K
Keisuke Horiuchi
Researcher at National Defense Medical College
Publications - 139
Citations - 5834
Keisuke Horiuchi is an academic researcher from National Defense Medical College. The author has contributed to research in topics: Ectodomain & Tumor necrosis factor alpha. The author has an hindex of 35, co-authored 132 publications receiving 4989 citations. Previous affiliations of Keisuke Horiuchi include Temple University & Kettering University.
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Journal ArticleDOI
Dysbiosis and Staphylococcus aureus Colonization Drives Inflammation in Atopic Dermatitis.
Tetsuro Kobayashi,Tetsuro Kobayashi,Martin Glatz,Keisuke Horiuchi,Hiroshi Kawasaki,Haruhiko Akiyama,Daniel H. Kaplan,Heidi H. Kong,Masayuki Amagai,Keisuke Nagao,Keisuke Nagao +10 more
TL;DR: It is demonstrated that Adam17(fl/fl)Sox9-(Cre) mice, generated to model ADAM17-deficiency in human, developed eczematous dermatitis with naturally occurring dysbiosis, similar to that observed in atopic dermatitis.
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Substrate Selectivity of Epidermal Growth Factor-Receptor Ligand Sheddases and their Regulation by Phorbol Esters and Calcium Influx
Keisuke Horiuchi,Keisuke Horiuchi,Sylvain Le Gall,Marc Schulte,Takafumi Yamaguchi,Karina Reiss,Gillian Murphy,Yoshiaki Toyama,Dieter Hartmann,Paul Saftig,Carl P. Blobel,Carl P. Blobel +11 more
TL;DR: It is demonstrated that dysregulated EGFR-ligand shedding may be caused by increased expression of constitutively active sheddases or activation of different sheddase by distinct stimuli, including phorbol esters and calcium influx.
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Cutting Edge: TNF-α-Converting Enzyme (TACE/ADAM17) Inactivation in Mouse Myeloid Cells Prevents Lethality from Endotoxin Shock
Keisuke Horiuchi,Tokuhiro Kimura,Takeshi Miyamoto,Hironari Takaishi,Yasunori Okada,Yoshiaki Toyama,Carl P. Blobel +6 more
TL;DR: It is reported that TACE inactivation in myeloid cells or temporal inactivation at 6 wk offers strong protection from endotoxin shock lethality in mice by preventing increased TNF serum levels, further validating TACE as a principal target for the treatment of TNF-dependent pathologies.
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Stress-induced production of chemokines by hair follicles regulates the trafficking of dendritic cells in skin
Keisuke Nagao,Tetsuro Kobayashi,Kazuyo Moro,Manabu Ohyama,Takeya Adachi,Daniela Y. Kitashima,Satoshi Ueha,Keisuke Horiuchi,Hideaki Tanizaki,Kenji Kabashima,Akiharu Kubo,Young Hun Cho,Bjarn E. Clausen,Kouji Matsushima,Makoto Suematsu,Glaucia C. Furtado,Sergio A. Lira,Joshua M. Farber,Mark C. Udey,Masayuki Amagai +19 more
TL;DR: It is shown that in response to external stress, mouse hair follicles recruited Gr-1hi monocyte-derived precursors of LCs whose epidermal entry was dependent on the chemokine receptors CCR2 and CCR6, whereas the Chemokine receptor CCR8 inhibited the recruitment of LCS.
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ADAMs 10 and 17 Represent Differentially Regulated Components of a General Shedding Machinery for Membrane Proteins Such as Transforming Growth Factor α, L-Selectin, and Tumor Necrosis Factor α
Sylvain Le Gall,Pierre Bobe,Karina Reiss,Keisuke Horiuchi,Xiao Da Niu,Daniel Lundell,David R. Gibb,Daniel Conrad,Paul Saftig,Carl P. Blobel,Carl P. Blobel +10 more
TL;DR: It is shown that Ca++ influx and stimulation of the P2X7R signaling pathway activate ADAM10 as sheddase of many ADAM17 substrates in Adam17-/- fibroblasts and primary B cells, which has general implications for understanding the substrate selectivity of two major cellular sheddases, ADAMs 10 and 17.