B
Blair R. Renshaw
Researcher at Amgen
Publications - 23
Citations - 2727
Blair R. Renshaw is an academic researcher from Amgen. The author has contributed to research in topics: Interleukin & Receptor. The author has an hindex of 14, co-authored 21 publications receiving 2452 citations.
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Journal ArticleDOI
Interleukin-36–Receptor Antagonist Deficiency and Generalized Pustular Psoriasis
Slaheddine Marrakchi,Philippe Guigue,Blair R. Renshaw,Anne Puel,Xue-Yuan Pei,Sylvie Fraitag,Jihen Zribi,Elodie Bal,Céline Cluzeau,Maya Chrabieh,Jennifer E. Towne,Jason Douangpanya,Christian Pons,Sourour Mansour,Valérie Serre,Hafedh Makni,Nadia Mahfoudh,Faiza Fakhfakh,Christine Bodemer,Josué Feingold,Smail Hadj-Rabia,Michel Favre,Emmanuelle Génin,Mourad Sahbatou,Arnold Munnich,Jean-Laurent Casanova,John E. Sims,Hamida Turki,Hervé Bachelez,Asma Smahi +29 more
TL;DR: Aberrant interleukin-36Ra structure and function lead to unregulated secretion of inflammatory cytokines and generalized pustular psoriasis.
Journal ArticleDOI
Interleukin (IL)-1F6, IL-1F8, and IL-1F9 Signal through IL-1Rrp2 and IL-1RAcP to Activate the Pathway Leading to NF-κB and MAPKs
TL;DR: It is demonstrated that IL-1F6 and IL- 1F8, in addition to IL-2F9, activate the pathway leading to NF-κB in an IL-3Rrp2-dependent manner in Jurkat cells as well as in multiple other human and mouse cell lines, and thatIL-1RrP2 antibodies block activation of the pathwayLeading to NF -κB by IL-0F6, IL-8, and Il-1
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Four New Members Expand the Interleukin-1 Superfamily
TL;DR: The cloning and characterization of four new members of the interleukin-1 (IL-1) family (FIL1δ, FIL1ε, Fil1ζ, and FIL1η, with FIL1 standing for “Family of IL-1”) are reported here.
Journal ArticleDOI
Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36α, IL-36β, and IL-36γ) or antagonist (IL-36Ra) activity.
Jennifer E. Towne,Blair R. Renshaw,Jason Douangpanya,Brian P. Lipsky,Min Shen,Christopher A. Gabel,John E. Sims +6 more
TL;DR: It is demonstrated that IL-36Ra antagonist activity is dependent upon removal of its N-terminal methionine, and the mechanism of action is directly analogous to that of IL-1Ra, which suggests that protease(s) that activate IL- 36 cytokines could be excellent drug targets for psoriasis.
Journal ArticleDOI
Identification and characterization of SIGIRR, a molecule representing a novel subtype of the IL-1R superfamily.
TL;DR: It is concluded that the SIGIRR protein represents a novel subtype of the IL-1R superfamily, which has only one Ig domain in its extracellular portion and an unusually long cytoplasmic domain is reminiscent of the structure of drosophila Toll.