Brian Bai
Assistant Professor
Ph.D. Training Faculty
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Department of Genetics
School of Medicine
Case Western Reserve University
Biomedical Research Building 621
2109 Adelbert Road
Cleveland, Ohio 44106-4955
Tel: (216) 368-0305
Fax: (216) 368-3432
E-mail: chunyang.bai@case.edu
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About Brian Bai
Brian Bai received his Ph.D. in Genetics from New York University in 1998. He was a postdoctoral fellow in Alexandra Joyner’s laboratory within the Developmental Genetics Program at the Skirball Institute of New York University School of Medicine. There he used mouse genetics to dissect the function of genes required for development of the spinal cord. Dr. Bai joined the Department of Genetics in 2004.
Research
The Bai laboratory focuses on the development of mammalian central nervous system, in particular the genetic and cellular mechanisms controlling the generation of diverse neurons. One area of research is how different secreted signals establish neuronal progenitor identities and how they control the differentiation of neurons.
Several signaling pathways are known to be required for neuronal development in the spinal cord. One of such important pathways that functions in the ventral spinal cord is the Hedgehog signaling pathway. We showed that all Hedgehog signaling in the spinal cord is dependent on Gli family of transcription factors. Using knock-in gene targeting technology in mice, we further delineate the in vivo function of each Gli transcription factor in the generation of spinal cord neurons.
Currently we are attempting to address the following questions. First, what are the other signaling pathways required for the specification of distinct progenitors? It is likely that more than one signaling pathways are involved in this process and we are using mouse genetics to identify them. Second, how do these pathways integrate to control proliferation and migration of neurons? Finally, what are the molecular mechanisms underlying progenitor cell fate specification, proliferation and maintenance?
Selected Publications
| Yu W, Wang Y, McDonnell K, Stephen D, Bai CB (2009) | | Patterning of ventral telencephalon requires positive function of Gli transcription factors. | | Dev Biol;334(1):264-75 | | See PubMed abstract |
| Yu W, McDonnell K, Taketo MM, Bai CB (2008) | | Wnt signaling determines ventral spinal cord cell fates in a time-dependent manner. | | Development;135(22):3687-96 | | See PubMed abstract |
| Pan Y, Bai CB, Joyner AL, Wang B (2006) | | Sonic hedgehog signaling regulates Gli2 transcriptional activity by suppressing its processing and degradation | | Mol Cell Biol;26(9):3365-77 | | See PubMed abstract |
| Bai CB, Stephen D, Joyner AL (2004) | | All mouse ventral spinal cord patterning by hedgehog is Gli dependent and involves an activator function of Gli3. | | Dev Cell.;6(1):103-15 | | See PubMed abstract |
| Nakashima M, Tanese N, Ito M, Auerbach W, Bai C, Furukawa T, Toyono T, Akamine A, Joyner AL (2002) | | A novel gene, GliH1, with homology to the Gli zinc finger domain not required for mouse development. | | Mech Dev.;119(1):21-34. | | See PubMed abstract |
| Bai CB, Auerbach W, Lee JS, Stephen D, Joyner AL (2002) | | Gli2, but not Gli1, is required for initial Shh signaling and ectopic activation of the Shh pathway. | | Development;129(20):4753-61 | | See PubMed abstract |
| Bai CB, Joyner AL (2001) | | Gli1 can rescue the in vivo function of Gli2 | | Development;128(24):5161-72 | | See PubMed abstract |
| Park HL, Bai C, Platt KA, Matise MP, Beeghly A, Hui CC, Nakashima M, Joyner AL (2000) | | Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation | | Development;127(8):1593-605. | | See PubMed abstract |
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