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您的检索式：作者名="Zhekai Lin"
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| 1 | Vagal-mAChR4 signaling promotes Friend virus complex(FV)-induced acute erythroleukemia显示文摘Erythroleukemia belongs to acute myeloid leukemia(AML)type 6(M6),and treatment remains difficult due to the poor prognosis of the disease.Friend virus(FV)is a complex of two viruses:Friend murine leukemia virus(F-MuLV)strain along with a defective spleen focus-forming virus(SFFV),which can induce acute eryth-roleukemia in mice.We have previously reported that activation of vagalα7 nicotinic acetylcholine receptor(nAChR)signaling promotes HIV-1 transcription.Whether vagal muscarinic signaling mediates FV-induced erythroleukemia and the underlying mechanisms remain unclear.In this study,sham and vagotomized mice were intraperitoneally injected with FV.FV infection caused anemia in sham mice,and vagotomy reversed this change.FV infection increased erythroblasts ProE,EryA,and EryB cells in the spleen,and these changes were blocked by vagotomy.In bone marrow,FV infection reduced EryC cells in sham mice,an effect that was coun-teracted by vagotomy.FV infection increased choline acetyltransferase(ChAT)expression in splenic CD4^(+)and CD8þT cells,and this change was reversed by vagotomy.Furthermore,the increase of EryA and EryB cells in spleen of FV-infected wild-type mice was reversed after deletion of ChAT in CD4^(+)T cells.In bone marrow,FV infection reduced EryB and EryC cells in sham mice,whereas lack of ChAT in CD4^(+)T cells did not affect this change.Activation of muscarinic acetylcholine receptor 4(mAChR4)by clozapine N-oxide(CNO)significantly increased EryB in the spleen but decreased the EryC cell population in the bone marrow of FV-infected mice.Thus,vagal-mAChR4 signaling in the spleen and bone marrow synergistically promotes the pathogenesis of acute erythroleukemia.We uncover an unrecognized mechanism of neuromodulation in erythroleukemia. | Shuting Song Zhekai Lin Caiqi Zhao Jing Wen Jie Chen Shitao Xie Huaxin Qi Jianhua Wang Xiao Su | 2023 | Virologica Sinica2023，38，3： | 0 |
| 2 | Cytoskeleton-a crucial key in host cell for coronavirus infection显示文摘The emerging coronavirus(CoV)pandemic is threatening the public health all over the world.Cytoskeleton is an intricate network involved in controlling cell shape,cargo transport,signal transduction,and cell division.Infection biology studies have illuminated essential roles for cytoskeleton in mediating the outcome of host-virus interactions.In this review,we discuss the dynamic interactions between actin filaments,microtubules,intermediate filaments,and CoVs.In one round of viral life cycle,CoVs surf along filopodia on the host membrane to the entry sites,utilize specific intermediate filament protein as co-receptor to enter target cells,hijack microtubules for transportation to replication and assembly sites,and promote actin filaments polymerization to provide forces for egress.During CoV infection,disruption of host cytoskeleton homeostasis and modification state is tightly connected to pathological processes,such as defective cytokinesis,demyelinating,cilia loss,and neuron necrosis.There are increasing mechanistic studies on cytoskeleton upon CoV infection,such as viral protein-cytoskeleton interaction,changes in the expression and post-translation modification,related signaling pathways,and incorporation with other host factors.Collectively,these insights provide new concepts for fundamental virology and the control of CoV infection. | Zeyu Wen Yue Zhang Zhekai Lin Kun Shi Yarning jiu | 2020 | Journal of Molecular Cell Biology2020，12，12： | 0 |
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