TY - JOUR T1 - B-Myb and C-Myb Play Required Roles in Neuronal Apoptosis Evoked by Nerve Growth Factor Deprivation and DNA Damage JF - The Journal of Neuroscience JO - J. Neurosci. SP - 8720 LP - 8725 DO - 10.1523/JNEUROSCI.1821-04.2004 VL - 24 IS - 40 AU - David X. Liu AU - Subhas C. Biswas AU - Lloyd A. Greene Y1 - 2004/10/06 UR - http://www.jneurosci.org/content/24/40/8720.abstract N2 - Activation of cell cycle elements plays a required role in neuronal apoptosis associated with both development and neurodegenerative disorders. We demonstrated previously that neuron survival requires gene repression mediated by the cell cycle transcription factor E2F (E2 promoter binding factor) and that apoptotic stimuli lead to de-repression of E2F-regulated genes and consequent death. However, the downstream mediators of such death have been unclear. The transcription factors B- and C-myb are E2F-regulated genes that are induced in neurons by apoptotic stimuli. Here, we examine the role of B- and C-myb induction in neuron death. Antisense and siRNA constructs that effectively block the upregulation of B- and C-myb provide substantial protection against death of cultured neuronal PC12 cells, sympathetic neurons, and cortical neurons elicited by either NGF withdrawal or DNA damage. There is also significant protection from death induced by direct E2F-dependent gene de-repression. Our findings thus establish required roles for B- and C-myb in neuronal apoptosis. ER -