| My laboratory has been actively involved in skeletal muscle research for the past 10 years. We have discovered that, in addition to the positive regulators of myogenesis, there are negative regulators of myogenesis too. In 1997, my laboratory discovered that mutation in the gene Myostatin, a TGF beta super-family member, causes an increased growth in the prenatal and post natal skeletal muscle. We have demonstrated the function of myostatin in three independent models that is chicken, mice and cattle. Recently myostatin?s ability to regulate muscle growth has also been demonstrated in humans. Thus Myostatin is considered to be a well conserved potent negative regulator of myogenesis. The recent research from our lab indicates that myostatin is expressed in muscle resident stem cells, Satellite cells, and induces quiescence in satellite cells. Furthermore, our research also suggests that myostatin could be involved in the self-renewal of satellite cells and specification of satellite cell lineage. The future research projects in my laboratory thus will capitalize our significant findings to unravel the molecular mechanism behind satellite cell self renewal and specification. This research has tremendous scope in regenerative medicine and therefore has applications in gene therapy and cell based therapies for muscle wasting conditions. |
- An Integrated Approach to Overcome Sarcopenia and Frailty in Aging Humans
- Characterization of Smad3 function in skeletal muscle growth and atrophy
- Myostatin as a therapeutic target for obesity/type II diabetes
- Myostatin signalling during cachexia
- Regulation of muscle stem cell self renewal by myostatin
- The Effects of Steroid Therapy on Satellite Cells and Fibro-adipocytes in Duchenne and Becker Muscular Dystrophy
| Selected Publications | - Misra A, George B, Rajmohan R, Jain N, Wong MH, Kambadur R, Thanabalu T. (2012). Insulin Receptor Substrate protein 53kDa (IRSp53) is a negative regulator of myogenic differentiation.. International Journal of Biochemistry and Cell Biology, 44(6), 928-41.
- Ge, X., McFarlane, C., Vajjala, A., Lokireddy, S., Ng, Z.H., Tan, C.K., Tan, N.S., Wahli, W., Sharma, M. and Kambadur, R. (2011). Smad3 signaling is required for satellite cell function and myogenic differentiation of myoblasts. Cell Research, DOI: 10.1002/sm.
- Tan CK, Leuenberger N, Tan MJ, Yan YW, Chen YH, Kambadur R, Wahli W, Tan NS. (2011). Smad3 Deficiency in Mice Protects Against Insulin Resistance and Obesity Induced by a High-Fat Diet. Diabetes, 60, 464-476.
- McFarlane, C., Sharma, M., Kambadur, R. (2008). Myostatin is a procachectic growth factor during postnatal myogenesis. Current Opinion in Clinical Nutrition and Metabolic Care, 11(4).
- Ferenc Jeanplong, Mridula Sharma, Wayne G. Somers, John J. Bass and Ravi Kambadur. (2008). Genomic organisation and postnatal expression of the bovine myostatin gene. Molecular and Cellular Biochemistry, 220, 31-37.
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