User:Ian Tay: Difference between revisions
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==Contact Info== | ==Contact Info== | ||
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*MIT | *MIT | ||
*Blg 16-760, Engelward Laboratory | *Blg 16-760, Engelward Laboratory | ||
*iantayATmitDOTedu | |||
==Education== | |||
*2011 - present: MIT | |||
*2007 - 2010: Imperial College London, UK | |||
==Research interests== | ==Research interests== | ||
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==Current research== | ==Current research== | ||
I am working with Prof. Bevin Engelward and Dr. Scott Floyd at the Koch Institute to study how tumor cells respond to DNA damaging chemotherapeutic agents and genes that confer cellular resistance to those drugs. | |||
Currently I am working on 2 projects: | |||
1. To design a screen that will allow us to identify genes that can potentially affect cellular resistance to radiotherapy and chemotherapy via modulation of DNA damage and repair kinetics. | |||
2. To study the effects of cell cycle on the evolution and resolution of DNA damage after chemotherapeutic agent treatment. | |||
Feel free to talk to me in the lab about what I do! | |||
==Previous projects== | ==Previous projects== | ||
Development of a bioartificial hemodialysis device | |||
Investigating pore formation in endothelial cells by mechanical stimulation | *Development of a bioartificial hemodialysis device | ||
- When a patient suffers from chronic kidney failure, it is very likely that the patient will have to undergo dialysis for the rest of his/her life. Current dialysis methods are insufficient in that they result in drastic swings in waste and electrolyte concentrations in the blood as a result of the periodic nature of dialysis. They are also unable to replenish hormones and metabolites that normal kidney tubule cells produce in the human body as the dialysis machine has no living components. | |||
- In this project, my group designed and tested a bioartificial hemodialysis device whereby live kidney tubule cells are seeded onto the dialysis fibers of the device in an attempt to make the device suitable for a complete renal replacement therapy. | |||
*Investigating pore formation in endothelial cells by mechanical stimulation | |||
- Pore formation in endothelial cells is an event in the body that is critical to biological processes such as leukocyte trafficking in blood vessels and aqueous humor drainage in the Schlemm’s canal of the eye. It has been hypothesised that pore formation in endothelial cells is initiated by forces exerted by leukocytes or pressure gradients across the drainage system of the eye. | |||
- In this project, I designed a setup using a halbach array of magnets and magnetic microbeads to stimulate pore formation in endothelial cells. With the setup, I was able to observe that the magnetic beads were able to pass through a confluent monolayer of endothelial cells, mimicking pore formation. | |||
*Long non-coding RNAs in early neuronal differentiation | |||
- For several years, most of the genomic DNA in human cells were thought of as 'junk'. However, a huge percentage of these 'junk' DNA are being actively transcribed at least at some period of time during a human's lifespan. The transcripts of these 'junk' DNA are called long non-coding RNAs (linc- or lnc-RNA) if they are more than 200nt long and do not code for a polypeptide. Some of these RNAs play an important role in gene regulation, especially during embryonic development. For example, the linc-RNA named XIST is extremely important in sliencing the entire X chromosome in female cells as a mechanism for X-chromosome dosage compensation. | |||
- In my project, I studied a novel linc-RNA that becomes highly expressed when embryonic stem cells are coerced into differentiation along the neuronal lineage. This linc-RNA was shown to be interacting with chromosome modelling proteins and was also shown to be co- and anti- expressed with particular genes in its immediate vicinity. We think that this linc-RNA may be a crucial/master regulator of downstream genes and ultimately drive neuronal differentiation. | |||
Latest revision as of 20:08, 25 February 2013
Contact Info
- Ian Tay
- MIT
- Blg 16-760, Engelward Laboratory
- iantayATmitDOTedu
Education
- 2011 - present: MIT
- 2007 - 2010: Imperial College London, UK
Research interests
- DNA damage and repair
- Cellular responses to chemo-therapeutics
- Long non-coding RNA
Current research
I am working with Prof. Bevin Engelward and Dr. Scott Floyd at the Koch Institute to study how tumor cells respond to DNA damaging chemotherapeutic agents and genes that confer cellular resistance to those drugs.
Currently I am working on 2 projects:
1. To design a screen that will allow us to identify genes that can potentially affect cellular resistance to radiotherapy and chemotherapy via modulation of DNA damage and repair kinetics.
2. To study the effects of cell cycle on the evolution and resolution of DNA damage after chemotherapeutic agent treatment.
Feel free to talk to me in the lab about what I do!
Previous projects
- Development of a bioartificial hemodialysis device
- When a patient suffers from chronic kidney failure, it is very likely that the patient will have to undergo dialysis for the rest of his/her life. Current dialysis methods are insufficient in that they result in drastic swings in waste and electrolyte concentrations in the blood as a result of the periodic nature of dialysis. They are also unable to replenish hormones and metabolites that normal kidney tubule cells produce in the human body as the dialysis machine has no living components.
- In this project, my group designed and tested a bioartificial hemodialysis device whereby live kidney tubule cells are seeded onto the dialysis fibers of the device in an attempt to make the device suitable for a complete renal replacement therapy.
- Investigating pore formation in endothelial cells by mechanical stimulation
- Pore formation in endothelial cells is an event in the body that is critical to biological processes such as leukocyte trafficking in blood vessels and aqueous humor drainage in the Schlemm’s canal of the eye. It has been hypothesised that pore formation in endothelial cells is initiated by forces exerted by leukocytes or pressure gradients across the drainage system of the eye.
- In this project, I designed a setup using a halbach array of magnets and magnetic microbeads to stimulate pore formation in endothelial cells. With the setup, I was able to observe that the magnetic beads were able to pass through a confluent monolayer of endothelial cells, mimicking pore formation.
- Long non-coding RNAs in early neuronal differentiation
- For several years, most of the genomic DNA in human cells were thought of as 'junk'. However, a huge percentage of these 'junk' DNA are being actively transcribed at least at some period of time during a human's lifespan. The transcripts of these 'junk' DNA are called long non-coding RNAs (linc- or lnc-RNA) if they are more than 200nt long and do not code for a polypeptide. Some of these RNAs play an important role in gene regulation, especially during embryonic development. For example, the linc-RNA named XIST is extremely important in sliencing the entire X chromosome in female cells as a mechanism for X-chromosome dosage compensation.
- In my project, I studied a novel linc-RNA that becomes highly expressed when embryonic stem cells are coerced into differentiation along the neuronal lineage. This linc-RNA was shown to be interacting with chromosome modelling proteins and was also shown to be co- and anti- expressed with particular genes in its immediate vicinity. We think that this linc-RNA may be a crucial/master regulator of downstream genes and ultimately drive neuronal differentiation.
