ArticleThe Journal of investigative dermatology2011
Inhibition of NF-κB signaling retards eosinophilic dermatitis in SHARPIN-deficient mice.
Article in The Journal of investigative dermatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- SHARPIN restrains IL-33 release by stromal cells to control ILC2 inflammation.Science advances · 2026Article
- Central Facial Nervous System Biomolecules Involved in Peripheral Facial Nerve Injury Responses and Potential Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2023Review
- SHARPIN: Role in Finding NEMO and in Amyloid-Beta Clearance and Degradation (ABCD) Pathway in Alzheimer's Disease?Cellular and molecular neurobiology · 2022Review
- The Interactions Between Autoinflammation and Type 2 Immunity: From Mechanistic Studies to Epidemiologic Associations.Frontiers in immunology · 2022Review
- Dual roles for LUBAC signaling in thymic epithelial cell development and survival.Cell death and differentiation · 2021Article
- SHARPIN regulates cell proliferation of cutaneous basal cell carcinoma via inactivation of the transcriptional factors GLI2 and c‑JUN.Molecular medicine reports · 2020Article
- The Balance of TNF Mediated Pathways Regulates Inflammatory Cell Death Signaling in Healthy and Diseased Tissues.Frontiers in cell and developmental biology · 2020Review
- Linear ubiquitination of cFLIP induced by LUBAC contributes to TNFα-induced apoptosis.The Journal of biological chemistry · 2018Article
- IL1RAP potentiates multiple oncogenic signaling pathways in AML.The Journal of experimental medicine · 2018Article
- Autoinflammatory Skin Disorders: The Inflammasomme in Focus.Trends in molecular medicine · 2016Review
- The intersection of cell death and inflammasome activation.Cellular and molecular life sciences : CMLS · 2016Review
- Dermal lymphatic dilation in a mouse model of alopecia areata.Experimental and molecular pathology · 2016Article
- SHARPIN controls regulatory T cells by negatively modulating the T cell antigen receptor complex.Nature immunology · 2016Article
- When Beauty Is Skin Deep: Regulation of the Wound Response by Caspase-8, RIPK3, and the Inflammasome.The Journal of investigative dermatology · 2015Article
- Human HOIP and LUBAC deficiency underlies autoinflammation, immunodeficiency, amylopectinosis, and lymphangiectasia.The Journal of experimental medicine · 2015Article
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- The linear ubiquitin assembly complex (LUBAC) is essential for NLRP3 inflammasome activation.The Journal of experimental medicine · 2014Article
- Article
- SHARPIN regulates uropod detachment in migrating lymphocytes.Cell reports · 2013Article
- Immunodeficiency, autoinflammation and amylopectinosis in humans with inherited HOIL-1 and LUBAC deficiency.Nature immunology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The NF-κB pathway performs pivotal roles in diverse physiological processes such as immunity, inflammation, proliferation, and apoptosis. NF-κB is kept inactive in the cytoplasm through association with inhibitors (IκB), and translocates to the nucleus to activate its target genes after the IκBs are phosphorylated and degraded. Here, we demonstrate that loss of function of SHANK-associated RH domain interacting protein (SHARPIN) leads to activation of NF-κB signaling in skin, resulting in the development of an idiopathic hypereosinophilic syndrome (IHES) with eosinophilic dermatitis in C57BL/KaLawRij-Sharpin(cpdm)/RijSunJ mice, and clonal expansion of B-1 B cells and CD3(+)CD4(-)CD8(-) T cells. Transcription profiling in skin revealed constitutive activation of classical NF-κB pathways, predominantly by overexpressed members of IL1 family. Compound-null mutants for both the IL1 receptor accessory protein (Il1rap(tm1Roml)) and SHARPIN (Sharpin(cpdm)) resulted in mice having decreased skin disease severity. Inhibition of IκBA degradation by the proteasome inhibitor bortezomib alleviated the dermatitis in Sharpin(cpdm) mice. These results indicate that absence of SHARPIN causes IHES with eosinophilic dermatitis by NF-κB activation, and bortezomib may be an effective treatment for skin problems of IHES.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.