Replication, establishment of latency, and induced reactivation of herpes simplex virus gamma 1 34.5 deletion mutants in rodent models.
about
A conserved domain of herpes simplex virus ICP34.5 regulates protein phosphatase complex in mammalian cellsA herpes simplex virus-derived replicative vector expressing LIF limits experimental demyelinating disease and modulates autoimmunityAn African swine fever virus virulence-associated gene NL-S with similarity to the herpes simplex virus ICP34.5 geneInhibition of herpes simplex virus replication by a 2-amino thiazole via interactions with the helicase component of the UL5-UL8-UL52 complexPresage of oncolytic virotherapy for oral cancer with herpes simplex virus.Herpes simplex virus 1 open reading frames O and P are not necessary for establishment of latent infection in mice.Association of a M(r) 90,000 phosphoprotein with protein kinase PKR in cells exhibiting enhanced phosphorylation of translation initiation factor eIF-2 alpha and premature shutoff of protein synthesis after infection with gamma 134.5- mutants of herAttenuated, replication-competent herpes simplex virus type 1 mutant G207: safety evaluation in miceAttenuated, replication-competent herpes simplex virus type 1 mutant G207: safety evaluation of intracerebral injection in nonhuman primates.Sequence variability in clinical and laboratory isolates of herpes simplex virus 1 reveals new mutations.Genetically engineered HSV in the treatment of glioma: a review.Functional interaction between fluorodeoxyuridine-induced cellular alterations and replication of a ribonucleotide reductase-negative herpes simplex virus.AlaArg motif in the carboxyl terminus of the gamma(1)34.5 protein of herpes simplex virus type 1 is required for the formation of a high-molecular-weight complex that dephosphorylates eIF-2alpha.Oncolytic Viruses for Cancer Therapy: Overcoming the Obstacles.HSV-1-based vectors for gene therapy of neurological diseases and brain tumors: part I. HSV-1 structure, replication and pathogenesis.HSV-1-based vectors for gene therapy of neurological diseases and brain tumors: part II. Vector systems and applicationsThe dominant-negative herpes simplex virus type 1 (HSV-1) recombinant CJ83193 can serve as an effective vaccine against wild-type HSV-1 infection in mice.Up to four distinct polypeptides are produced from the γ34.5 open reading frame of herpes simplex virus 2Replication-selective virotherapy for cancer: Biological principles, risk management and future directions.Second-site mutation outside of the U(S)10-12 domain of Deltagamma(1)34.5 herpes simplex virus 1 recombinant blocks the shutoff of protein synthesis induced by activated protein kinase R and partially restores neurovirulence.Signals that dictate nuclear, nucleolar, and cytoplasmic shuttling of the gamma(1)34.5 protein of herpes simplex virus type 1Structure and sequence of the saimiriine herpesvirus 1 genome.Failure of thymidine kinase-negative herpes simplex virus to reactivate from latency following efficient establishment.Oncolytic herpes viral therapy is effective in the treatment of hepatocellular carcinoma cell lines.Comparison of genetically engineered herpes simplex viruses for the treatment of brain tumors in a scid mouse model of human malignant glioma.A herpesvirus virulence factor inhibits dendritic cell maturation through protein phosphatase 1 and Ikappa B kinase.p32 is a novel target for viral protein ICP34.5 of herpes simplex virus type 1 and facilitates viral nuclear egress.Current good manufacturing practice production of an oncolytic recombinant vesicular stomatitis viral vector for cancer treatment.Replication of herpes simplex virus 1 depends on the gamma 134.5 functions that facilitate virus response to interferon and egress in the different stages of productive infection.Characterization of herpes simplex virus 2 primary microRNA Transcript regulationNeutralizing innate host defenses to control viral translation in HSV-1 infected cells.Activation of NF-κB in CD8+ dendritic cells Ex Vivo by the γ134.5 null mutant correlates with immunity against herpes simplex virus 1.Neuronal Interferon Signaling Is Required for Protection against Herpes Simplex Virus Replication and Pathogenesis.Specific phenotypic restoration of an attenuated virus by knockout of a host resistance geneInhibition of TANK binding kinase 1 by herpes simplex virus 1 facilitates productive infectionTwo overlapping transcription units which extend across the L-S junction of herpes simplex virus type 1.An avirulent ICP34.5 deletion mutant of herpes simplex virus type 1 is capable of in vivo spontaneous reactivation.The carboxyl terminus of the murine MyD116 gene substitutes for the corresponding domain of the gamma(1)34.5 gene of herpes simplex virus to preclude the premature shutoff of total protein synthesis in infected human cells.The spontaneous reactivation function of the herpes simplex virus type 1 LAT gene resides completely within the first 1.5 kilobases of the 8.3-kilobase primary transcript.Phenotypic properties of herpes simplex virus 1 containing a derepressed open reading frame P gene.
