James P. White

ORCID: 0000-0003-2667-0806
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About
Contact & Profiles
Research Areas
  • Muscle Physiology and Disorders
  • Adipose Tissue and Metabolism
  • Exercise and Physiological Responses
  • Nutrition and Health in Aging
  • Muscle metabolism and nutrition
  • Genomics and Phylogenetic Studies
  • Microbial Community Ecology and Physiology
  • Fire dynamics and safety research
  • Legume Nitrogen Fixing Symbiosis
  • Genetics, Aging, and Longevity in Model Organisms
  • Gut microbiota and health
  • interferon and immune responses
  • Combustion and flame dynamics
  • Viral Infections and Immunology Research
  • Epigenetics and DNA Methylation
  • Mosquito-borne diseases and control
  • RNA Research and Splicing
  • RNA regulation and disease
  • Metabolism, Diabetes, and Cancer
  • Wastewater Treatment and Nitrogen Removal
  • Cancer, Hypoxia, and Metabolism
  • Peroxisome Proliferator-Activated Receptors
  • Combustion and Detonation Processes
  • Genetic Neurodegenerative Diseases
  • Autophagy in Disease and Therapy

Duke University
2017-2024

Providence College
2023

FM Global (United States)
2023

Duke Medical Center
2016-2022

Washington University in St. Louis
2014-2021

Resphera Biosciences
2021

University of Rochester
2010-2019

University of Maryland, College Park
2015-2019

Dana-Farber Cancer Institute
2013-2018

Harvard University
2012-2018

Muscle wasting that occurs with cancer cachexia is caused by an imbalance in the rates of muscle protein synthesis and degradation. The Apc(Min/+) mouse a model colorectal develops dependent on circulating IL-6. However, IL-6 regulation turnover during initiation progression not known. Cachexia was studied mice were either weight stable (WS) or had initial (≤5%), intermediate (6-19%), extreme (≥20%) body loss. reduced %MPS 19% further ∼50% additional IGF-1 mRNA expression mTOR targets...

10.1371/journal.pone.0024650 article EN cc-by PLoS ONE 2011-09-19

Muscle protein turnover regulation during cancer cachexia is being rapidly defined, and skeletal muscle mitochondria function appears coupled to processes regulating wasting. Skeletal oxidative capacity the expression of proteins mitochondrial biogenesis dynamics are disrupted in severely cachectic ApcMin/+ mice. It has not been determined if these changes occur at onset necessary for progression Exercise anti-cytokine therapies have proven effective preventing development tumor bearing...

10.1186/2044-5040-2-14 article EN cc-by Skeletal Muscle 2012-07-06

One of the largest contributions to biologically available nitrogen comes from reduction N 2 ammonia by rhizobia in symbiosis with legumes. Plants supply dicarboxylic acids as a carbon source bacteroids, and return they receive ammonia. However, metabolic exchange must be more complex, because effective fixation Rhizobium leguminosarum bv viciae bacteroids requires either one two broad-specificity amino acid ABC transporters (Aap Bra). It was proposed that cycle between plant but model...

10.1073/pnas.0903653106 article EN Proceedings of the National Academy of Sciences 2009-07-14

Although catabolic signaling has a well-established role in muscle wasting during cancer cachexia, the suppression of anabolic also warrants further investigation. In cachectic tumor-bearing mice, circulating IL-6 levels are associated with suppressed protein synthesis and mTORC1 signaling. We have found AMPK IGF-I/insulin signaling, two well-known regulators mammalian target rapamycin (mTOR), altered progression cachexia. How can induce remains to be established. The purpose this study was...

10.1152/ajpendo.00410.2012 article EN AJP Endocrinology and Metabolism 2013-03-27

Many diseases are associated with catabolic conditions that induce skeletal muscle wasting. These various states may have similar and distinct mechanisms for inducing protein loss. Mechanisms related to wasting also be metabolism since glycolytic fibers greater susceptibility several diseases. The purpose of this study was determine the relationship between oxidative capacity mass loss in red white hindlimb muscles during cancer cachexia development Apc Min/+ mouse. Gastrocnemius soleus were...

10.1152/ajpregu.00300.2010 article EN AJP Regulatory Integrative and Comparative Physiology 2010-12-10

10.1016/j.bbadis.2011.08.010 article EN publisher-specific-oa Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 2011-09-03

Abstract The pace of repair declines with age and, while exposure to a young circulation can rejuvenate fracture repair, the cell types and factors responsible for rejuvenation are unknown. Here we report that macrophage cells produce promote osteoblast differentiation old bone marrow stromal cells. Heterochronic parabiosis exploiting mice in which macrophages be depleted fractionated transplantation experiments show slow healing mice. Proteomic analysis secretomes identify differential...

10.1038/s41467-018-07666-0 article EN cc-by Nature Communications 2018-11-29

Type I IFNs promote cellular responses to viruses, and IFN receptor (IFNAR) signaling regulates the of endothelial cells blood-brain barrier (BBB) during neurotropic viral infection. However, role astrocytes in innate immune BBB infection CNS remains be fully elucidated. Here, we have demonstrated that type IFNAR permeability protects cerebellum from immunopathology. Mice with astrocyte-specific loss showed decreased survival after West Nile virus Accelerated mortality was not due expanded...

10.1172/jci88720 article EN Journal of Clinical Investigation 2017-01-29

Significance The work reported in this paper describes a previously unknown signaling pathway skeletal muscle acting through G protein-coupled receptor 56-Galpha12/13. This discovery elucidates mechanism of anabolism and gives another target investigation for therapies against the loss mass seen with aging various wasting diseases.

10.1073/pnas.1417898111 article EN Proceedings of the National Academy of Sciences 2014-10-21
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