Publications
For more publications, visit Pubmed, Google Scholar, and ORCID.
The Genetics of Primary Microcephaly
Jayaraman D, Bae BI, Walsh CA. (2018) Annu. Rev. Genomics Hum. Genet. 19: 177-200. Genetic microcephaly and other related cerebral cortical malformations are comprehensively reviewed.
ASPM Knockout Ferret Reveals an Evolutionary Mechanism Governing Cerebral Cortical Size
Johnson MB, Sun X, Kodani A, Borges-Monroy R, Girskis KM, Ryu SC, Wang PP, Patel K, Gonzalez DM, Woo YM, Yan Z, Liang B, Smith RS, Chatterjee M, Coman D, Papademetris X, Staib LH, Hyder F, Mandeville JB, Grant PE, Im K, Kwak H, Engelhardt JF, Walsh CA*, Bae BI*. (2018) Nature. 556(7701): 370-375. (*, co-corresponding) Highlighted in Cell 173: 1059-1061 and Nature Rev. Neurosci. 19: 320-321. Genetically engineered ferrets are a superb and rigorous model organism for cerebral cortical development research.
Microcephaly Proteins Wdr62 and Aspm Define a Mother Centriole Complex Regulating Centriole Biogenesis, Apical Complex, and Cell Fate
Jayaraman D^, Kodani A^, Gonzalez DM, Mancias JD, Mochida GH, Vagnoni C, Johnson J, Krogan N, Harper JW, Reiter JF, Yu TW*, Bae BI*, Walsh CA*. (2016) Neuron. 92(4): 813-828. (*, co-corresponding; ^, co-first) (cover article). Mechanisms by which the centrosomal proteins WDR62 and ASPM together control cerebral cortical development.
Mutations in Human Accelerated Regions Disrupt Cognition and Social Behavior
Doan RN, Bae BI, Cubelos B, Chang C, Hossain AA, Al-Saad S, Mukaddes NM, Oner O, Al-Saffar M, Balkhy S, Gascon GG; Homozygosity Mapping Consortium for Autism, Nieto M, Walsh CA. (2016) Cell. 167(2): 341-354. Mutations in “human accelerated regions”, specific noncoding regions that are uniquely distinct in humans, cause autism spectrum disorder.
Allele-Specific Regulation of Mutant Huntingtin by Wig1, a Downstream Target of P53
Kim SH, Shahani N, Bae BI, Sbodio JI, Chung Y, Nakaso K, Paul BD, Sawa A. (2016) Hum. Mol. Genet. 25(12): 2514-2524. Wig1, a downstream target of the transcription factor p53, plays an important role in stabilizing mutant Huntingtin mRNA and thereby accelerating Huntington’s Disease pathology.
Genetic Changes Shaping the Human Brain
Bae BI, Jayaraman D, Walsh CA. (2015) Dev. Cell. 32(4): 423-434. How genetic changes during a lifetime or during evolution affect human brain development is reviewed with noteworthy examples.
New Functions and Signaling Mechanisms for the Class of Adhesion G Protein-Coupled Receptors
Liebscher I, Ackley B, Araç D, Ariestanti DM, Aust G, Bae BI, Bista BR, Bridges JP, Duman JG, Engel FB, Giera S, Goffinet AM, Hall RA, Hamann J, Hartmann N, Lin HH, Liu M, Luo R, Mogha A, Monk KR, Peeters MC, Prömel S, Ressl S, Schiöth HB, Sigoillot SM, Song H, Talbot WS, Tall GG, White JP, Wolfrum U, Xu L, Piao X. (2014) Ann. N. Y. Acad. Science. 1333: 43-64. Advancements in understanding the functions, mechanisms, and disease associations of adhesion G protein-coupled receptors are discussed.
Evolutionarily Dynamic Alternative Splicing of Gpr56 Regulates Regional Cerebral Cortical Patterning
Bae BI*, Tietjen I*, Atabay KD, Evrony GD, Johnson MB, Asare E, Wang PP, Murayama AY, Im K, Lisgo SN, Overman L, Šestan N, Chang BS, Barkovich AJ, Grant PE, Topçu M, Politsky J, Okano H, Piao X, Walsh CA. (2014) Science. 343(6172): 764-768. (*, co-first). Evolutionarily dynamic promoters of GPR56 regulate regional cerebral cortical folding, neural stem cell proliferation, and, potentially, cortical evolution.
What Are Mini-Brains?
Bae BI, Walsh CA. (2013) Science. 342(6155): 200-201. Some speculations on how human cerebral organoids, or three-dimensional in vitro culture systems for human neural stem cells, may benefit the studies of brain development in health and disease.
Nitric Oxide-Induced Nuclear Gapdh Activates P300/Cbp and Mediates Apoptosis
Sen N, Hara MR, Kornberg MD, Cascio MB, Bae BI, Shahani N, Thomas B, Dawson TM, Dawson VL, Snyder SH, Sawa A. (2008) Nat. Cell Biol. 10(7): 866-873. GAPDH initiates a cell death cascade when stimulated with nitric oxide.
Neuroprotection by Pharmacologic Blockade of the Gapdh Death Cascade
Hara MR, Thomas B, Cascio MB, Bae BI, Hester LD, Dawson VL, Dawson TM, Sawa A, Snyder SH. (2006) Proc Natl Acad Sci USA. 103(10): 3887-3889. Blocking the GAPDH death cascade using low doses of deprenyl provides neuroprotection in a pharmacologic mouse model of Parkinson’s Disease.
Mutant Huntingtin: Nuclear Translocation and Cytotoxicity Mediated by Gapdh
Bae BI, Hara MR, Cascio MB, Wellington CL, Hayden MR, Ross CA, Ha HC, Li XJ, Snyder SH, Sawa A. (2006) Proc. Natl. Acad. Sci. USA. 103(9): 3405-3409. Nuclear localization of mutant Huntingtin, a critical step in the pathogenesis of Huntington’s Disease, is mediated by GAPDH.
P53 Mediates Cellular Dysfunction and Behavioral Abnormalities in Huntington's Disease
Bae BI, Xu H, Igarashi S, Fujimuro M, Agrawal N, Taya Y, Hayward SD, Moran TH, Montell C, Ross CA, Snyder SH, Sawa A. (2005) Neuron. 47(1): 29-41. Highlighted in Neuron 47(1): 1-3, Nature 436(7048): 154-155, Science 310(5745): 43-45, The Lancet Neurology 4(9): 528-529, and Chemical & Engineering News 53(29): 9. The transcription factor and tumor suppressor p53 links nuclear and mitochondrial pathologies characteristic of Huntington’s Disease.
Inositol Hexakisphosphate Kinase-2, a Physiologic Mediator of Cell Death
Nagata E, Luo HR, Saiardi A, Bae BI, Suzuki N, Snyder SH. (2005) J. Biol. Chem. 280(2): 1634-1640. Endogenous InsP6K2, by generating InsP7, provides physiologic regulation of the apoptotic process.
Mechanisms of Neuronal Cell Death in Huntington's Disease
Sawa A, Tomoda T, Bae BI. (2003) Cytogenet. Genome Res. 100(1-4): 287-295. A review of the current understanding on mechanisms of how mutant Huntingtin can elicit cytotoxicity, as well as how the selective sets of neuronal cell death occur in Huntington’s Disease brains.
A Mammalian Iron Atpase Induced by Iron
Barañano DE, Wolosker H, Bae BI, Barrow RK, Snyder SH, Ferris CD. (2000) J. Biol. Chem. 275(20): 15166-15173. A characterization of an ATP-requiring iron transporter for iron efflux in mammalian cells.