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Mihail S. Iordanov

Researcher at Oregon Health & Science University

Publications -  31
Citations -  3034

Mihail S. Iordanov is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Kinase & p38 mitogen-activated protein kinases. The author has an hindex of 24, co-authored 31 publications receiving 2865 citations.

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Ribotoxic stress response: activation of the stress-activated protein kinase JNK1 by inhibitors of the peptidyl transferase reaction and by sequence-specific RNA damage to the alpha-sarcin/ricin loop in the 28S rRNA.

TL;DR: It is found that aminohexose pyrimidine nucleoside antibiotics, which bind to the same region in the 28S rRNA that is the target site for anisomycin, are also potent activators of SAPK/JNK1.
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Th17 cytokines stimulate CCL20 expression in keratinocytes in vitro and in vivo: implications for psoriasis pathogenesis.

TL;DR: It is shown that Th17 cytokines stimulate CCL20 production in vitro and in vivo, and thus provide a potential explanation of how CCR6-positive Th17 cells maintain their continual presence in psoriasis through a positive chemotactic feedback loop.
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UV-Induced Signal Transduction

TL;DR: UV is absorbed by several target molecules relevant for cellular signaling, and it appears that numerous signal transduction pathways are stimulated.
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CREB is activated by UVC through a p38/HOG‐1‐dependent protein kinase

TL;DR: It is found that UVC‐induced transcriptional activation depends also on the CRE at position −60 of the c‐fos promoter and on the functionality of a CREB, which represents an as yet unrecognized route of U VC‐induced signal transduction, independent of suramin‐inhibitable growth factor receptors and different from the Erk 1,2–p62TCF pathway.
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Activation of p38 Mitogen-Activated Protein Kinase and c-Jun NH2-Terminal Kinase by Double-Stranded RNA and Encephalomyocarditis Virus: Involvement of RNase L, Protein Kinase R, and Alternative Pathways

TL;DR: A novel form of dsRNA-triggered signaling that leads to the stimulation of the p38 mitogen-activated protein kinase (p38 MAPK) and the c-Jun NH2-terminal Kinase (JNK) and of their respective activators MKK3/6 and SEK1/MKK4 is described.