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Yung-Feng Liao|Institute of Cellular and Organismic Biology, Academia Sinica

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Professional ExperienceOpenClose
Research Fellow, Institute of Cellular and Organismic Biology, Academia
Associate Research Fellow, Institute of Cellular and Organismic Biology, Academia
Assistant Research Fellow, Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan.
Assistant Research Fellow, Institute of Zoology, Academia Sinica, Taipei, Taiwan.
Postdoctoral Research Fellow, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA
Postdoctoral Research Fellow, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
Ph.D., Dept. of Biochemistry and Molecular Biology, University of Georgia, Athens, GA, USA.
Adjunct Associate Professor, Department of Life Science, National Taiwan University.
Adjunct Assist./Assoc. Professor, Institute of Zoology, National Taiwan University.
Research InterestOpenClose

1. The molecular mechanisms underlying the pathogenic activity of γ-secretase in Alzheimer’s disease.
The deposition of the amyloid-β (Aβ) peptide in neuritic plaques plays a central role in the pathogenesis of Alzheimer’s disease (AD). Aβ is generated through the proteolysis of amyloid precursor protein (APP) by the sequential actions of β- and γ-secretases. We have demonstrated that a number of inflammatory molecules can modulate γ-secretase activity through various signaling pathways. Our recent data have revealed that the protein-protein interactions between γ-secretase and its substrates could be subject to endogenous regulation mediated by intracellular signaling mediators. These newly identified endogenous modulators of γ-secretase exhibit the differential regulation in governing the γ-cleavage of APP-C99 and Notch. These γ-secretase-modulating signaling pathways could thus form intrinsic networks to regulate the substrate selectivity of γ-secretase, and be superior pharmacological targets for anti-AD therapy with minimal side effects.

2. The tumorigenesis of neuroblastoma and the differentiation of neural progenitor cells.
Neuroblastoma (NB) is a heterogeneous neoplasm, and the tumor behavior of neuroblastoma is closely associated with the histological state of differentiation. We have found a number of prognostic marker proteins in human NB tumors that are tightly associated with the histological grade of differentiation and play active roles in governing the molecular mechanisms underlying the neuronal differentiation of NB. Our studies will also shed new insight to the molecular mechanisms that govern the tumor behaviors of neuroblastoma in patients.

Selected PublicationOpenClose
  1. N. Bhore, B.-J. Wang, P.-F. Wu, Y.-L. Lee, Y.-W. Chen, W.- M. Hsu, H. Lee, Y.-S. Huang, D.-I Yang, and Y.-F. Liao*. (2021) Dual-specificity phosphatase 15 (DUSP15) modulates Notch signaling by enhancing the stability of Notch protein. Mol. Neurobiol., 58: 2204-2214.
  2. P.-F. Wu, N. Bhore, Y.-L. Lee, J.-Y. Chou, Y.-W. Chen, P.-Y. Wu, W.-M. Hsu, H. Lee, Y.-S. Huang, P.-J. Lu, Y.-F. Liao*. (2020) Phosphatidylinositol-4-Phosphate 5-Kinase Type 1α Attenuates Aβ Production by Promoting Non-amyloidogenic Processing of Amyloid Precursor Protein. FASEB J., 34: 12127-12146. 
  3. P.-Y. Wu, I-S. Yu, Y.-C. Lin, Y.-T. Chang, C.-C. Chen, K.-H. Lin, T.-H. Tseng, M. Kargren, Y.-L. Tai, T.-L. Shen, Y.-L. Liu, B.-J. Wang, C.-H. Chang, W.-M. Chen, H.-F. Juan, S.-F. Huang, Y.-Y. Chan, Y.-F. Liao*, W.-M. Hsu*, and H. Lee*. (2019) Activation of Aryl Hydrocarbon Receptor by Kynurenine Impairs Progression and Metastasis of Neuroblastoma. Cancer Res., 79: 5550-5562. 
  4. P.-Y. Wu, P.-Y. Chuang, G.-D. Chang, Y.-Y. Chan, T.-C. Tsai, B.-J. Wang, K.-H. Lin, W.-M. Hsu*, Y.-F. Liao*, and H. Lee*. (2019) Novel Endogenous Ligands of Aryl Hydrocarbon Receptor Mediate Neural Development and Differentiation of Neuroblastoma. ACS Chem. Neurosci., 10: 4031-4042. 
  5. B.-J. Wang, G. M. Her, M.-K. Hu, Y.-W. Chen, Y.-T. Tung, P.-Y. Wu, W.-M. Hsu, H. Lee, L.-W. Jin, S.-P. L. Hwang, R. P.-Y. Chen, C.-J. Huang, and Y.-F. Liao*. (2017) ErbB2 regulates autophagic flux to modulate the proteostasis of APP-CTFs in Alzheimer's disease. Proc. Natl. Acad. Sci. U.S.A., 114: E3129-E3138. 
  6. Y.-T. Tung, B.-J. Wang, W.-M. Hsu, M.-K. Hu, G. M. Her, W.-P. Huang*, Y.-F. Liao*. (2014) Presenilin-1 regulates the expression of p62 to govern p62-dependent Tau degradation. Mol. Neurobiol., 49, 10-27. 
  7. A. Kapoor, B.-J. Wang, W.-M. Hsu, M.-Y. Chang, S.-M. Liang*, Y.-F. Liao*. (2013) Retinoic acid-elicited RARα/RXRα signaling attenuates Aβ production by directly inhibiting γ-secretase-mediated cleavage of amyloid precursor protein. ACS Chem. Neurosci., 4, 1093-1100. 
  8. H.-H. Chang, H. Lee, M.-K. Hu, P.-N. Tsao, H.-F. Juan, M.-C. Huang, Y.-Y. Shih, B.-J. Wang, Y.-M. Jeng, C. L. Chang, S.-F. Huang, Y.-G. Tsay, F.-J. Hsieh, K.-H. Lin*, W.-M. Hsu*, and Y.-F. Liao*. (2010) Notch1 expression predicts an unfavorable prognosis and serves as a therapeutic target of patients with neuroblastoma. Clin. Cancer Res., 16, 4411-4420. (Highlights: Selected articles from this issue by editors) 
  9. L.-H. Kuo, M.-K. Hu, W.-M. Hsu, Y.-T. Tung, B.-J. Wang, W.-W. Tsai, C.-T. Yen, and Y.-F. Liao*. (2008) TNF-α-elicited stimulation of γ-secretase is mediated by JNK-dependent phosphorylation of presenilin and nicastrin. Mol. Biol. Cell, 19, 4201-4212.  
  10. Y.-F. Liao*, Wang, B.-J., Cheng, H.-T., Kuo, L.-H., Wolfe, M. S. (2004) TNF-α, IL-1β, and IFN-γ stimulate γ-secretase-mediated cleavage of amyloid precursor protein through a JNK-dependent MAPK pathway. J. Biol. Chem. 279, 49523-49532.