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Research Interests
The overall research interests of this laboratory are to understand, at the molecular and cellular levels, how the human retroviruses, human immunodeficiency virus (HIV) and human T-cell leukemia virus (HTLV), cause AIDS and cancer, respectively. We are also developing gene therapy reagents and modeling these reagents utilizing the SCID-hu mouse, which allows stem cell reconstitution and thymic T-cell development. Some of the specific projects ongoing in this laboratory are: 1. The mechanism by which HIV-1 causes CD4+ T-cell death is unknown. We have found that HIV-1 causes perturbation of the cell cycle, leading to arrest of the cells at a particular point in the cycle. Furthermore, this ability of HIV-1 to arrest T-cells can be abrogated by specific mutations within one of the non-structural genes of the virus. We are investigating the role of this gene, termed vpr, and the specific cell cycle kinases, cyclins and cell cycle inhibitors that may be involved in this process. 2. Immune reconstitution is theoretically a viable approach to AIDS therapy. However, the new T-cells need to be protected from the effects of residual HIV-1. We are modeling gene therapy utilizing the SCID-hu mouse for introduction of "protected" CD34+ stem cells, reconstitution of the SCID-hu animal and finally, challenge with HIV-1. This is the only model for human stem cell gene therapy, and allows for more rapid experimental design of vectors, reagents, etc.
The overall research interests of this laboratory are to understand, at the molecular and cellular levels, how the human retroviruses, human immunodeficiency virus (HIV) and human T-cell leukemia virus (HTLV), cause AIDS and cancer, respectively. We are also developing gene therapy reagents and modeling these reagents utilizing the SCID-hu mouse, which allows stem cell reconstitution and thymic T-cell development. Some of the specific projects ongoing in this laboratory are: 1. The mechanism by which HIV-1 causes CD4+ T-cell death is unknown. We have found that HIV-1 causes perturbation of the cell cycle, leading to arrest of the cells at a particular point in the cycle. Furthermore, this ability of HIV-1 to arrest T-cells can be abrogated by specific mutations within one of the non-structural genes of the virus. We are investigating the role of this gene, termed vpr, and the specific cell cycle kinases, cyclins and cell cycle inhibitors that may be involved in this process. 2. Immune reconstitution is theoretically a viable approach to AIDS therapy. However, the new T-cells need to be protected from the effects of residual HIV-1. We are modeling gene therapy utilizing the SCID-hu mouse for introduction of "protected" CD34+ stem cells, reconstitution of the SCID-hu animal and finally, challenge with HIV-1. This is the only model for human stem cell gene therapy, and allows for more rapid experimental design of vectors, reagents, etc.
研究兴趣
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Anjie Zhen,Shallu Tomer,Li Wang,Ng Hwee,Wally Wennerberg, Jeyashree Alagarsamy,Valerie Rezek,Heather Martin,Mayra Carrillo,Scott G. Kitchen,Irvin S. Y. Chen, Steven Lee,
MOLECULAR THERAPYno. 4 (2023): 71-72
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Isaac M Barber-Axthelm, Valerie Barber-Axthelm, Kai Yin Sze,Anjie Zhen,Gajendra W Suryawanshi,Irvin Sy Chen,Jerome A Zack,Scott G Kitchen,Hans-Peter Kiem,Christopher W Peterson
Anjie Zhen,Christopher W Peterson,Mayra A Carrillo,Sowmya Somashekar Reddy, Cindy S Youn, Brianna B Lam, Nelson Y Chang,Heather A Martin,Jonathan W Rick,Jennifer Kim, Nick C Neel,Valerie K Rezek,
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