In the adult mature brain, once the neurons of the central nervous system leave the ventricular, they will be permanently post mitotic, and never complete a full cell cycle again. But despite this non-mitotic state, a neuron is still capable of initiating a cell cycle. The cell cycle is a highly conserved mechanism that controls the cells decision to proliferate and regulate the process once it starts. Typically, the cell cycle is divided into four phases, namely G1 (first gap), S (DNA synthesis), G2 (second gap), and M (mitosis). The consistency of the cell cycle suppression role of Cdk5 in a variety of cell types, in stressful situations both in vivo and in vitro, proves that the nuclear localization of Cdk5 that plays an unexpected but widespread role in neuronal cell cycle suppression. The types of stress that can induce a cell cycle related neuronal death are wide ranging and include oxidation (H2O2), DNA damage (camptothecin, etoposide), as well as the Alzheimerâs peptide (AÎ²). In exploring the mechanism by which Cdk5 suppress neuronal cell cycle, our attention was drawn to the transcriptional factor E2F1. E2F1 is a well-known transcription factor that is involved in the regulation of cell proliferation, differentiation, and apoptosis through transcriptional regulation.
A journal is a periodical publication intended to further progress of science, usually by reporting new research. Most journals are highly specialized, although some of the oldest journals publish articles, reviews, editorials, short communications, letters, and scientific papers across a wide range of scientific fields. Journals contain articles that peer reviewed, in an attempt to ensure that articles meet the journal's standards of quality, and scientific validity. Each such journal article becomes part of the permanent scientific record.
Last date updated on June, 2014