| ORIGINAL ARTICLE |
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| Year : 2006 | Volume
: 21
| Issue : 1 | Page : 1-11 |
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Hypothetical Model for the Suppression of Stress Induced Apoptosis in Hematopoietic Stem Cells by Bcl-2 Mutants
Gurudatta U Gangenahalli1, Yogeah Kumar Verma1, Vimal Kishor Singh1, Pallavi Gupta1, Ramesh Chandra2, Rakesh Kumar Sharma3, HG Raj4
1 Stem Cell Gene Therapy Research Group, Delhi, India
2 Dr. B. R. Ambedkar Centre for Biomedical Research, Delhi, India
3 INMAS, Delhi, India
4 Department of Biochemistry, V. P. Chest Institute, Delhi, India
Correspondence Address:
Gurudatta U Gangenahalli
Stem Cell Gene Therapy Research Group (INMAS), Lucknow Road, Timar Pur, Delhi-110054
India
 Source of Support: None, Conflict of Interest: None  | Check |
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Hematopoietic stem cells (HSC), which are responsible for maintaining continuous pool of blood cells, are being used for bone marrow transplantation (BMT). However, the programmed cell death/ apoptosis poses a serious problem for their optimum proliferation and differentiation after radio- and/ or chemotherapy. The role of Bcl-2 (B Cell Lymphoma) protein, a Bcl-2 family member, is well established in suppressing apoptosis of HSC on irradiation and serum withdrawal. The anti-apoptotic activity of Bcl-2 is regulated by inter- and intra-family homo-/ heterodimerization. Here we are proposing that the potential of Bcl-2 and its survival enhancing mutants, such as D34A and S70E, may be harnessed (gene therapy) to suppress the radiation and growth factor withdrawal induced apoptosis provided the neoplastic outcomes of these genes are regulated. The suggested hypothetical model is likely to be helpful in treating blood borne disorders and radiation injury through BMT. |
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