Karumbayaram Saravanan, Novitch Bennett G, Patterson Michaela, Umbach Joy A, Richter Laura, Lindgren Anne, Conway Anne E, Clark Amander T, Goldman Steve A, Plath Kathrin, Wiedau-Pazos Martina, Kornblum Harley I, Lowry William E Directed differentiation of human-induced pluripotent stem cells
generates active motor neurons..
Stem cells (Dayton, Ohio).
2009;
27(4):
806-11.
Rousso David L, Gaber Zachary B, Wellik Deneen, Morrisey Edward E, Novitch Bennett G Coordinated actions of the forkhead protein Foxp1 and Hox proteins in the columnar organization of spinal motor neurons..
Neuron.
2008;
59(2):
226-40.
Dessaud Eric, Yang Lin Lin, Hill Katy, Cox Barny, Ulloa Fausto, Ribeiro Ana, Mynett Anita, Novitch Bennett G, Briscoe James Interpretation of the sonic hedgehog morphogen gradient by a temporal adaptation mechanism..
Nature.
2007;
450(7170):
717-20.
Novitch Bennett G, Wichterle Hynek, Jessell Thomas M, Sockanathan Shanthini A requirement for retinoic acid-mediated transcriptional activation in ventral neural patterning and motor neuron specification..
Neuron.
2003;
40(1):
81-95.
Qu, J. Li, X. Novitch, B. G. Zheng, Y. Kohn, M. Xie, J. M. Kozinn, S. Bronson, R. Beg, A. A. Minden, A. PAK4 kinase is essential for embryonic viability and for proper neuronal development.
Mol Cell Biol.
2003;
23( 20):
7122-33.
Bylund Magdalena, Andersson Elisabeth, Novitch Bennett G, Muhr Jonas Vertebrate neurogenesis is counteracted by Sox1-3 activity..
Nature neuroscience.
2003;
6(11):
1162-8.
Novitch, B. G. Chen, A. I. Jessell, T. M. Coordinate regulation of motor neuron subtype identity and pan-neuronal properties by the bHLH repressor Olig2.
Neuron.
2001;
31( 5):
773-89.
Novitch, B. G. Spicer, D. B. Kim, P. S. Cheung, W. L. Lassar, A. B. pRb is required for MEF2-dependent gene expression as well as cell-cycle arrest during skeletal muscle differentiation.
Curr Biol.
1999;
9( 9):
449-59.
Sellers, W. R. Novitch, B. G. Miyake, S. Heith, A. Otterson, G. A. Kaye, F. J. Lassar, A. B. Kaelin, W. G., Jr. Stable binding to E2F is not required for the retinoblastoma protein to activate transcription, promote differentiation, and suppress tumor cell growth.
Genes Dev.
1998;
12( 1):
95-106.
Skapek, S. X. Rhee, J. Kim, P. S. Novitch, B. G. Lassar, A. B. Cyclin-mediated inhibition of muscle gene expression via a mechanism that is independent of pRB hyperphosphorylation.
Mol Cell Biol.
1996;
16( 12):
7043-53.
Novitch, B. G. Mulligan, G. J. Jacks, T. Lassar, A. B. Skeletal muscle cells lacking the retinoblastoma protein display defects in muscle gene expression and accumulate in S and G2 phases of the cell cycle.
J Cell Biol.
1996;
135( 2):
441-56.
Halevy, O. Novitch, B. G. Spicer, D. B. Skapek, S. X. Rhee, J. Hannon, G. J. Beach, D. Lassar, A. B. Correlation of terminal cell cycle arrest of skeletal muscle with induction of p21 by MyoD.
Science.
1995;
267( 5200):
1018-21.
Lassar, A. B. Skapek, S. X. Novitch, B. Regulatory mechanisms that coordinate skeletal muscle differentiation and cell cycle withdrawal.
Curr Opin Cell Biol.
1994;
6( 6):
788-94.
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The development of the central nervous system (CNS) depends upon the remarkable ability of undifferentiated neural stem and progenitor cells to produce hundreds of distinct types of neurons and glial cells in a stereoyped manner. However, little is known about the molecular mechanisms that operate within neural stem and progenitor cells to control the production of each differentiated cell type in the CNS. Research in my laboratory aims to understand the process by neural stem and progenitor cells become committed to the production of different cell types, and in determining the mechanisms that control the appropriate cell division and expansion of each group of committed progenitors, as well as their eventual cell cycle exit and differentiation into mature neurons and glia. To study how this process works at a molecular level, we are focusing on the formation of three main cell types, spinal motor neurons and interneurons, which control the movement of muscles in the body, and oligodendrocytes, which support the function of motor neurons. Our main objectives are to identify the extracellular signals in developing embryos that instruct stem and progenitor cells to form these and other cell types in the central nervous system, ascertain how these signals regulate the expression and activity of transcription factors within stem and progenitor cells, and ultimately determine how these transcription factors control the division, differentiation, and identity of neurons and glia. Insights into these fundamental mechanisms are essential for determining the function of stem and progenitor cells in normal development and in diseased states, as well as for developing methods to manipulate stem and progenitor cells to direct the generation of specific types of neurons and glial cells and facilitate the repair of damaged neural circuits.
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