Author

H. Kudo

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Evolutionary Biology· 1 Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:proteomics· 2 Organism:Arabidopsis· 1 Organism:bacteria (other)· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1 Organism:mouse· 1

Frequent Co-Authors

D. Matsuike· 1 shared G. Britton· 1 shared G. Foster· 1 shared G. Renney· 1 shared H. Heath· 1 shared H. Kimura· 1 shared H. N. Wu· 1 shared J. Obokata· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 12 mutual co-author links

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1 shared paperMicrobiology

D. Matsuike

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Structure and Function of Gli123 Involved in Mycoplasma mobile Gliding

D. Matsuike, Y. O. Tahara, T. Nonaka, H. N. Wu, T. Hamaguchi, H. Kudo, Y. Hayashi, M. Arai, M. Miyata

This study investigates the structure and function of Gli123, a surface protein essential for Mycoplasma mobile gliding, revealing its conformational changes and evolutionary implications.

bioRxiv · Sep 7, 2022Microbiology

Cryptic promoter activation occurs by at least two different mechanisms in the Arabidopsis genome

H. Kudo, M. Matsuo, S. Satoh, R. Hachisu, M. Nakamura, Y. Y. Yamamoto, T. Hata, H. Kimura, M. Matsui, J. Obokata

The paper identifies two mechanisms of cryptic promoter activation in Arabidopsis: chromatin capture of pre-existing promoter-like regions and de novo promoter formation near inserted LUC ORF sequences.

bioRxiv · Nov 28, 2020Evolutionary Biology

Stat2 loss disrupts damage signalling and is protective in acute pancreatitis

H. Heath, G. Britton, H. Kudo, G. Renney, M. Ward, R. Hutchins, G. Foster, R. Goldin, W. Alazawi

This study shows that Stat2 deficiency protects against acute pancreatitis by disrupting damage signaling pathways independent of type I interferon, with reduced cytokine levels and NF-κB activation.

bioRxiv · Sep 18, 2019Immunology