samuel</au><au>Shin, Alexandra</au><au>Mayagoitia, Karina</au><au>Siebold, Lorraine</au><au>Rubini, Marsilio</au><au>Wilson, Christopher</au><au>Bellinger, Denise</au><au>Soriano, Salvador</au><format>book</format><genre>unknown</genre><ristype>GEN</ristype><title>MOESM5 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C</title><date>2019-12-18</date><risdate>2019</risdate><abstract>Additional file 5: Figure S5. Loss of APP function results in the exacerbation of DEGs functionally related to antiviral response in Npc1-/-/App-/- mouse cerebella. All differentially expressed genes (DEGs) are localized to their sub-cellular location. All plotted DEGs meet the significance cutoff of fold-change (absolute FC > 1.5) and p-value (p < 0.05). *Duplicate identifiers used for the same gene. A detailed key for IPA molecular shape, color, and interaction is provided in Fig. 2.</abstract><pub>figshare</pub><doi>10.6084/m9.figshare.11393514</doi><oa>free_for_read</oa></addata></record> |
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subjects | Biochemistry Biophysics Cell Biology Developmental Biology FOS: Biological sciences FOS: Health sciences Genetics Infectious Diseases Medicine Mental Health Molecular Biology Neuroscience Physiology |
title | MOESM5 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C |
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