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Nek2 (EC 220.127.116.11), also known as Never in Mitosis (NIMA) related kinase 2, is a 48 kDa homodimeric serine/threonine kinase that is regulated by the cell cycle and is involved in separation of the centrosomes at the start of mitosis.
Nek2 (EC 18.104.22.168), also known as Never in Mitosis (NIMA) related kinase 2, is a 48 kDa homodimeric serine/threonine kinase that is regulated by the cell cycle. Nek2 is involved in separation of the centrosomes at the start of mitosis, which ensures proper chromosome separation upon cell division.
Nek2 is localized to the centrosomes and is a member of the Nek family of kinases of which there are eleven members. All Nek kinases have an N-terminal kinase domain and a C-terminal domain containing several regulatory motifs. The regulatory domain differs in size between Nek kinases allowing them to perform different roles within the cell cycle. At least three Nek2 variants exist, Nek2A, Nek2B and Nek2A-T, which result from alternate gene splicing and differ in the length of their C-terminus.
Nek2A dissolves the links between the two centrioles of the centrosome during the G2 phase of the cell cycle. It does this by phosphorylating rootletin, a filamentous linker between the two centrioles, and C-Nap1, which attaches rootletin to the centriole. Phosphorylation allows centriolar separation and the formation of spindle poles enabling correct chromosome separation during mitosis.
Nek2 is overexpressed in numerous cancers, which commonly have an abnormal number of chromosomes, and is associated with cell survival and drug resistance. Inhibition of Nek2 reduces cell growth and increases susceptibility to chemotherapeutic treatments and so Nek2 is of interest in cancer research.
Tocris offers the following scientific literature for Nek2 Kinase to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the main targets for cancer metabolism researchers. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways. These distinct metabolic circuits could provide viable cancer therapeutic targets.
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.