Shi Yan NG
                       
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  Shi Yan NG  
  Lab Location: #5-07

email:
syng@imcb.a-star.edu.sg

 
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  Key Publications  
 

Shi-Yan Ng, Boon Seng Soh, Natalia Rodriguez-Muela, David G. Hendrickson, Feodor Price, John L. Rinn, Lee L. Rubin.
Genome-wide RNA-seq of human motor neurons implicates selective ER stress activation in Spinal Muscular Atrophy. (Advanced Online Publication:
Cell Stem Cell 27 August 2015)

Boon Seng Soh, Kristina Buac, Huansheng Xu, Edward Li, Shi-Yan Ng, Hao Wu, Jolanta Chmielowiec, Xin Jiang, Lei Bu, Ronald Li, Chad Cowan, Kenneth R. Chien (2014).
N-cadherin prevents the premature differentiation of second heart field progenitors in the pharyngeal mesoderm microenvironment.
Cell Res. 24: 1420-32.

Shi-Yan Ng, Gireesh K. Bogu, Boon Seng Soh, Lawrence W. Stanton (2013).
The long non-coding RNA RMST interacts with SOX2 to regulate neurogenesis.
Mol. Cell 51: 349-59.

Shi-Yan Ng, Lin Lin, Boon Seng Soh, Lawrence W. Stanton (2013).
Long non-coding RNAs in development and disease of the central nervous system.
Trends in Genetics 29:461-8.

Shi-Yan Ng, Lawrence W Stanton (2013).
Long non-coding RNAs in stem cell pluripotency.
Wiley Interdiscip. Rev RNA 4: 121-8.

Boon Seng Soh, Dahai Zheng, Julie Su Li Yeo, Henry He Yang, Shi-Yan Ng, Lan Hiong Wong, Wencai Zhang, Pin Li, Massimo Nichane, Atasha Asmat et al. (2012). CD166(pos) subpopulation from differentiated human ES and iPS cells support repair of acute lung injury.
Mol. Ther. 20: 2335-46.

Shi-Yan Ng, Rory Johnson, Lawrence W. Stanton (2012).
Human long non-coding RNAs promote pluripotency and neuronal differentiation by association with chromatin modifiers and transcription factors.
EMBO J. 31: 522-533.
Featured article and accompanied by Preview in EMBO J. 31: 515-516.

Xu Jiang, Hao Qing Cao, Li Ya Shi, Shi-Yan Ng, Lawrence W. Stanton, Sing Yian Chew (2012).
Nanofiber topography and sustained biochemical signaling enhance human mesenchymal stem cell neural commitment.
Acta Biomater. 8: 1290-1302.

 

 

 
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  Shi Yan NG


Shi Yan obtained her Ph.D in 2012 for her thesis work in the laboratory of Lawrence Stanton, Ph.D (Genome Institute of Singapore) on regulatory long non-coding RNAs in human cell fate determination. For her discovery of long non-coding RNAs that promote stem cell identity and neurogenesis, Shi-Yan also won the Merck Millipore Young Scientist Award (Third Prize).

From 2012 to 2015, Shi-Yan was a postdoctoral researcher at the laboratory of Lee Rubin, Ph.D at Harvard University and the Harvard Stem Cell Institute. There, she collaborated with academic partners and pharmaceutical companies on translational projects aimed at treating neurodegeneration. She has since developed a keen interest in discovering therapeutics for human neurodegenerative disorders.
     
  Neurotherapeutics Laboratory
 


The Neurotherapeutics Lab is broadly interested in using human induced pluripotent stem cells to model neurodegeneration, and using this as a platform for therapeutic discovery.

Spinal Muscular Atrophy (SMA)
SMA is a genetic disease affecting mainly spinal motor neurons, and is the leading cause of infant mortality. SMA is a result of mutations in the SMN1 gene, which produces functional SMN protein. Because loss of SMN affects primarily spinal motor neurons even though SMN is ubiquitously expressed, we are interested in the biology underlying specific motor neuron death in SMA. Preventing such motor neuron-specific death may result in a therapeutic strategy for children with SMA.
•  RNA-seq of purified patient-derived motor neurons reveals disease pathways
•  Super-enhancer analysis of purified patient-derived motor neurons reveals key    regulatory elements of disease


Amyotrophic Lateral Sclerosis (ALS)
ALS or Lou Gehrig's Disease is a progressive neurodegenerative disease affecting motor neurons in the brain and spinal cord. Approximately 90% of ALS cases are sporadic where the cause of disease is not known and the remaining are familial forms of ALS. Familial ALS means the disease is inherited.
To date, a number of genetic mutations have been associated with the disease, such as SOD1, FUS, TDP-43, HNRNPA1, C9ORF72 and so on. The long term goal of the laboratory is to model the disease using iPSCs from patients with a known ALS-causing mutation, and to extend our understanding of disease progression in familial cases to sporadic ALS so as to better diagnose, and treat ALS in future.



Frontotemporal Dementia (FTD)
FTD refers to a group of disorders causing progressive neuronal loss in the brain's frontal lobes and/or temporal lobes, the areas generally associated with language, behavior and personality. Signs and symptoms vary depending on the area of the brain affected. Some people with FTD undergo dramatic changes in their personality and become socially inappropriate, impulsive or emotionally indifferent, while others lose the ability to use language.
FTD is often misdiagnosed as psychiatric disease or Alzheimer's disease, which greatly hampers the treatment of FTD. The laboratory is especially interested in using the C9ORF72 expansion mutant model to understand the pathogenesis of FTD and using this as a platform to identify new therapeutic targets for prevention of FTD.


Astrocyte Biology
Astrocytes are the most abundant cell type in the central nervous system, and support normal neuronal health and function by providing metabolic support, modulating synaptic transmission, and their involvement in uptake and release of factors. There is strong evidence for astrocyte (non-cell autonomous) toxicity in many neurodegenerative diseases including ALS. Our ultimate goal is to be able to decipher the basis of astrocyte toxicity and to discover therapeutics that may counter neuronal death caused by diseased astrocytes.