P2860
Q24302506-4D1A1881-D7DE-4B37-9FFE-F0882E5AE72DQ27319470-144DEC7F-DEC8-4DD7-86F5-7BBC2F416E6BQ27480762-8C7F1624-CD94-4122-92C4-4888CAE38291Q28368363-EE7E5048-3E95-4E51-B02E-26018B34BDF3Q33603748-2993DDA5-30A0-4807-9A5C-02F7EB55DFCBQ33604367-F3B4FEAA-2CF3-4319-B6F2-51EEA8D50516Q33780588-D55AC14B-527E-47C6-9DDE-6D8FDA820354Q33802747-43A61F1D-7CF6-4DFD-8421-050DFBEA0ACAQ33816579-019528B7-C7A0-4F40-B1E3-1589845F1C2DQ33826925-EA89B126-945F-4B8B-A45B-8FD116F47850Q33827571-5A650A8C-5A6B-4635-A3BA-9FD4B05F50F2Q33844465-0BAFA68C-FCC0-46B7-A0E9-77E515BB8F41Q33851189-F40F6D3C-C3BB-49C5-A112-EDE9725ED297Q33906116-0F9C122E-B44F-4CE0-87C4-944497A81E10Q33995747-BE7CED4A-4F11-4332-91E8-26663BDB199BQ33995752-0769335C-B742-45A9-82A2-2099BD7EC7D4Q34150713-A2D30B21-AB48-4641-B033-B8E38774994EQ34261842-3288E78C-69F4-4404-9A64-F2B9A48EADAFQ34297058-C4AE9226-471C-4A76-B1B6-841B6EB83D55Q34328502-0D60AA14-4B85-441E-913A-D9D846694C7FQ34344979-5038A395-A91C-4D44-968E-DAF09FED0C51Q34474333-102D81AF-A0A0-4857-837F-192FFB7B1977Q34553254-A422E072-5C68-4085-A9F1-666BDC6A65E0Q34557399-81E86240-A4E6-407E-9780-CA8AE5A0A9C8Q34616722-C901E11B-3272-4776-AFD7-EBCFF948612CQ34742621-824D4F21-3DE5-4A79-A462-2A53FDD3A587Q34774447-15B518ED-9164-4AF6-84ED-ADF6042D9BF1Q34774805-E11C31FE-1FF2-4A3F-BAE9-3C81B5893BE6Q35123297-FEDA8377-3AFB-48C9-AAC4-CC444C3403C2Q35488636-FF78D4D5-7EED-4652-BE4E-6DB2B1627C2BQ35613824-BFC43054-0B34-423E-9B4C-4A56073FE2E5Q35665813-69EB909E-128D-4023-912F-F67EA79D2AE9Q35685766-BF752F43-C4F1-4D31-9F0C-8AFE88297784Q35760833-BAB724A7-AB1B-4EE3-8D37-DE660DFEF7EBQ35826469-E55D120E-E8C4-4A0C-BC2A-D82FE80DE5DDQ35838735-C3DCD715-94CC-4B6D-8485-587403C1499AQ35839010-E6633775-B44F-46CF-8D9D-5965CDDA62E2Q35853252-2D9C77C1-FF00-4EB5-977B-FDD58A5DEA28Q35854629-E842AA06-2962-4E9A-B082-FF85DF306DF0Q35857171-B6B66A32-C981-4425-A7CA-553ECF8EAE89
P2860
Replication, establishment of latency, and induced reactivation of herpes simplex virus gamma 1 34.5 deletion mutants in rodent models.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年論文
@yue
1993年論文
@zh-hant
1993年論文
@zh-hk
1993年論文
@zh-mo
1993年論文
@zh-tw
1993年论文
@wuu
1993年论文
@zh
1993年论文
@zh-cn
name
Replication, establishment of ...... tion mutants in rodent models.
@ast
Replication, establishment of ...... tion mutants in rodent models.
@en
type
label
Replication, establishment of ...... tion mutants in rodent models.
@ast
Replication, establishment of ...... tion mutants in rodent models.
@en
prefLabel
Replication, establishment of ...... tion mutants in rodent models.
@ast
Replication, establishment of ...... tion mutants in rodent models.
@en
P2093
P2860
P356
P1476
Replication, establishment of ...... tion mutants in rodent models.
@en
P2093
P2860
P304
P356
10.1172/JCI116527
P407
P577
1993-06-01T00:00:00Z