Dataset Information

Anti-hsp70 pull down CIK cells lysis infected GCRV and MS for identify the proteins

ABSTRACT: HSP70 of grass carp and outer capsid protein VP7 of GCRV determines the early stage of viral entry. Multi-transcriptomic analysis identified HSP70 as a key player in the pathogenesis of GCRV infection. Temperature-dependent, and primarily plasma membrane anchored HSP70 interacts with VP7 to facilitate viral entry during the early phase of GCRV infection. We indentified the interaction of vp7 and hsp70 by MS.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Ctenopharyngodon Idella

TISSUE(S): Kidney

SUBMITTER: guoli hou

LAB HEAD: Guoli Hou

PROVIDER: PXD036008 | Pride | 2023-05-09

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	22042204_SG_HSP70-3_MGFPeaklist.mgf	Mgf
	22042204_SG_HSP70_20220501061050.raw	Raw
	22042204_SG_HSP70_PeptideSummary.txt	Txt
	22042204_SG_HSP70_ProteinSummary.txt	Txt
	Add.22042204.fasta	Fasta

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Project description:The major inducible 70 kDa heat shock protein (hsp70) is host protective in a mouse model of measles virus (MeV) brain infection. Transgenic constitutive expression of hsp70 in neurons, the primary target of MeV infection, abrogates neurovirulence in neonatal H-2d congenic C57BL/6 mice. A significant level of protection is retained after depletion of T lymphocytes, implicating innate immune mechanisms. Focus of the present work was to elucidate the basis for hsp70-dependent innate immunity using this model. Transcriptome analysis of brains from transgenic (TG) and non-transgenic (NT) mice 5 days after infection identified type 1 interferon (IFN) signaling and macrophage activation/antigen presentation as the main differences linked to survival. The pivotal role for type 1 IFN in hsp70-mediated protection was demonstrated in mice with a genetically disrupted type 1 IFN receptor (IFNAR-/-), where IFNAR-/- eliminated the difference in survival between TG and NT mice. Brain macrophages, not neurons, are the predominant source of type 1 IFN in the virus-infected brain, and in vitro studies provided a mechanistic basis by which MeV-infected neurons can induce IFN-β in uninfected microglia in an hsp70-dependent manner. MeV infection induced extracellular release of hsp70 from mouse neuronal cells that constitutively express hsp70, and extracellular hsp70 induced IFN-β transcription in mouse microglial cells through Toll-like receptors 2 and 4. Collectively, results support a novel axis of type 1 IFN-dependent antiviral immunity in the virus-infected brain that is driven by hsp70. Hsp70 expression in mice enhances gene expression related to antiviral immune response against MeV neurovirulence. We performed microarrays on whole brain tissues in mice to obtain an unbiased picture of how hsp70 alters host innate responses to viral infection. Hsp70-overexpressing transgenic (TG) and non-transgenic (NT) mice were infected with MeV intracranially, and total brain mRNA harvested at 5 and 10 days post infection (d.p.i.) was analyzed, sampling the hemisphere opposite the side of viral inoculation. Analysis includes 6 groups: infected TG at 5 d.p.i. (n=4), infected TG at 10 d.p.i. (n=5), infected NT at 5 d.p.i. (n=4), infected NT at 10 d.p.i. (n=5), uninfected TG at 5 d.p.i. (n=4), and uninfected NT at 5 d.p.i. (n=4).

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Anti-hsp70 pull down CIK cells lysis infected GCRV and MS for identify the proteins

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