Kenneth M. Baldwin
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Kenneth M. Baldwin

Since joining the Dept of Physiology and Biophysics at UCI my research has focused on the general theme of plasticity of striated muscle. Over the years, our research group has developed several approaches to manipulate the structure and function of cardiac and Skeletal muscle in the in vivo setting using the primarily models of altered loading states such as functional overload, resistance training exercise, and limb unloading including spaceflight. Using these models, we have primarily focused on the myosin heavy chain (MHC) gene family of motor proteins as the marker genes of study. Consequently, our research has gradually evolved over many years into the molecular biology/physiology field by assembling a cadre of Co-Investigators (see below). Our research spanning ~ 45 years has been funded by three primary research entities: The National Heart, Lung, and Blood Institute; The National Institute of Arthritis and Musculoskeletal and Skin Diseases; and the NASA Life Sciences.

Our research on MHC plasticity expands our studies concerning the transcriptional regulation of the four adult MHC genes. In recent years we have made important findings suggesting that the fast MHC genes are transcriptionally regulated as a gene loci in which they communicate with one another through expression of non coding antisense RNA regulated by intergenic promoters. This area is one of the primary aims in the theme of genomic/epigenetic interaction and cooperative regulation of MHC genes that we have focused on in recent years. Also, we have explored these novel findings concerning muscle unloading targets that reduce expression of slow motor unit fibers by rapidly shutting down transcription of the slow MHC gene while expressing de novo the fastest MHC genes IIx and IIb as a functional mechanism to compensate for the weakness of the slow motor units.

A new area of focus for these studies is to ascertain the mechanisms whereby fast muscle fibers expressing chiefly the IIx/IIb isoforms have an impaired capability to express the slow antigravity type I MHC gene, there by limiting the ability of the muscle to increase its economy of function and fidelity of movement. Furthermore, we have observed epigenetic phenomena suggesting that histone modifications are also playing a key role in the regulation of MHC gene switching and in limiting slow MHC expression in fast type fibers. Hence we will delve further into this area as part of the layering of MHC transcriptional processes. In pursuing these future studies we also will take advantage of new technologies (ChIP, RNA interference, fluorescent labeling of muscle fibers) developed in our laboratory. Thus, the projects that we have identified will spearhead other research groups in pursuing new areas of study that have not been pursued before in the muscle plasticity field.


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