IL-17-driven intestinal fibrosis is inhibited by Itch-mediated ubiquitination of HIC-5

Hic-5 is required for myofibroblast differentiation by regulating mechanically dependent MRTF-A nuclear accumulation

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Hic-5 deficiency attenuates the activation of hepatic stellate cells and liver fibrosis through upregulation of Smad7 in mice

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Itch inhibits IL-17-mediated colon inflammation and tumorigenesis by ROR-γt ubiquitination

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Losartan Reduces Trinitrobenzene Sulphonic Acid-Induced Colorectal Fibrosis in Rats

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Negative Regulation of NADPH Oxidase 4 by Hydrogen Peroxide-inducible Clone 5 (Hic-5) Protein

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IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation

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The Deubiquitinase A20 Mediates Feedback Inhibition of Interleukin-17 Receptor Signaling

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Cbl and Itch binding sites in ERBB4 CYT-1 and CYT-2 mediate K48- and K63-polyubiquitination, respectively

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Hydrogen Peroxide-Inducible Clone 5 (Hic-5) as a Potential Therapeutic Target for Vascular and Other Disorders

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Noncanonical K27-Linked Polyubiquitination of TIEG1 Regulates Foxp3 Expression and Tumor Growth

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Novel Regulation of Parkin Function through c-Abl-Mediated Tyrosine Phosphorylation: Implications for Parkinson's Disease

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The E3 ligase Itch and deubiquitinase Cyld act together to regulate Tak1 and inflammation

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IL-1 and IL-23 Mediate Early IL-17A Production in Pulmonary Inflammation Leading to Late Fibrosis

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Human ITCH E3 Ubiquitin Ligase Deficiency Causes Syndromic Multisystem Autoimmune Disease

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K33-Linked Polyubiquitination of T Cell Receptor-ζ Regulates Proteolysis-Independent T Cell Signaling

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In vitro and in vivo evidence of pathogenic roles of Hic-5/ARA55 in keloids through Smad pathway and profibrotic transcription

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IL-17 and Th17 Cells

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ITCH K63-Ubiquitinates the NOD2 Binding Protein, RIP2, to Influence Inflammatory Signaling Pathways

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Intestinal fibrosis in IBD—a dynamic, multifactorial process

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Upregulation of GRAIL is associated with remission of ulcerative colitis

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Interactions among the transcription factors Runx1, RORγt and Foxp3 regulate the differentiation of interleukin 17–producing T cells

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TGF-β1 Slows the Growth of Pathogenic Myofibroblasts through a Mechanism Requiring the Focal Adhesion Protein, Hic-5

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