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January 1, 1996Journal of VirologyOpen Access

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

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Authors

BHBin HeShanghai Chest HospitalJCJ ChouPrecision for Medicine (United States)DLDan A. LiebermannAmerican Association For Cancer Research

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He et al. (1996) studied this question.

synapsesocial.com/papers/6a71b375439bab0cabc3a6aahttps://doi.org/10.1128/jvi.70.1.84-90.1996
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Herpes simplex virus 1 gamma(1)34.5 gene function, which blocks the host response to infection, maps in the homologous domain of the genes expressed during growth arrest and DNA damage.1994 · 205 citations
  2. 2The gamma 1(34.5) gene of herpes simplex virus 1 precludes neuroblastoma cells from triggering total shutoff of protein synthesis characteristic of programed cell death in neuronal cells.1992 · 396 citations
  3. 3Replication, establishment of latency, and induced reactivation of herpes simplex virus gamma 1 34.5 deletion mutants in rodent models.1993 · 188 citations
  4. 4Mapping of Herpes Simplex Virus-1 Neurovirulence to γ 1 34.5, a Gene Nonessential for Growth in Culture1990 · 715 citations
  5. 5Sequence of MyD116 cDNA: a novel myeloid differentiation primary response gene induced by IL61990 · 87 citations