Marita A. Wallace

ORCID: 0000-0003-1814-2480
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About
Contact & Profiles
Research Areas
  • Muscle Physiology and Disorders
  • Adipose Tissue and Metabolism
  • Muscle metabolism and nutrition
  • Exercise and Physiological Responses
  • Diet and metabolism studies
  • Genetics and Physical Performance
  • Genetics, Aging, and Longevity in Model Organisms
  • Genetic Neurodegenerative Diseases
  • Sirtuins and Resveratrol in Medicine
  • Histone Deacetylase Inhibitors Research
  • Coenzyme Q10 studies and effects
  • Cellular Mechanics and Interactions
  • Amyotrophic Lateral Sclerosis Research
  • Diet, Metabolism, and Disease
  • Cardiomyopathy and Myosin Studies
  • Parkinson's Disease Mechanisms and Treatments
  • Muscle activation and electromyography studies
  • Ubiquitin and proteasome pathways
  • Spaceflight effects on biology
  • Neurogenetic and Muscular Disorders Research

Virginia Tech
2023

University of California, Davis
2015-2022

Deakin University
2009-2021

University of California, Los Angeles
2012

University of North Carolina at Chapel Hill
2012

Toyohashi University of Technology
2012

Abstract The causes of the decline in skeletal muscle mass and function with age, known as sarcopenia, are poorly understood. Nutrition (calorie restriction) interventions impact many cellular processes increase lifespan preserve age. As we previously observed an life span aging mice on a ketogenic diet (KD), aimed to investigate effect KD maintenance age potential molecular mechanisms this action. Twelve‐month‐old were assigned isocaloric control or until 16 26 months at which time was...

10.1111/acel.13322 article EN Aging Cell 2021-03-06

The loss of muscle strength with age has been studied from the perspective a decline in mass and neuromuscular junction (NMJ) stability. A third potential factor is force transmission. purpose this study was to determine changes transfer apparatus within aging impact on membrane integrity NMJ We measured an age-related dystrophin protein that greatest flexor muscles. occurred despite twofold increase mRNA. Importantly, disparity could be explained by four- fivefold upregulation dystromir...

10.1093/gerona/glw109 article EN The Journals of Gerontology Series A 2016-07-05

Skeletal muscle atrophy is a severe consequence of ageing, neurological disorders and chronic disease. Identifying the intracellular signalling pathways controlling changes in skeletal size function vital for future development potential therapeutic interventions. Striated activator Rho (STARS), an actin-binding protein, has been implicated rodent cardiac hypertrophy; however its role human not determined. This study aimed to establish if STARS, as well downstream targets, RhoA,...

10.1113/jphysiol.2009.168674 article EN The Journal of Physiology 2009-03-03

The striated muscle activator of Rho signalling (STARS) is an actin-binding protein specifically expressed in cardiac, skeletal and smooth muscle. STARS has been suggested to provide important link between the transduction external stress signals intracellular pathways controlling genes involved maintenance function. aims this study were firstly, establish if STARS, as well members its downstream pathway, are upregulated following acute endurance cycling exercise; secondly, determine a...

10.1113/jphysiol.2011.205468 article EN The Journal of Physiology 2011-02-22

Knowledge from human exercise studies on regulators of muscle atrophy is lacking, but it important to understand the underlying mechanisms influencing skeletal protein turnover and net gain. This study examined regulation atrophy-related factors, including atrogin-1 MuRF1, their upstream transcription factors FOXO1 FOXO3A substrate eIF3-f, in response unilateral isolated eccentric (ECC) vs. concentric (CONC) training. Exercise was performed with whey hydrolysate (WPH) or isocaloric...

10.1152/japplphysiol.00136.2013 article EN Journal of Applied Physiology 2014-01-24

The striated muscle activator of Rho signalling (STARS) pathway is suggested to provide a link between external stress responses and transcriptional regulation in muscle. However, the sensitivity STARS different mechanical stresses has not been investigated. In comparative study, we examined response unilateral resistance exercise performed as either eccentric (ECC) or concentric (CONC) contractions well prolonged training; with without whey protein supplementation. Skeletal STARS,...

