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LC-MS of rabies virus glycoproteins in human cells

ABSTRACT: Rabies virus (RABV), causes a fatal encephalitis disease contributing to an estimated annual death toll of 40 000–70 000 people worldwide. Without effective therapeutic treatment, RABV has a mortality rate approaching 100%. However, it remains unclear how RABV hijack cellular factors to subvert antiviral defenses and enable virus replication. As interactions with these proteins are critical for viral infection and pathogenesis, small molecules or biologics therapies targeting these interfaces may serve as potential antiviral agents. In this study, to better understand how RABV G protein rewire the host cell, we generated a different strains RABV G proteins-human protein interaction map.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human) Lyssavirus Rabies

TISSUE(S): Epithelial Cell, Cell Culture

SUBMITTER: Yuelan zhang

LAB HEAD: Bishi Fu

PROVIDER: PXD046741 | Pride | 2025-08-25

REPOSITORIES: Pride

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			Action	DRS
	73359_B19_G_1.raw	Raw
	73427_B19_G_2.raw	Raw
	73448_Nishi_G_2.raw	Raw
	73694_Nishi_G_1.raw	Raw
	74783_B19_G_G_1.raw	Raw

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Publications

AP3B1 facilitates PDIA3/ERP57 function to regulate rabies virus glycoprotein selective degradation and viral entry.

Zhang Yuelan Y Zhang Xinyi X Yang Xue X Lv Linyue L Wang Qinyang Q Zeng Shaowei S Zhang Zhuyou Z Dorf Martin M Li Shitao S Zhao Ling L Fu Bishi B

Autophagy 20240817 12

Rabies virus causes an estimated 59,000 annual fatalities worldwide and promising therapeutic treatments are necessary to develop. In this study, affinity tag-purification mass spectrometry was employed to delineate RABV glycoprotein and host protein interactions, and PDIA3/ERP57 was identified as a potential inhibitor of RABV infection. PDIA3 restricted RABV infection with follow mechanisms: PDIA3 mediated the degradation of RABV G protein by targeting lysine 332 via the selective macroautophag ...[more]

PMID: 39128851

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Project description:Rabies, caused by the rabies virus (RABV), is the oldest known zoonotic infectious disease. Although the molecular mechanisms of RABV pathogenesis have been investigated extensively, the interactions between host and RABV are not clearly understood. It is now known that long non-coding RNAs (lncRNAs) participate in various physiological and pathological processes, but their possible roles in the host response to RABV infection remain to be elucidated. To better understand the pathogenesis of RABV, RNAs from RABV-infected and uninfected human neuroblastoma cells (SK-N-SH) were analyzed using human lncRNA microarrays. We identified 896 lncRNAs and 579 mRNAs that were differentially expressed after infection, indicating a potential role for lncRNAs in the immune response to RABV. Differentially expressed RNAs were examined using Gene Ontology (GO) analysis and were tentatively assigned to biological pathways using the Kyoto Encyclopedia of Genes and Genomes (KEGG). A lncRNA-mRNA-transcription factor co-expression network was constructed to relate lncRNAs to regulatory factors and pathways that may be important in virus-host interactions. The network analysis suggests that E2F4, TAF7 and several lncRNAs function as transcriptional regulators in various signaling pathways. This study is the first global analysis of lncRNA and mRNA co-expression during RABV infection, provides deeper insight into the mechanism of RABV pathogenesis, and reveals promising candidate for future investigation.

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