Robert Sanders Williams

Journal article Proc Natl Acad Sci U S A · January 21, 2003 Featured Publication The calcium/calmodulin-dependent protein phosphatase calcineurin stimulates cardiac hypertrophy in response to numerous stimuli. Calcineurin activity is suppressed by association with modulatory calcineurin-interacting protein (MCIP)1DSCR1, which is up-reg ... Full text Link to item Cite

The role of modulatory calcineurin-interacting proteins in calcineurin signaling.

Journal article Trends Cardiovasc Med · January 2003 Featured Publication Modulatory calcineurin-interacting proteins (MCIPs), also known as the Down syndrome critical region 1 (DSCR1) and DSCR1-like proteins, are a recently described family of small, structurally related proteins that are preferentially expressed in heart, skel ... Full text Link to item Cite

Another surprise from the mitochondrial genome.

Journal article N Engl J Med · August 22, 2002 Featured Publication Full text Link to item Cite

Multiple domains of MCIP1 contribute to inhibition of calcineurin activity.

Journal article J Biol Chem · August 16, 2002 Featured Publication Calcineurin is a serine/threonine protein phosphatase that plays a critical role in many physiologic processes such as T-cell activation, apoptosis, skeletal myocyte differentiation, and cardiac hypertrophy. Calcineurin-dependent signals are transduced to ... Full text Link to item Cite

Calcineurin signaling in human cardiac hypertrophy.

Journal article Circulation · May 14, 2002 Featured Publication Full text Link to item Cite

Regulation of mitochondrial biogenesis in skeletal muscle by CaMK.

Journal article Science · April 12, 2002 Featured Publication Endurance exercise training promotes mitochondrial biogenesis in skeletal muscle and enhances muscle oxidative capacity, but the signaling mechanisms involved are poorly understood. To investigate this adaptive process, we generated transgenic mice that se ... Full text Link to item Cite

Targeted inhibition of calcineurin in pressure-overload cardiac hypertrophy. Preservation of systolic function.

Journal article J Biol Chem · March 22, 2002 Featured Publication Calcineurin is a Ca(2+)/calmodulin-activated protein phosphatase that transduces hypertrophic stimuli to regulate transcriptional control of myocyte transformation. It is not known whether overexpression of MCIP1, a recently described endogenous inhibitor ... Full text Link to item Cite

Activation of MEF2 by muscle activity is mediated through a calcineurin-dependent pathway.

Journal article EMBO J · November 15, 2001 Featured Publication Gene expression in skeletal muscles of adult vertebrates is altered profoundly by changing patterns of contractile work. Here we observed that the functional activity of MEF2 transcription factors is stimulated by sustained periods of endurance exercise or ... Full text Link to item Cite

Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo.

Journal article Proc Natl Acad Sci U S A · March 13, 2001 Featured Publication Signaling events controlled by calcineurin promote cardiac hypertrophy, but the degree to which such pathways are required to transduce the effects of various hypertrophic stimuli remains uncertain. In particular, the administration of immunosuppressive dr ... Full text Link to item Cite

Calcineurin signaling and muscle remodeling.

Journal article Cell · June 23, 2000 Featured Publication Full text Link to item Cite

Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis.

Journal article Cell · May 12, 2000 Featured Publication Cytochrome c released from mitochondria has been proposed to be an essential component of an apoptotic pathway responsive to DNA damage and other forms of cell stress. Murine embryos devoid of cytochrome c die in utero by midgestation, but cell lines estab ... Full text Link to item Cite

Myogenic stem cell function is impaired in mice lacking the forkhead/winged helix protein MNF.

Journal article Proc Natl Acad Sci U S A · May 9, 2000 Featured Publication Myocyte nuclear factor (MNF) is a winged helix transcription factor that is expressed selectively in myogenic stem cells (satellite cells) of adult animals. Using a gene knockout strategy to generate a functional null allele at the Mnf locus, we observed t ... Full text Link to item Cite

MEF2 responds to multiple calcium-regulated signals in the control of skeletal muscle fiber type.

Journal article EMBO J · May 2, 2000 Featured Publication Different patterns of motor nerve activity drive distinctive programs of gene transcription in skeletal muscles, thereby establishing a high degree of metabolic and physiological specialization among myofiber subtypes. Recently, we proposed that the influe ... Full text Link to item Cite

A protein encoded within the Down syndrome critical region is enriched in striated muscles and inhibits calcineurin signaling.

Journal article J Biol Chem · March 24, 2000 Featured Publication Here we describe a small family of proteins, termed MCIP1 and MCIP2 (for myocyte-enriched calcineurin interacting protein), that are expressed most abundantly in striated muscles and that form a physical complex with calcineurin A. MCIP1 is encoded by DSCR ... Full text Link to item Cite

Mice without myoglobin.

Journal article Nature · October 29, 1998 Featured Publication Myoglobin, an intracellular haemoprotein expressed in the heart and oxidative skeletal myofibres of vertebrates, binds molecular oxygen and may facilitate oxygen transport from erythrocytes to mitochondria, thereby maintaining cellular respiration during p ... Full text Link to item Cite

A calcineurin-dependent transcriptional pathway controls skeletal muscle fiber type.

Journal article Genes Dev · August 15, 1998 Featured Publication Slow- and fast-twitch myofibers of adult skeletal muscles express unique sets of muscle-specific genes, and these distinctive programs of gene expression are controlled by variations in motor neuron activity. It is well established that, as a consequence o ... Full text Link to item Cite