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Expression of the neural specific protein, GAP‐43, dramatically lengthens the cell cycle in fibroblasts
Author(s) -
Zhao Junpeng,
Yao Yajuan,
Xu Changlei,
Jiang Xiaohua,
Xu Qunyuan
Publication year - 2009
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2009.06.013
Subject(s) - neurogenesis , cell cycle , microbiology and biotechnology , neuroblast , biology , neural stem cell , cell growth , bromodeoxyuridine , restriction point , progenitor cell , cell division , cell , stem cell , cell cycle progression , biochemistry
It has been demonstrated that during neurogenesis in the mammalian brain, cell‐cycle lengthening in neuronal progenitors may cause them to switch from proliferation to neuron‐generating division. However, little is known about the cellular mechanisms involved in lengthening of the cell cycle. Growth‐associated protein‐43 (GAP‐43) is a nervous system‐specific protein whose expression in proliferating neuroblasts is related to neurogenesis. In this study, we investigated the effect of GAP‐43 on cell‐cycle progression in transgenic fibroblast cells. Using cumulative bromodeoxyuridine labeling, cell‐cycle kinetics in GAP‐43‐transgenic and control NIH 3T3 cells were analyzed. Our data demonstrate that expression of GAP‐43 in fibroblasts results in lengthening of the cell cycle compared to control fibroblasts. The mechanism by which GAP‐43 mediated this effect appeared to involve increasing the time spent by the cells in the G 1 phase of the cell cycle.