دورية أكاديمية

KCTD15 deregulation is associated with alterations of the NF-κB signaling in both pathological and physiological model systems

التفاصيل البيبلوغرافية
العنوان: KCTD15 deregulation is associated with alterations of the NF-κB signaling in both pathological and physiological model systems
المؤلفون: Giovanni Smaldone, Luigi Coppola, Katia Pane, Monica Franzese, Giuliana Beneduce, Rosanna Parasole, Giuseppe Menna, Luigi Vitagliano, Marco Salvatore, Peppino Mirabelli
المصدر: Scientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
بيانات النشر: Nature Portfolio, 2021.
سنة النشر: 2021
المجموعة: LCC:Medicine
LCC:Science
مصطلحات موضوعية: Medicine, Science
الوصف: Abstract Like other KCTD proteins, KCTD15 is involved in important albeit distinct biological processes as cancer, neural crest formation, and obesity. Here, we characterized the role of KCTD15 in different physiological/pathological states to gain insights into its diversified function(s). The silencing of KCTD15 in MLL-rearranged leukemia models induced attenuation of the NF-κB pathway associated with a downregulation of pIKK-β and pIKB-α. Conversely, the activation of peripheral blood T cells upon PMA/ionomycin stimulation remarkably upregulated KCTD15 and, simultaneously, pIKK-β and pIKB-α. Moreover, a significant upregulation of KCTD15 was also observed in CD34 hematopoietic stem/progenitor cells where the NF-κB pathway is physiologically activated. The association between KCTD15 upregulation and increased NF-κB signaling was confirmed by luciferase assay as well as KCTD15 and IKK-β proximity ligation and immunoprecipitation experiments. The observed upregulation of IKK-β by KCTD15 provides a novel and intriguing interpretative key for understanding the protein function in a wide class of physiological/pathological conditions ranging from neuronal development to cancer and obesity/diabetes.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2045-2322
Relation: https://doaj.org/toc/2045-2322
DOI: 10.1038/s41598-021-97775-6
URL الوصول: https://doaj.org/article/fa0ca22740494c77810ada74d6a4b4ba
رقم الأكسشن: edsdoj.fa0ca22740494c77810ada74d6a4b4ba
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20452322
DOI:10.1038/s41598-021-97775-6