Tohoku University · Biochemistry, Genetics and Molecular Biology
Professor Keiko Nakayama's research lab focuses on the molecular mechanisms regulating cell survival, apoptosis, and cell cycle control during development and disease. Her work centers on the roles of key regulatory genes such as Bcl-2 family members and cyclin-dependent kinase inhibitors (CKIs), particularly in hematopoietic system development and tumorigenesis. The lab investigates how precise control of apoptosis and cell cycle progression contributes to normal physiology and how their disruption leads to developmental defects or cancer. Using genetically engineered mouse models, the lab explores the functional specificity of these regulators in lymphocyte homeostasis and tissue maintenance.
Figures are computed from collected data and may differ slightly.
Mice carrying ablated coding regions of the bcl-2 alpha and bcl-2 beta transcripts have been made. bcl-2-/- mutants are smaller but viable, although about half of them die by 6 weeks of age. As shown earlier with somatic bcl-2 gene-targeted mice, the number of lymphocytes markedly decreased within few weeks after birth while other hematopoietic lineages remained unaffected. Among lymphocytes, CD8+ T cells disappeared most quickly followed by CD4+ T cells, whereas B cells were least affected. bcl
Precise control of cell-cycle progression is believed to be critical for normal development, while oncogenesis may be a direct result of its disturbance. Cell-cycle progression is regulated predominantly by a series of serine/threonine kinases, the cyclin-dependent kinases (CDKs). The activities of the CDKs are controlled by a variety of mechanisms, and a group of molecules that inhibit CDK activity, CDK inhibitors (CKIs), has recently become the focus of interest, particularly in the fields of
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