10.1113/jphysiol.2012.249755 article EN The Journal of Physiology 2013-06-11

Background: Skeletal muscle growth and regeneration depend on the activation of satellite cells, which leads to myocyte proliferation, differentiation fusion with existing fibres. cell proliferation are tightly coordinated by a continuum molecular signalling pathways. The striated activator Rho (STARS) is an actin binding protein that regulates transcription genes involved in growth, structure function via stimulation polymerization serum-response factor (SRF) signalling. While STARS...

10.3389/fphys.2016.00007 article EN cc-by Frontiers in Physiology 2016-02-08

Healthy living throughout the lifespan requires continual growth and repair of cardiac, smooth, skeletal muscle. To effectively maintain these processes muscle cells detect extracellular stress signals efficiently transmit them to activate appropriate intracellular transcriptional programs. The striated activator Rho signaling (STARS) protein, also known as Myocyte Stress-1 (MS1) protein Actin-binding Rho-activating (ABRA) is highly enriched in skeletal, smooth STARS binds actin,...

10.3389/fphys.2012.00469 article EN cc-by Frontiers in Physiology 2012-01-01

Skeletal muscle mass is regulated by sensing and transmitting extracellular mechanical stress signals to intracellular signaling pathways controlling protein synthesis degradation. Striated activator of Rho (STARS) a muscle-specific actin-binding that sensitive signals. STARS stimulates actin polymerization influences serum response factor (SRF) peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α transcription genes involved in growth, structure, contraction. The role skeletal...

10.1152/ajpcell.00421.2012 article EN AJP Cell Physiology 2013-05-30

Skeletal muscle dysfunction may contribute to the progression and severity of amyotrophic lateral sclerosis (ALS). In present study, we characterized skeletal pathophysiology in an inducible transgenic mouse model (rNLS8) that develops a TAR-DNA binding protein (TDP-43) proteinopathy ALS-like neuropathology disease progression; representative >90% all familial sporadic ALS cases. As previously observed elevated levels miR-23a patients with ALS, also investigated effect suppression on rNLS8...

10.1016/j.nbd.2021.105559 article EN cc-by-nc-nd Neurobiology of Disease 2021-11-10

We tested the effects of prolonged voluntary wheel running on muscle function mdx mice treated with one two different microdystrophin constructs. At 7 weeks age were injected a single dose AAV9-CK8-microdystrophin (gene therapy 1, GT1) or without 2, GT2) nNOS-binding domain and assigned to four gene groups: mdxRGT1 (run, GT1), mdxGT1 (no run, mdxRGT2 (run,GT2), mdxGT2 GT2). There untreated groups excipient: mdxR no therapy) therapy). A third treatment group, Wildtype (WT) received injection...

10.3389/fphys.2023.1166206 article EN cc-by Frontiers in Physiology 2023-06-26

What is the central question of this study? Striated muscle activator rho signalling (STARS) an actin-binding protein that regulates transcriptional pathways controlling function, growth and myogenesis, processes are impaired in dystrophic muscle: what regulation STARS pathway Duchenne muscular dystrophy (DMD)? main finding its importance? Members reduced quadriceps patients with DMD mouse models dystrophy. Overexpression deficient mdx model increased maximal isometric specific force...

10.1113/ep089253 article EN Experimental Physiology 2021-05-09

Abstract Muscle mass and strength are predictors of longevity. We have previously identified a series molecular brakes that slow muscle growth in response to stress. One potential stress we hypothesized would limit is caloric through the activation SIRT1. therefore natural product inhibitors SIRT1 tested their effects on load-induced increases fiber cross-sectional area (fCSA) using an incomplete factorial design. Supplying varying amounts three products for full two-week period overload...

10.1101/2022.06.27.497838 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-06-29

Abstract We have previously identified a series of molecular brakes that slow muscle growth. One potential brake is SIRT1, which activated by negative caloric balance. In this work, we natural product inhibitors SIRT1 and tested their effects on load-induced increases in fiber cross-sectional area (fCSA) using an incomplete factorial design. Supplying varying amounts three products during two-week overload resulted fCSA varied from − 2 to 113%. Using these data, produced model predicted the...

10.21203/rs.3.rs-1855726/v1 preprint EN cc-by Research Square (Research Square) 2022-08-16
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