IκBζ is a key transcriptional regulator of IL-36–driven psoriasis-related gene expression in keratinocytes
出版年份 2018 全文链接
标题
IκBζ is a key transcriptional regulator of IL-36–driven psoriasis-related gene expression in keratinocytes
作者
关键词
-
出版物
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume -, Issue -, Pages 201801377
出版商
Proceedings of the National Academy of Sciences
发表日期
2018-09-18
DOI
10.1073/pnas.1801377115
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- Regulation and function of interleukin-36 cytokines
- (2017) Esen Yonca Bassoy et al. IMMUNOLOGICAL REVIEWS
- Overview of the IL-1 family in innate inflammation and acquired immunity
- (2017) Charles A. Dinarello IMMUNOLOGICAL REVIEWS
- GM-CSF in murine psoriasiform dermatitis: Redundant and pathogenic roles uncovered by antibody-induced neutralization and genetic deficiency
- (2017) Tatjana Scholz et al. PLoS One
- An analysis of IL-36 signature genes and individuals with IL1RL2 knockout mutations validates IL-36 as a psoriasis therapeutic target
- (2017) Satveer K. Mahil et al. Science Translational Medicine
- The psoriasis-associated IL-17A induces and cooperates with IL-36 cytokines to control keratinocyte differentiation and function
- (2017) Carolina M. Pfaff et al. Scientific Reports
- Distinct expression of interleukin (IL)-36α, βandγ, their antagonist IL-36Ra and IL-38 in psoriasis, rheumatoid arthritis and Crohn's disease
- (2016) M.-A. Boutet et al. CLINICAL AND EXPERIMENTAL IMMUNOLOGY
- Atypical IκB proteins in immune cell differentiation and function
- (2016) Michaela Annemann et al. IMMUNOLOGY LETTERS
- IL-17A plays a central role in the expression of psoriasis signature genes through the induction of IκB-ζ in keratinocytes
- (2016) Ryuta Muromoto et al. INTERNATIONAL IMMUNOLOGY
- The role of IFN-γ in regulating Nfkbiz expression in epidermal keratinocytes
- (2015) Toshina ISHIGURO-OONUMA et al. BIOMEDICAL RESEARCH-TOKYO
- Proteolytic Processing of Interleukin-1 Family Cytokines: Variations on a Common Theme
- (2015) Inna S. Afonina et al. IMMUNITY
- IL-36γ (IL-1F9) Is a Biomarker for Psoriasis Skin Lesions
- (2015) Angelo Massimiliano D'Erme et al. JOURNAL OF INVESTIGATIVE DERMATOLOGY
- IκBζ is a key driver in the development of psoriasis
- (2015) Claus Johansen et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Enhanced meta-analysis and replication studies identify five new psoriasis susceptibility loci
- (2015) Lam C. Tsoi et al. Nature Communications
- Immunology of Psoriasis
- (2014) Michelle A. Lowes et al. Annual Review of Immunology
- Akirin2 is critical for inducing inflammatory genes by bridging I B- and the SWI/SNF complex
- (2014) S. Tartey et al. EMBO JOURNAL
- Enhanced Apoptosis by Disruption of the STAT3-IκB-ζ Signaling Pathway in Epithelial Cells Induces Sjögren’s Syndrome-like Autoimmune Disease
- (2013) Atsushi Okuma et al. IMMUNITY
- Keratinocyte Overexpression of IL-17C Promotes Psoriasiform Skin Inflammation
- (2013) A. Johnston et al. JOURNAL OF IMMUNOLOGY
- I B Is a Transcriptional Key Regulator of CCL2/MCP-1
- (2013) D. G. Hildebrand et al. JOURNAL OF IMMUNOLOGY
- NF-κB and STAT3 Inhibition as a Therapeutic Strategy in Psoriasis: In Vitro and In Vivo Effects of BTH
- (2013) Rosa M. Andrés et al. JOURNAL OF INVESTIGATIVE DERMATOLOGY
- Psoriasiform dermatitis is driven by IL-36–mediated DC-keratinocyte crosstalk
- (2012) Luigi Tortola et al. JOURNAL OF CLINICAL INVESTIGATION
- An Alternative Pathway of Imiquimod-Induced Psoriasis-Like Skin Inflammation in the Absence of Interleukin-17 Receptor A Signaling
- (2012) Khalifa El Malki et al. JOURNAL OF INVESTIGATIVE DERMATOLOGY
- Mutations in IL36RN/IL1F5 Are Associated with the Severe Episodic Inflammatory Skin Disease Known as Generalized Pustular Psoriasis
- (2011) Alexandros Onoufriadis et al. AMERICAN JOURNAL OF HUMAN GENETICS
- Interleukin-36 (IL-36) Ligands Require Processing for Full Agonist (IL-36α, IL-36β, and IL-36γ) or Antagonist (IL-36Ra) Activity
- (2011) Jennifer E. Towne et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- IL-1F5, -F6, -F8, and -F9: A Novel IL-1 Family Signaling System That Is Active in Psoriasis and Promotes Keratinocyte Antimicrobial Peptide Expression
- (2011) A. Johnston et al. JOURNAL OF IMMUNOLOGY
- Inter-Regulation of Th17 Cytokines and the IL-36 Cytokines In Vitro and In Vivo: Implications in Psoriasis Pathogenesis
- (2011) Yijun Carrier et al. JOURNAL OF INVESTIGATIVE DERMATOLOGY
- Hierarchies of NF-κB target-gene regulation
- (2011) Stephen T Smale NATURE IMMUNOLOGY
- Interleukin-36–Receptor Antagonist Deficiency and Generalized Pustular Psoriasis
- (2011) Slaheddine Marrakchi et al. NEW ENGLAND JOURNAL OF MEDICINE
- Induction of Neutrophil Gelatinase-associated Lipocalin Expression by Co-stimulation with Interleukin-17 and Tumor Necrosis Factor-α Is Controlled by IκB-ζ but neither by C/EBP-β nor C/EBP-δ
- (2010) Joachim R. Karlsen et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- IL-1RL2 and Its Ligands Contribute to the Cytokine Network in Psoriasis
- (2010) H. Blumberg et al. JOURNAL OF IMMUNOLOGY
- Stat3 as a Therapeutic Target for the Treatment of Psoriasis: A Clinical Feasibility Study with STA-21, a Stat3 Inhibitor
- (2010) Ken Miyoshi et al. JOURNAL OF INVESTIGATIVE DERMATOLOGY
- IκBζ regulates TH17 development by cooperating with ROR nuclear receptors
- (2010) Kazuo Okamoto et al. NATURE
- The NIH Roadmap Epigenomics Mapping Consortium
- (2010) Bradley E Bernstein et al. NATURE BIOTECHNOLOGY
- Regulation and Function of NF-κB Transcription Factors in the Immune System
- (2009) Sivakumar Vallabhapurapu et al. Annual Review of Immunology
- Autoregulatory feedback loops terminating the NF-κB response
- (2009) Florian Renner et al. TRENDS IN BIOCHEMICAL SCIENCES
- Class-specific Regulation of Pro-inflammatory Genes by MyD88 Pathways and IκBζ
- (2008) Hisako Kayama et al. JOURNAL OF BIOLOGICAL CHEMISTRY
Discover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversationPublish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn More