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HGNC Genes

SARS-CoV-2 proteins

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    FYN HGNC, SARS-CoV-2, and IFITM3 HGNC in the Neurobiology of Alzheimer’s Disease MESHD: A Regulatory Feedback Loop Governing Tau and Aβ Pathology

    Authors: George Vavougios; Marianthi Breza; Theodore Mavridis; Karen Krogfelt

    id:202012.0739/v2 Date: 2021-02-02 Source: Preprints.org

    Introduction: IFITM3 HGNC, an innate immune protein linked to COVID-19 MESHD severity, has recently been identified as a novel γ-secretase modulator. Independent research has shown that IFITM3 HGNC may facilitate SARS-CoV-2 neurotropism MESHD in an ACE2 HGNC-independent manner. In a previous study, we had detected perturbations in IFITM3 HGNC networks in both the CNS and peripheral immune cells donated by AD MESHD patients. The purpose of this study is to explore the transcriptomic evidence of the SARS-CoV-2 / IFITM3 HGNC / AD interplay, validating previous findings from our group. Methods: Exploratory analyses involved meta-analysis of bulk and single cell RNA data for IFITM3 HGNC and FYN HGNC differential expression. For confirmatory analyses, we performed gene set enrichment analysis (GSEA) on an AD gene signature from AD Consensus transcriptomics; using the Enrichr platform, we scrutinized COVID-19 MESHD datasets for significant, overlapping enriched biological networks. Results: Bulk RNA data analysis revealed that IFITM3 HGNC and FYN HGNC were differentially expressed in two CNS regions in AD MESHD: the temporal cortex ( AD MESHD vs. Controls, adj.p-value=1.3e-6) and the parahippocampal cortex ( AD MESHD vs. controls, adj.p-value=0.012). Correspondingly, single cell RNA analysis of IFITM3 HGNC and FYN HGNC revealed that it was differentially expressed in neuronal cells donated from AD MESHD patients (astrocytes, microglia and oligodendrocyte precursor cells), when compared to controls. Discussion: IFITM3 HGNC and by extent FYN HGNC were found as interactors within biological networks overlapping between AD MESHD and SARS-CoV-2 infection MESHD. SARS-CoV-2-mediated FYN HGNC/ IFITM3 HGNC induction would mechanistically result in increased Tau fibrilization and Aβ oligomerization. FYN HGNC recruitment by viral processes results in abrogation of both fusion of IFITM3 HGNC vesicles with lysosomes; immunoevasion, by FYN HGNC-mediated impairment of autophagy would then serve to promote impaired detoxification from Aβ, while propagating Tau pathology in an IFITM3 HGNC-independent manner.

    FYN HGNC, SARS-CoV-2, and IFITM3 HGNC in the Neurobiology of Alzheimer’s Disease MESHD: A Regulatory Feedback Loop Governing Tau and Aβ Pathology

    Authors: George Vavougios; Marianthi Breza; Sofia Nikou; Karen Krogfelt

    id:10.20944/preprints202012.0739.v1 Date: 2020-12-29 Source: Preprints.org

    Introduction IFITM3 HGNC, an innate immune protein linked to COVID-19 MESHD severity, has recently been identified as a novel γ-secretase modulator. Independent research has shown that IFITM3 HGNC may facilitate SARS-CoV-2 neurotropism MESHD in an ACE2 HGNC-independent manner. In a previous study, we had detected perturbations in IFITM3 HGNC networks in both the CNS and peripheral immune cells donated by AD MESHD patients.The purpose of this study is to explore the transcriptomic evidence of the SARS-CoV-2 / IFITM3 HGNC / AD interplay, validating previous findings from our group. Methods Exploratory analyses involved meta-analysis of bulk and single cell RNA data for IFITM3 HGNC and FYN HGNC differential expression. For confirmatory analyses, we performed gene set enrichment analysis (GSEA) on an AD gene signature from AD Consensus transcriptomics; using the Enrichr platform, we scrutinized COVID-19 MESHD datasets for significant, overlapping enriched biological networks. Results Bulk RNA data analysis revealed that IFITM3 HGNC and FYN HGNC were differentially expressed in two CNS regions in AD MESHD: the temporal cortex ( AD MESHD vs. Controls, adj.p-value=1.3e-6) and the parahippocampal cortex ( AD MESHD vs. controls, adj.p-value=0.012). Correspondingly, single cell RNA analysis of IFITM3 HGNC and FYN HGNC revealed that it was differentially expressed in neuronal cells donated from AD MESHD patients (astrocytes, microglia and oligodendrocyte precursor cells), when compared to controls. Discussion IFITM3 HGNC and by extent FYN HGNC were found as interactors within biological networks overlapping between AD MESHD and SARS-CoV-2 infection MESHD. SARS-CoV-2 SARS-CoV-2-mediated IFITM3 HGNC induction would mechanistically result in increased Aβ production. FYN HGNC recruitment by viral processes results in abrogation of both fusion of IFITM3 HGNC vesicles with lysosomes; immunoevasion, by FYN HGNC-mediated impairment of autophagy would then serve to promote impaired detoxification from Aβ, while propagating Tau pathology in an IFITM3 HGNC-independent manner.

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MeSH Disease
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SARS-CoV-2 Proteins


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