ArticleThe Journal of clinical investigation2018
ASK1/2 signaling promotes inflammation in a mouse model of neutrophilic dermatosis.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- The Pathophysiology and Treatment of Pyoderma Gangrenosum-Current Options and New Perspectives.International journal of molecular sciences · 2024Review
- Biphasic JNK signaling reveals distinct MAP3K complexes licensing inflammasome formation and pyroptosis.Cell death and differentiation · 2023Article
- CD47 haltsScience advances · 2023Article
- A novel murine model of pyoderma gangrenosum reveals that inflammatory skin-gut crosstalk is mediated by IL-1β-primed neutrophils.Frontiers in immunology · 2023Article
- Cellular miR-6741-5p as a Prognostic Biomarker Predicting Length of Hospital Stay among COVID-19 Patients.Viruses · 2022Article
- Pyoderma Gangrenosum: An Updated Literature Review on Established and Emerging Pharmacological Treatments.American journal of clinical dermatology · 2022Review
- Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy.Signal transduction and targeted therapy · 2022Review
- Ets-2 deletion in myeloid cells attenuates IL-1α-mediated inflammatory disease caused by a Ptpn6 point mutation.Cellular & molecular immunology · 2021Article
- Immune-Mediated Dermatoses in Patients with Haematological Malignancies: A Comprehensive Review.American journal of clinical dermatology · 2020Review
- Pyoderma gangrenosum.Nature reviews. Disease primers · 2020Review
- Improved mouse models and advanced genetic and genomic technologies for the study of neutrophils.Drug discovery today · 2020Review
- The nonreceptor tyrosine kinase SYK drives caspase-8/NLRP3 inflammasome-mediated autoinflammatory osteomyelitis.The Journal of biological chemistry · 2020Article
- Inflammasomes in the pathophysiology of autoinflammatory syndromes.Journal of leukocyte biology · 2020Review
- Ox-LDL Causes Endothelial Cell Injury Through ASK1/NLRP3-Mediated Inflammasome Activation via Endoplasmic Reticulum Stress.Drug design, development and therapy · 2020Article
- KLICK Syndrome Linked to aFrontiers in immunology · 2020Review
- Ptpn6 inhibits caspase-8- and Ripk3/Mlkl-dependent inflammation.Nature immunology · 2020Article
- FGF1Cell death & disease · 2019Article
- Mechanisms of Inflammation in Neutrophil-Mediated Skin Diseases.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mice homozygous for the Tyr208Asn amino acid substitution in the carboxy terminus of Src homology region 2 (SH2) domain-containing phosphatase 1 (SHP-1) (referred to as Ptpn6spin mice) spontaneously develop a severe inflammatory disease resembling neutrophilic dermatosis in humans. Disease in Ptpn6spin mice is characterized by persistent footpad swelling and suppurative inflammation. Recently, in addition to IL-1α and IL-1R signaling, we demonstrated a pivotal role for several kinases such as SYK, RIPK1, and TAK1 in promoting inflammatory disease in Ptpn6spin mice. In order to identify new kinases involved in SHP-1-mediated inflammation, we took a genetic approach and discovered apoptosis signal-regulating kinases 1 and 2 (ASK1 and ASK2) as novel kinases regulating Ptpn6-mediated footpad inflammation. Double deletion of ASK1 and ASK2 abrogated cutaneous inflammatory disease in Ptpn6spin mice. This double deletion further rescued the splenomegaly and lymphomegaly caused by excessive neutrophil infiltration in Ptpn6spin mice. Mechanistically, ASK regulates Ptpn6spin-mediated disease by controlling proinflammatory signaling in the neutrophils. Collectively, the present study identifies SHP-1 and ASK signaling crosstalk as a critical regulator of IL-1α-driven inflammation and opens future avenues for finding novel drug targets to treat neutrophilic dermatosis in humans.
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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.