ArticleCell death & disease2012
Anti-apoptotic effects of suppressor of cytokine signaling 3 and 1 in psoriasis.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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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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
52 citing papers in PubMed, 88 citations in OpenAlex.
- First-in-human studies of seletalisib, an orally bioavailable small-molecule PI3Kδ inhibitor for the treatment of immune and inflammatory diseases.European journal of clinical pharmacology · 2017Trial
- αCGRP Activates PI3K/Akt to Exert Antioxidant Effects and Improve the Survival Rate and Functional Status of Cortical Neurons.Molecular neurobiology · 2026Article
- Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026Review
- Reduction of primary tumor growth and metastasis in models of triple-negative breast cancer following tilorone administration via type I interferon signaling.Breast cancer research : BCR · 2026Article
- BIRC5 modulates keratinocyte proliferation and apoptosis via PI3K/AKT/mTOR-mediated autophagy.Scientific reports · 2026Article
- Article
- In vitro HIV DNA integration in STAT3 drives T cell persistence-A model of HIV-associated T cell lymphoma.PLoS pathogens · 2025Article
- CARD14 signalosome formation is associated with its endosomal relocation and mTORC1-induced keratinocyte proliferation.The Biochemical journal · 2024Article
- Prevalence and trends of contact sensitization in patients with psoriasis in Lithuania.JAAD international · 2024Article
- Targeting dependency on a paralog pair of CBP/p300 against de-repression of KREMEN2 in SMARCB1-deficient cancers.Nature communications · 2024Article
- Inflammatory Skin Diseases: Focus on the Role of Suppressors of Cytokine Signaling (SOCS) Proteins.Cells · 2024Review
- SOCS1 and SOCS3 as key checkpoint molecules in the immune responses associated to skin inflammation and malignant transformation.Frontiers in immunology · 2024Review
- β-endorphin suppresses ultraviolet B irradiation-induced epidermal barrier damage by regulating inflammation-dependent mTORC1 signaling.Scientific reports · 2023Article
- miRNA-559 and MTDH as possible diagnostic markers of psoriasis: Role of PTEN/AKT/FOXO pathway in disease pathogenesis.Molecular and cellular biochemistry · 2023Article
- Chinese Medicine as Supporting Therapy for Psoriasis: Past, Present, and Future.Chinese journal of integrative medicine · 2023Review
- Predominant Role of mTOR Signaling in Skin Diseases with Therapeutic Potential.International journal of molecular sciences · 2022Review
- The regulation of skin homeostasis, repair and the pathogenesis of skin diseases by spatiotemporal activation of epidermal mTOR signaling.Frontiers in cell and developmental biology · 2022Review
- Post-Translational Modifications in Atopic Dermatitis: Current Research and Clinical Relevance.Frontiers in cell and developmental biology · 2022Review
- Dysregulation of Survivin-Targeting microRNAs in Autoimmune Diseases: New Perspectives for Novel Therapies.Frontiers in immunology · 2022Review
- Novel Therapeutic Target(s) for Psoriatic Disease.Frontiers in medicine · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Because of their genetically determined capacity to respond to pro-inflammatory stimuli, keratinocytes have a crucial role in the pathogenesis of psoriasis. Upon IFN-γ and TNF-α exposure, psoriatic keratinocytes express exaggerated levels of inflammatory mediators, and show aberrant hyperproliferation and terminal differentiation. The thickening of psoriasic skin also results from a peculiar resistance of keratinocytes to cytokine-induced apoptosis. In this study, we investigated on the molecular mechanisms concurring to the resistance of psoriatic keratinocytes to cell death, focusing on the role having suppressor of cytokine signaling (SOCS)1 and SOCS3, two molecules abundantly expressed in IFN-γ/TNF-α-activated psoriatic keratinocytes, in sustaining anti-apoptotic pathways. We found that SOCS1 and SOCS3 suppress cytokine-induced apoptosis by sustaining the activation of the PI3K/AKT pathway in keratinocytes. The latter determines the activation of the anti-apoptotic NF-κB cascade and, in parallel, the inhibition of the pro-apoptotic BAD function in keratinocytes. For the first time, we report that phosphorylated AKT and phosphorylated BAD are strongly expressed in lesional psoriatic skin, compared with healthy or not lesional skin, and they strictly correlate to the high expression of SOCS1 and SOCS3 molecules in the psoriatic epidermis. Finally, the depletion of SOCS1 and SOCS3, as well as the chemical inactivation of PI3K activity in psoriatic keratinocytes, definitively unveils the role of PI3K/AKT cascade on the resistance of diseased keratinocytes to apoptosis.
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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.