Редактирование: FBXW7

F-box/WD repeat-containing protein 7 (Archipelago homolog) (hAgo) (F-box and WD-40 domain-containing protein 7) (F-box protein FBX30) (SEL-10) (hCdc4) [FBW7] [FBX30] [SEL10]

==Publications==

{{medline-entry
|title=[[MYC]] Modulation around the CDK2/p27/SKP2 Axis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28665315
|abstract=[[MYC]] is a pleiotropic transcription factor that controls a number of fundamental cellular processes required for the proliferation and survival of normal and malignant cells, including the cell cycle. [[MYC]] interacts with several central cell cycle regulators that control the balance between cell cycle progression and temporary or permanent cell cycle arrest (cellular senescence). Among these are the cyclin E/A/cyclin-dependent kinase 2 (CDK2) complexes, the CDK inhibitor p27  (p27) and the E3 ubiquitin ligase component S-phase kinase-associated protein 2 (SKP2), which control each other by forming a triangular network. [[MYC]] is engaged in bidirectional crosstalk with each of these players; while [[MYC]] regulates their expression and/or activity, these factors in turn modulate [[MYC]] through protein interactions and post-translational modifications including phosphorylation and ubiquitylation, impacting on [[MYC]]'s transcriptional output on genes involved in cell cycle progression and senescence. Here we elaborate on these network interactions with [[MYC]] and their impact on transcription, cell cycle, replication and stress signaling, and on the role of other players interconnected to this network, such as [[CDK1]], the retinoblastoma protein (pRB), protein phosphatase 2A (PP2A), the F-box proteins [[FBXW7]] and [[FBXO28]], the RAS oncoprotein and the ubiquitin/proteasome system. Finally, we describe how the [[MYC]]/CDK2/p27/SKP2 axis impacts on tumor development and discuss possible ways to interfere therapeutically with this system to improve cancer treatment.

|keywords=* cancer
* cell cycle
* cellular senescence
* oncogenes
* phosphorylation
* post-translational modifications
* protein–protein interactions
* the ubiquitin/proteasome system
* transcription
* tumor suppressor genes
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541307
}}