Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
6 authors.
Naoto KoyanagiDivision of Molecular Virology, Department of Microbiology and Immunology, the Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.ORCID 0009-0007-1419-3578
Kosuke TakeshimaDivision of Molecular Virology, Department of Microbiology and Immunology, the Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Saori ShioDivision of Molecular Virology, Department of Microbiology and Immunology, the Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Yuhei MaruzuruDivision of Molecular Virology, Department of Microbiology and Immunology, the Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Akihisa KatoDivision of Molecular Virology, Department of Microbiology and Immunology, the Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Yasushi KawaguchiDivision of Molecular Virology, Department of Microbiology and Immunology, the Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.ORCID 0000-0001-8232-6925
Funding
GlaxoSmithKline Japan Research Grant 2019Grant for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Science, Sports and Technology of Japan 21H00338Grant for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Science, Sports and Technology of Japan 21H00417Grant for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Science, Sports and Technology of Japan 22H04803Grant for Transformative Research Areas from the Ministry of Education, Culture, Science, Sports and Technology of Japan 22H05584Grants for Scientific Research and Grant-in-Aid for Scientific Research (S) from the Japan Society for Promotion of Science (JSPS) 20H05692International Joint Research Project of the Institute of Medical Science, the University of TokyoJapan Agency for Medical Research and Development JP20wm0125002Japan Agency for Medical Research and Development JP223fa627001Japan Agency for Medical Research and Development JP22fk0108640Japan Agency for Medical Research and Development JP22gm1610008Japan Agency for Medical Research and Development JP23wm0225031Japan Agency for Medical Research and Development JP23wm0225035Japan Science and Technology Agency JPMJPR22R5Mitsubishi FoundationTakeda Science FoundationUehara Memorial FoundationWaksman Foundation of Japan
6 · The paper itself
Abstract
Although previous studies reported that the herpes simplex virus 2 (HSV-2) UL13 protein kinase mediates the phosphorylation of elongation factor 1δ (EF-1δ) in infected cells, we found here that individual expression of UL13 was insufficient to induce phosphorylation of EF-1δ in mammalian cells. This led us to hypothesize that HSV-2 UL13 requires viral cofactors for full kinase activity and prompted us to identify such cofactors. Our results were as follows. (i) Co-expression of UL13 with UL55 or Us10 significantly enhanced phosphorylation of EF-1δ compared to UL13 alone. (ii) UL13 was co-precipitated with UL55 or Us10 upon co-expression, and its kinase activity was significantly increased in their presence, as demonstrated by
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Identification of viral activators of the HSV-2 UL13 protein kinase. · full record | OpenQuestion