High impact information on CCNA2

• Their cyclin A and B expression level suggests that they are in the mitotic phase of the cell cycle [1].
• Matrix-independent activation of phosphatidylinositol 3-kinase, Stat3, and cyclin A-associated Cdk2 Is essential for anchorage-independent growth of v-Ros-transformed chicken embryo fibroblasts [2].
• c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2 [3].
• We conclude that up-regulation of cyclin A expression and CDK2 activity can represent important link between the c-Jun protein, cell cycle machinery, and programmed cell death pathway in leukemic cells [3].
• Transient induction of cyclin A in loaded chicken skeletal muscle [4].

Biological context of CCNA2

• These data show that the cell cycle protein cyclin A is induced in fiber-associated cells during the early growth response in loaded ALD but also implicate an activation of interstitial cells as playing an early role in this model for muscle growth [4].

Other interactions of CCNA2

• In vitro kinase assays demonstrated a corresponding massive activation of the cyclin A-regulated, cyclin-dependent kinase 2 but not of cyclin-dependent kinase 2 protein level in muscle homogenates after 1.5 days of muscle loading [4].

Analytical, diagnostic and therapeutic context of CCNA2

• Immunoblotting analysis identified that cyclin A protein per total protein was dramatically increased in ALD muscle after 1.5 days of loading but returned to control level at 7 days [4].
• Immunofluorescence experiments demonstrated that the increase of cyclin A in 1.5 days of loaded ALD was primarily confined to nuclei of interstitial cells (92%) but was also found in fiber-associated cells (8%) [4].

References