دورية أكاديمية

IKBKE-driven TPL2 and MEK1 phosphorylations sustain constitutive ERK1/2 activation in tumor cells

التفاصيل البيبلوغرافية
العنوان: IKBKE-driven TPL2 and MEK1 phosphorylations sustain constitutive ERK1/2 activation in tumor cells
المؤلفون: Serkan Ismail Göktuna
المصدر: EXCLI Journal : Experimental and Clinical Sciences, Vol 21, Pp 436-453 (2022)
بيانات النشر: IfADo - Leibniz Research Centre for Working Environment and Human Factors, Dortmund, 2022.
سنة النشر: 2022
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
LCC:Biology (General)
مصطلحات موضوعية: cancer cells, signal transduction, ikkɛ (ikbke), tpl2 (map3k8), mek1 (map2k1), erk1/2 (mapk1/2), Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Biology (General), QH301-705.5
الوصف: IKBKE have been associated with numerous cancers. As a result, IKBKE have emerged as potential target for cancer therapy. Accumulating evidence support that IKBKE orchestrate tumor cell survival in cancers. Here we evaluated the possible link between IKBKE and ERK phosphorylation. The effects of IKBKE silencing on MAPK activation in tumor vs. normal cells were evaluated via WB and RT-PCR. Ectopically expressed IKBKE, TPL2 or MEK1 constructs were used to examine the possible interactions among them via co-IP. In vitro kinase assays were performed to understand nature of the observed interactions. In tumors, IKBKE regulates MEK/ERK constitutive activations in vitro and in vivo. IKBKE and TPL2 physically interact and this interaction leads to TPL2 phosphorylation. We describe here a novel regulatory link between IKBKE and constitutive ERK1/2 activation in tumor cells. This new circuitry may be relevant for tumor cell survival in various malignancies.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1611-2156
Relation: https://www.excli.de/index.php/excli/article/view/4578; https://doaj.org/toc/1611-2156
DOI: 10.17179/excli2021-4578
URL الوصول: https://doaj.org/article/61f437f8d8724caf8f6e5af7c053c9a1
رقم الأكسشن: edsdoj.61f437f8d8724caf8f6e5af7c053c9a1
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16112156
DOI:10.17179/excli2021-4578