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Alterations in human skeletal muscle proteins in amyotrophic lateral sclerosis

dc.contributor.advisorChin, Evaen_US
dc.contributor.authorDeRusso, Alicia Laurenen_US
dc.date.accessioned2015-07-17T05:37:41Z
dc.date.available2015-07-17T05:37:41Z
dc.date.issued2015en_US
dc.identifierhttps://doi.org/10.13016/M27D0Z
dc.identifier.urihttp://hdl.handle.net/1903/16814
dc.description.abstractAmyotrophic lateral sclerosis (ALS) is the most common fatal neurodegenerative disease, resulting in loss of voluntary muscle control, atrophy, paralysis, and eventually death. Although the pathophysiology of ALS is not completely understood, recent research in Dr. Chin's lab has identified alterations in skeletal muscle proteins in ALS mice. The purpose of this study was to investigate alterations in proteins involved in calcium handling (SERCA1 and SERCA2), endoplasmic reticulum (ER) stress (Grp78/BiP, PDI, and CHOP) and protein synthesis (Akt) in human ALS skeletal muscle. The ER chaperone protein Grp78/BiP and Akt, a protein involved in protein synthesis, were higher in ALS compared to CON. The calcium pump SERCA1 was lower in diaphragm compared to quadriceps muscles of ALS cases. These data highlight alterations in skeletal muscle proteins not only between ALS and CON, but also between different muscles in ALS, which are helpful for informing future research study designs.en_US
dc.language.isoenen_US
dc.titleAlterations in human skeletal muscle proteins in amyotrophic lateral sclerosisen_US
dc.typeThesisen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.contributor.departmentKinesiologyen_US
dc.subject.pqcontrolledPhysiologyen_US
dc.subject.pqcontrolledCellular biologyen_US
dc.subject.pquncontrolledALSen_US
dc.subject.pquncontrolledamyotrophic lateral sclerosisen_US
dc.subject.pquncontrolledER stressen_US
dc.subject.pquncontrolledprotein alterationsen_US
dc.subject.pquncontrolledproteinsen_US
dc.subject.pquncontrolledskeletal muscleen_US


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