Boon Seng SOH 
                       
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  Boon Seng SOH  
  Lab Location: #6-07

tel: 65869530

Email: bssoh@imcb.a-star.edu.sg
 
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  Key Publications  
 


Ng SY*, Soh BS*, Rodriguez-Muela N, Hendrickson DG, Price F, Rinn JL, Rubin LL.
Genome-wide RNA-seq of human motor neurons implicates selective ER stress activation in Spinal Muscular Atrophy.
Cell Stem Cell. 2015 Aug 26. pii: S1934-5909(15)00358-6. (*co-first author)

Soh BS*, Buac K*, Xu H*, Li E, Ng SY, Wu H, Chmielowiec J, Jiang X, Bu L, Li RA, Cowan C, Chien KR.
N-cadherin prevents the premature differentiation of second heart field progenitors in the pharyngeal mesoderm microenvironment.
Cell Res. 2014 Dec;24(12):1420-32. (Featured article) (*co-first author).

Tam WL, Lu H, Buikhuisen J, Soh BS, Lim E, Reinhardt F, Wu ZJ, Krall JA, Bierie B, Guo W, Chen X, Liu XS, Brown M, Lim B, Weinberg RA.
Protein kinase C α is a central signaling node and therapeutic target for breast cancer stem cells.
Cancer Cell
. 2013 Sep 9;24(3):347-64.

Soh BS, Wu H, Chien KR.
Cardiac regenerative medicine 2.0.
Nat Biotechnol. 2013 Mar;31(3):209-11.

Soh BS*, Zheng D, Yeo SL, Yang H, Ng SY, Wong LH, Zhang W, Li P, Nichane M, Asmat A, Wong PS, Wong PC, Su LL, Mantalaris A, Lu J, Xian W, McKeon F, Chen J, Lim EH* and Lim B*.
CD166(pos) subpopulation from differentiated human ES and iPS cells support repair of acute lung injury.
Mol Ther. 2012 Dec;20(12):2335-46. (*Co-corresponding)

Han J, Yuan P, Yang H, Zhang J, Soh BS, Li P, Lim SL, Cao S, Tay J, Orlov YL, Lufkin T, Ng HH, Tam WL, Lim B.
Tbx3 improves the germ-line competency of induced pluripotent stem cells.
Nature. 2010 Feb 25;463(7284):1096-100.

Soh BS, Song CM, Vallier L, Li P, Choong C, Yeo BH, Lim EH, Pedersen RA, Yang HH, Rao M, Lim B.
Pleiotrophin enhances clonal growth and long-term expansion of human embryonic stem cells.
Stem Cells. 2007 Dec;25(12):3029-37.

 

 

 
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  Boon Seng SOH


Boon Seng obtained his B.Sc. (1st Class Honours) from the National University of Singapore. As an A*STAR Graduate Scholarship (Overseas) recipient, he did his Ph.D thesis on the optimization of hES cell culture and differentiation towards pulmonary stem cells under the co-supervision of Prof. Athanasios Mantalaris, Ph.D (Imperial College) and Prof. Bing Lim, MD, Ph.D (Genome Institute of Singapore). In 2011, he joined the laboratory of Prof. Kenneth Chien, MD, Ph.D at Harvard University to work on the biology of multipotent cardiac stem cells, in both murine and human based model systems. His research focus has always been clinically driven with emphasis on understanding the underlying molecular and cellular mechanisms in diseases and development of therapies. His current research interests focus on modeling human diseases of the heart and lung, and establishing both in vitro and in vivo therapeutic screening platforms. He is currently a Group Leader in IMCB, under the Infrastructure, Technology and Translational Division (ITTD).

     
  Disease Modeling and Therapeutics Unit
 


My research aims to understand the underlying molecular and cellular mechanisms that underpin disease progression of the human heart and lung, and to develop novel screening platform for the evaluation of potential therapeutic intervention. At present, most drug screening processes involve screening a single cell type against a large number of compounds using defined biochemical assays in a high throughput format. However, such chemical screens often overlook the effects of a drug on an organism, which is complex and involves interactions at multiple levels that cannot be predicted using simple biochemical assays. Thus, recapitulation of the in vivo cellular microenvironment would provide a more biologically relevant surrogate to predict the response of the organism. Currently, the main research areas include the followings:

  1. Therapeutics development to enhance adult cardiomyocyte proliferation after myocardial infarction.
  2. Examination of cardiac phenotypes in other disease models.
  3. Genetic manipulation of key genes governing cardiac or pulmonary diseases, and screening for potential therapeutics.


Figure legend: Schematic summarizing the role of N-cadherin in the maintenance of anterior heart field cardiac progenitor cells (AHF-CPC).

In wild-type mice, N-cadherin expression by CPCs allows the cells to be properly adhered in the microenvironment of the pharyngeal mesoderm, thereby allowing the cells to be sufficiently exposed to paracrine factors that promote multipotency and proliferation. In addition, N-cadherin serves to maintain β-catenin levels by sequestering the molecules at the cell membrane. These allow the AHFCPCs from wild-type mice to achieve higher Wnt signaling activity as compared to single mutant (AHF-Cre;Cdh2fl/fl), where an overall downregulation of Wnt signaling activity was observed, which consequently resulted in premature differentiation of CPCs to cardiomyocytes in the AHF. Expectedly, activating Wnt signaling by overexpression of β-catenin in the double mutant (AHF-Cre; Cdh2fl/fl; bCat(e3)fl/+) was able to partially rescue the premature differentiation phenotype of the CPCs observed in Cdh2 single mutant.