MOESM12 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C
Additional file 12: Figure S12. Activation of APC-associated co-stimulatory molecules is implicated in Npc1-/-/App-/- mouse cerebella. In Npc1-/-/App-/- mouse cerebella, 32 genes related to CD40, 12 genes related to ICAM1, and 6 genes related to CD86 were differentially expressed when compared with...
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creator | Shin, Samuel Shin, Alexandra Mayagoitia, Karina Siebold, Lorraine Rubini, Marsilio Wilson, Christopher Bellinger, Denise Soriano, Salvador |
description | Additional file 12: Figure S12. Activation of APC-associated co-stimulatory molecules is implicated in Npc1-/-/App-/- mouse cerebella. In Npc1-/-/App-/- mouse cerebella, 32 genes related to CD40, 12 genes related to ICAM1, and 6 genes related to CD86 were differentially expressed when compared with wildtype littermates (Npc1+/+/App+/+). 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. 4. |
doi_str_mv | 10.6084/m9.figshare.11393469 |
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Activation of APC-associated co-stimulatory molecules is implicated in Npc1-/-/App-/- mouse cerebella. In Npc1-/-/App-/- mouse cerebella, 32 genes related to CD40, 12 genes related to ICAM1, and 6 genes related to CD86 were differentially expressed when compared with wildtype littermates (Npc1+/+/App+/+). 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. 4.</description><identifier>DOI: 10.6084/m9.figshare.11393469</identifier><language>eng</language><publisher>figshare</publisher><subject>Biochemistry ; Cell Biology ; Developmental Biology ; FOS: Biological sciences ; FOS: Clinical medicine ; Genetics ; Immunology ; 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.11393469$$EView_record_in_DataCite.org$$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>MOESM12 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C</title><description>Additional file 12: Figure S12. Activation of APC-associated co-stimulatory molecules is implicated in Npc1-/-/App-/- mouse cerebella. In Npc1-/-/App-/- mouse cerebella, 32 genes related to CD40, 12 genes related to ICAM1, and 6 genes related to CD86 were differentially expressed when compared with wildtype littermates (Npc1+/+/App+/+). 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. 4.</description><subject>Biochemistry</subject><subject>Cell Biology</subject><subject>Developmental Biology</subject><subject>FOS: Biological sciences</subject><subject>FOS: Clinical medicine</subject><subject>Genetics</subject><subject>Immunology</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>eNqdjk0KwjAQRrNxIeoNXMwFWhtbil0XxYV_oPswtlMdbZKSRLC3V0Ev4Op93-LBE2IqkzhPFtlMF3HDF39FR7GUaZFmeTEUt-1-edzKOdgGNtb7D1H3reUaOkfVw3nr3ssGYgP0xIrcGQN5IHRtD2yaFrXGwNa8D-yYNBoTHbi6Q82e0BOEviMox2LQYOtp8uVIZKvlqVxHNQasOJDqHGt0vZKJ-iQrXahfsvolp39qLz7hVXs</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>MOESM12 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_113934693</frbrgroupid><rsrctype>images</rsrctype><prefilter>images</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Biochemistry</topic><topic>Cell Biology</topic><topic>Developmental Biology</topic><topic>FOS: Biological sciences</topic><topic>FOS: Clinical medicine</topic><topic>Genetics</topic><topic>Immunology</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>MOESM12 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 12: Figure S12. Activation of APC-associated co-stimulatory molecules is implicated in Npc1-/-/App-/- mouse cerebella. In Npc1-/-/App-/- mouse cerebella, 32 genes related to CD40, 12 genes related to ICAM1, and 6 genes related to CD86 were differentially expressed when compared with wildtype littermates (Npc1+/+/App+/+). 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. 4.</abstract><pub>figshare</pub><doi>10.6084/m9.figshare.11393469</doi><oa>free_for_read</oa></addata></record> |
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subjects | Biochemistry Cell Biology Developmental Biology FOS: Biological sciences FOS: Clinical medicine Genetics Immunology Molecular Biology Neuroscience Physiology |
title | MOESM12 of Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C |
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