ArticleInternational journal of biological sciences2023
Keratin 17 covalently binds to alpha-enolase and exacerbates proliferation of keratinocytes in psoriasis.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 17 citations in OpenAlex.
- Therapeutic potential of polygonatum polysaccharides in modulating gut microbiota and alleviating psoriasis-like inflammation in a mouse model.Molecular and cellular biochemistry · 2026Article
- Enolase-1 and Inflammation.Biomolecules · 2026Review
- Mitochondrial Metabolic Reprogramming and Skin Immune Homeostasis: From Basic Mechanisms to Therapeutic Perspectives.Immune network · 2026Review
- GPR107 promotes autophagy secretion in psoriatic keratinocytes by inhibiting BECN1 K48-linked ubiquitination.Cell death & disease · 2026Article
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- Tm4sf19 inhibition alleviates imiquimod-induced psoriatic dermatitis by regulating inflammatory signaling pathways and keratinocyte proliferation in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- FUT11-Driven fucosylation coordinates K63 ubiquitination of keratin 17 to sustain psoriatic keratinocytes hyperproliferation.Cell communication and signaling : CCS · 2025Article
- Targeting Kupffer Cell Enolase 1 Attenuates Liver Inflammation and Injury in Hemorrhagic Shock.International journal of molecular sciences · 2025Article
- The methylation site cg06972019 regulates the succinylation-related gene ENO1 to inhibit the occurrence of erectile dysfunction.Hereditas · 2025Article
- Expression Distribution of Keratins in Normal and Pathological Corneas and the Regulatory Role of Krt17 on Limbal Stem Cells.Investigative ophthalmology & visual science · 2025Article
- Keratins 6, 16, and 17 in Health and Disease: A Summary of Recent Findings.Current issues in molecular biology · 2024Review
- CYSLTR1 antagonist inhibits Th17 cell differentiation by regulating the NF-κB signaling for the treatment of psoriasis.International journal of biological sciences · 2024Article
- Research Progress on Glycolysis Mechanism of Psoriasis.Psoriasis (Auckland, N.Z.) · 2024Review
- RNA Sequencing Reveals That the Genes Related to Cell Cycle and Glycolysis Play an Essential Role in IL-27-Induced Keratinocyte Hyperproliferation.Journal of inflammation research · 2024Article
- Targeted siRNA Therapy for Psoriasis: Translating Preclinical Potential into Clinical Treatments.ImmunoTargets and therapy · 2024Review
- Metabolic dysfunction associated steatotic liver disease in patients with plaque psoriasis: a case-control study and serological comparison.Frontiers in medicine · 2024Article
- Key Factors in the Complex and Coordinated Network of Skin Keratinization: Their Significance and Involvement in Common Skin Conditions.International journal of molecular sciences · 2023Review
- A Route for Investigating Psoriasis: From the Perspective of the Pathological Mechanisms and Therapeutic Strategies of Cancer.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated glucose metabolism is an important characteristic of psoriasis. Cytoskeletal protein keratin 17 (K17) is highly expressed in the psoriatic epidermis and contributes to psoriasis pathogenesis. However, whether K17 is involved in the dysregulated glucose metabolism of keratinocytes (KCs) in psoriasis remains unclear. In the present study, loss- and gain-of-function studies showed that elevated K17 expression was critically involved in glycolytic pathway activation in psoriatic KCs. The level of α-enolase (ENO1), a novel potent interaction partner of K17, was also elevated in psoriatic KCs. Knockdown of ENO1 by siRNA or inhibition of ENO1 activity by the inhibitor ENOBlock remarkably suppressed KCs glycolysis and proliferation. Moreover, ENO1 directly interacted with K17 and maintained K17-Ser
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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.