Studies of herpes simplex virus type 1 （HSV-1） infection have shown that many known and unknown cellular molecules in- volved in viral proliferation are up-regulated following HSV-1 infection. In this study, using t...Studies of herpes simplex virus type 1 （HSV-1） infection have shown that many known and unknown cellular molecules in- volved in viral proliferation are up-regulated following HSV-1 infection. In this study, using two-dimensional polyacrylamide gel electrophoresis, we found that the expression of the HSV-1 infection response repressive protein （HIRRP, GI 16552881） was up-regulated in human L02 cells infected with HSV-1. HIRRP, an unknown protein, was initially localized in the cytoplasm and then translocated into the nucleus of HSV-l-infected cells. Further analysis showed that HIRRP represses HSV-1 proliferation by inhibiting transcription of the viral genome by interacting with the cellular transcription factor, ATFS, via its N-terminal domain. ATF5 represses the transcription of many host genes but can also act as an activator of genes containing a specific motif. We found that ATF5 promotes the proliferation of HSV-1 via a potential mechanism by which ATF5 enhances the transcription of viral genes during the course of an HSV-1 infection; HIRRP then induces feedback repression of this tran- scription by interacting with ATFS.展开更多
Wnt signaling directs cell-fate choices during embryonic development and tissue tumorigenesis. T cell fac-tor 4 (TCF4) plays a pivotal role in the Wnt signaling path-way. We demonstrate that a specific protein-protein...Wnt signaling directs cell-fate choices during embryonic development and tissue tumorigenesis. T cell fac-tor 4 (TCF4) plays a pivotal role in the Wnt signaling path-way. We demonstrate that a specific protein-protein interac-tion occurs between TCF4 and ATF5 (activating transcrip-tion factor 5) —— a new member of cAMP response element binding protein (CREB) with the yeast two-hybrid system. The N-terminal and DNA binding domain of TCF4 (TCF4ND, 1—495 aa) and the C-terminal spanning bZIP domain of ATF5 (162—282 aa) were found to be responsible for the interaction, and the C-terminal of ATF5 (ATF5/C) showed a much stronger interaction with TCF4ND than the full-length of ATF5 by detecting the b-gal activity. Further-more, overexpression of ATF5/C enhanced transcriptional activation by TCF4 proteins in luciferase assay by transient transfection. Taken together, these data suggest that ATF5 may function as a co-activator to potentiate the ability of TCF4 to activate transcription.展开更多
Broiler ascites syndrome(AS)is one of the main diseases threatening the health of broilers.It is well documented that myocardial hypertrophy and failure is one of the key mechanisms of broiler ascites syndrome.Therefo...Broiler ascites syndrome(AS)is one of the main diseases threatening the health of broilers.It is well documented that myocardial hypertrophy and failure is one of the key mechanisms of broiler ascites syndrome.Therefore,prevention of cardiac hypertrophy and failure would be one goal to reduce broiler ascites syndrome incidence.Myocardial hyper-trophy and failure are closely related to endoplasmic reticulum stress(ERS)in cardiac myocytes,and the endoplasmic reticulum stress signaling system(ATF6-DR5)is one of the important pathways of myocardial apoptosis.Excessive hyper-trophy will affect the heart muscle's normal contraction and diastole function,and the heart will turn from compen-sated to decompensate thus causing myocardial injury.Myocardial apoptosis is a core component of the pathological changes of this myocardial injury.Nano-selenium is a kind of red elemental selenium nanoparticle.Due to its excellent physical,chemical and biological properties,it has attracted extensive academic attention in recent years.It has been proven to have excellent antioxidant,antibacterial,antitumor,antihypertrophic,and antiapoptotic abilties.Herein,nano-selenium(1μmol/L)can inhibit hydrogen peroxide(H_(2)O_(2))-induced oxidative stress in broiler primary cardiomyocytes,and at the same time reduce cardiomyocyte apoptosis.In vivo,nano-selenium can reduce broiler myocardial injury-related enzyme indicators(AST,CK and LDH),and alleviate myocardial injury.It can also activate the antioxidant enzyme system(SOD,GSH-Px and CAT)and reduce MDA,and make the recovery ofT-AOC ability in the organization.Meanwhile,nano-selenium can down-regulate the genes and proteins expression of ATF-6,GRP-78,CHOP and caspase 12 in the ERS-related signaling pathway,and inhibit that of downstream-related caspase 3,Bax and caspase 9,and increase that of the downstream anti-apoptotic Bcl-2,thereby maintaining the homeostasis of the endoplasmic reticulum and alleviating cardiomyocyte apoptosis.It can be seen that nano-selenium can protect the damaged myocardium in the broiler ascites caused by high-salt drinking by regulating the ATF6-DR5 signaling pathway.This study was performed in chickens and cardiomyocyte cells and attempted to demonstrate that selenium nanoparticles can protect the damaged myocar-dium in broiler ascites.This paper provides a new idea for preventing and treating broiler ascites syndrome.展开更多
基金supported by the National Basic Research Program of China(2012CB518901)the National Natural Science Foundation of China(31100127)
文摘Studies of herpes simplex virus type 1 （HSV-1） infection have shown that many known and unknown cellular molecules in- volved in viral proliferation are up-regulated following HSV-1 infection. In this study, using two-dimensional polyacrylamide gel electrophoresis, we found that the expression of the HSV-1 infection response repressive protein （HIRRP, GI 16552881） was up-regulated in human L02 cells infected with HSV-1. HIRRP, an unknown protein, was initially localized in the cytoplasm and then translocated into the nucleus of HSV-l-infected cells. Further analysis showed that HIRRP represses HSV-1 proliferation by inhibiting transcription of the viral genome by interacting with the cellular transcription factor, ATFS, via its N-terminal domain. ATF5 represses the transcription of many host genes but can also act as an activator of genes containing a specific motif. We found that ATF5 promotes the proliferation of HSV-1 via a potential mechanism by which ATF5 enhances the transcription of viral genes during the course of an HSV-1 infection; HIRRP then induces feedback repression of this tran- scription by interacting with ATFS.
