PO Box 9227
216 Annex HSC North
- Curriculum Vitae
- Download CV
- BS, Madurai Kamaraj University, 1989
- MS, Bharathidasan University, 1992
- PhD, M. S. University, 2001
- Coarfa C, Fiskus W, Eedunuri VK, Rajapakshe K, Foley C, Chew SA, Shah SS, Geng C, Shou J, Mohamed JS, O'Malley BW, Mitsiades N. 2016. Comprehensive proteomic profiling identifies the androgen receptor axis and other signaling pathways as targets of microRNAs suppressed in metastatic prostate cancer. Oncogene. 35(18):2345-2356
- Mohamed JS, Hajira A, Lopez ML, Boriek AM. 2015. Genome-wide Mechanosensitive MicroRNA (MechanomiR) Screen Uncovers Dysregulation of their Regulatory Networks in the mdm Mouse Model of Muscular Dystrophy. J Biol Chem. 290(41): 24986-5011
- Eedunuri VK, Rajapakshe K, Fiskus W, Geng C, Chew SA, Foley C, Shah SS, Shou J, Mohamed JS, Coarfa C, O'Malley BW, Mitsiades N. 2015. miR-137 Targets p160 Steroid Receptor Coactivators SRC1, SRC2, and SRC3 and Inhibits Cell Proliferation. Mol Endocrinol. 29(8):1170-83.
- Alway SE, Bennett BT, Wilson JC, Sperringer J, Mohamed JS, Edens NK, Pereira SL. 2015. Green tea extract attenuates muscle loss and improves muscle function during disuse, but fails to improve muscle recovery following unloading in aged rats. J Appl Physiol. 118(3):319-30.
- Mohamed JS, Wilson JC, Myers MJ, Sisson KJ, Alway SE. 2014. Dysregulation of SIRT-1 in aging mice increases skeletal muscle fatigue by a PARP-1-dependent mechanism. Aging. (Albany NY). 6(10):820-34.
- Alway SE, Myers MJ, Mohamed JS. 2014. Regulation of satellite cell function in sarcopenia. Front Aging Neurosci. 6(246): 1-15.
- *Mohamed JS, Hajira A, Pardo PS, Boriek AM. 2014. MicroRNA-149 inhibits PARP-2 and promotes mitochondrial biogenesis via SIRT-1/PGC-1α network in skeletal muscle. Diabetes. 63(5):1546-59.
*Highlighted in Svensson K, Handschin C. 2014. MicroRNAs emerge as modulators of NAD+-dependent energy metabolism in skeletal muscle. Diabetes. 63(5): 1451-1453.
- Bennett BT, Mohamed JS, Alway SE. 2013. Effects of resveratrol on the recovery of muscle mass following disuse in the plantaris muscle of aged rats. PLoS One. 8(12):e83518.
- Mohamed JS, Lopez MA, Cox GA, Boriek AM. 2013. Ankyrin repeat domain protein 2 and inhibitor of DNA binding 3 cooperatively inhibit myoblast differentiation by physical interaction. J Biol Chem. 288(34):24560-8.
- Wang Y, Mohamed JS, Alway SE. 2013. M-cadherin-inhibited phosphorylation of ß-catenin augments differentiation of mouse myoblasts. Cell Tissue Res. 351(1):183-200.
About Junaith S Mohamed
Our current research focuses on systematic investigations into the underlying physiology, biology and genetics of aging and age-associated diseases, with an emphasis on the following aspects:
Skeletal Muscle Fatigue
Skeletal muscle fatigue is any decline in muscle performance associated with muscle activity. Muscle fatigue is an extremely common and debilitating symptom in aging people. Changes in ATP production, accumulation of metabolic by-products, such as reactive oxygen species (ROS) and cellular stress are the main causes of muscle fatigue. A balance between free radicals (such as ROS) and antioxidants also plays a key role in the initiation of muscle fatigue. Our research focuses on identifying the molecular and cellular signaling mechanisms, which contribute to the initiation of muscle fatigue during aging.
Skeletal Muscle Regeneration
Skeletal muscle is remarkable among tissues because of its robust capacity for regeneration that relies on muscle satellite cells (stem cells) to self-renew, expand, and undergo myogenic differentiation to fuse and restore damaged muscle fibers. Impairment in any of these processes severely affects the formation of new muscle fibers, leading to the loss of skeletal muscle, which is more common in sarcopenia (the age-related loss of muscle mass, strength and function). In this regard, our research focuses on identifying the molecular and cellular signaling mechanisms, which impair skeletal muscle regeneration in different pathophysiological contexts.
Skeletal Muscle Metabolic Disorders
Skeletal muscles compose the largest metabolic tissue in the body and are a major site of lipid and glucose oxidation. Thus, the maintenance of muscle metabolic activity is critical for whole-body energy homeostasis and for preventing aging associated metabolic disorders such as diabetes and obesity. Mitochondria are important sub-cellular organelles that play a central role in glucose and lipid oxidation, especially in skeletal muscles. Thus, one of our research goals is to study signaling pathways regulating the metabolic components of mitochondria in skeletal muscle.
To address our research questions, we use muscle stem cell specific or muscle specific knockout mice, and transgenic mice. We use advanced biochemical, genetic, cell & molecular biology and physiology techniques, bioinformatics tools, in vitro and in vivo experiments, and mouse models of human diseases. We also use microarray and next generation sequencing technology and proteomic analysis.