CDKs and CDK-Interacting Proteins/Kinase-Inhibitory Proteins in Human Health and Disease

Dear Colleagues,

Decades of cell cycle-related research have led to unravelling the molecular mechanisms of cell cycle progression. In this context, cyclins, cyclin-dependent kinases (CDKs) and cyclin-dependent kinase regulators (CKRs) are undoubtedly primary cell cycle regulators. However, to date, the paradigm that they are only involved in ensuring correct cell division has been overcome. Indeed, it is consolidated that they have additional roles, such as transcriptional regulation, cell differentiation, DNA damage response, cytoskeleton remodeling, regulation of metabolism, cell death, stem cell fate, tissue regeneration and development. Despite more than 30 years of research, the full comprehension of their physiological roles is still lacking due to their multiplicity, tissue specificity and frequent functional overlapping. In parallel, even if the known pathological implications of their alterations range from the onset of human tumors to diseases related to growth, development and metabolism, new evidence suggests their involvement in a broader spectrum of genetic and epigenetic pathologies. Finally, in the era of target therapy, the comprehension of the regulatory mechanisms of cyclin/CDK complexes has made it possible to formulate new anti-cancer drugs targeting cell cycle proteins, as well as recognize the mechanisms underlying sensitivity and resistance to the related therapies, and develop alternative therapeutic strategies.

This Special Issue will cover and focus on the role of cell cycle-related proteins in health and various pathologies, particularly cancer and growth-related diseases, as well as emerging therapeutic strategies, and the role of cell cycle-related proteins as sensitizing or resistance factors in therapy.

Dr. Emanuela Stampone
Prof. Dr. Adriana Borriello
Dr. Debora Bencivenga
Guest Editors

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• Cell cycle
• CDKs
• cyclins
• CIP/Kip proteins
• INK4 family
• p53
• transcriptional regulation
• DNA damage
• cytoskeleton, metabolism, senescence, cell death, cell commitment and differentiation
• stem cell
• tissue regeneration
• embryogenesis
• development
• growth-related diseases
• cancer, sensitivity/resistance to therapy
• target therapy