基金supported by the National Natural Science Foundation of China(Grant Nos.30070703 and 39970369).
文摘Wnt signaling directs cell-fate choices during embryonic development and tissue tumorigenesis. T cell fac-tor 4 (TCF4) plays a pivotal role in the Wnt signaling path-way. We demonstrate that a specific protein-protein interac-tion occurs between TCF4 and ATF5 (activating transcrip-tion factor 5) —— a new member of cAMP response element binding protein (CREB) with the yeast two-hybrid system. The N-terminal and DNA binding domain of TCF4 (TCF4ND, 1—495 aa) and the C-terminal spanning bZIP domain of ATF5 (162—282 aa) were found to be responsible for the interaction, and the C-terminal of ATF5 (ATF5/C) showed a much stronger interaction with TCF4ND than the full-length of ATF5 by detecting the b-gal activity. Further-more, overexpression of ATF5/C enhanced transcriptional activation by TCF4 proteins in luciferase assay by transient transfection. Taken together, these data suggest that ATF5 may function as a co-activator to potentiate the ability of TCF4 to activate transcription.
基金Central Fundamental Research Fund for Universities(No.2662020DKPY013)Thirteenth Five-Year Plan Key R&D Program(No.2016YFD0501208)Innovation and Entrepreneurship Training Program for College Students in Hubei Province(S202110504039).
文摘Broiler ascites syndrome(AS)is one of the main diseases threatening the health of broilers.It is well documented that myocardial hypertrophy and failure is one of the key mechanisms of broiler ascites syndrome.Therefore,prevention of cardiac hypertrophy and failure would be one goal to reduce broiler ascites syndrome incidence.Myocardial hyper-trophy and failure are closely related to endoplasmic reticulum stress(ERS)in cardiac myocytes,and the endoplasmic reticulum stress signaling system(ATF6-DR5)is one of the important pathways of myocardial apoptosis.Excessive hyper-trophy will affect the heart muscle's normal contraction and diastole function,and the heart will turn from compen-sated to decompensate thus causing myocardial injury.Myocardial apoptosis is a core component of the pathological changes of this myocardial injury.Nano-selenium is a kind of red elemental selenium nanoparticle.Due to its excellent physical,chemical and biological properties,it has attracted extensive academic attention in recent years.It has been proven to have excellent antioxidant,antibacterial,antitumor,antihypertrophic,and antiapoptotic abilties.Herein,nano-selenium(1μmol/L)can inhibit hydrogen peroxide(H_(2)O_(2))-induced oxidative stress in broiler primary cardiomyocytes,and at the same time reduce cardiomyocyte apoptosis.In vivo,nano-selenium can reduce broiler myocardial injury-related enzyme indicators(AST,CK and LDH),and alleviate myocardial injury.It can also activate the antioxidant enzyme system(SOD,GSH-Px and CAT)and reduce MDA,and make the recovery ofT-AOC ability in the organization.Meanwhile,nano-selenium can down-regulate the genes and proteins expression of ATF-6,GRP-78,CHOP and caspase 12 in the ERS-related signaling pathway,and inhibit that of downstream-related caspase 3,Bax and caspase 9,and increase that of the downstream anti-apoptotic Bcl-2,thereby maintaining the homeostasis of the endoplasmic reticulum and alleviating cardiomyocyte apoptosis.It can be seen that nano-selenium can protect the damaged myocardium in the broiler ascites caused by high-salt drinking by regulating the ATF6-DR5 signaling pathway.This study was performed in chickens and cardiomyocyte cells and attempted to demonstrate that selenium nanoparticles can protect the damaged myocar-dium in broiler ascites.This paper provides a new idea for preventing and treating broiler ascites syndrome.
