Profilling of aggregated proteome in human control and AD cases
Ontology highlight
ABSTRACT: Analyzing and comparing proteome profiling between human control and AD cases will be beneficial to understand the molecular changes of insoluble fractions of AD cases.
Project description:Analyzing and comparing proteome profiling N40K mouse cultured neurons will be beneficial to understand the contributing of RNA splicing dysfunction pathway to Alzheimer's Disease.
Project description:Analyzing and comparing proteome profiling among WT, N40K-Tg, 5xFAD and dTg will be beneficial to understand the interaction between RNA splicing dysfunction pathway and Amyloid cascade.
Project description:Analyzing and comparing proteome profiling among WT, N40K-Tg, 5xFAD and dTg will be beneficial to understand the interaction between RNA splicing dysfunction pathway and Amyloid cascade.
Project description:Analyzing and comparing proteome profiling between WT, N40K-Tg will be beneficial to understand the protein changes in insoluble fractions.
Project description:To assess changes in the muscle proteome that due to tumor burden and dexamethasone treatments and compare proteomic changes that occur in atrophy due to tumor burden and dexamethasone treatment with atrophy caused by aging. Regulators of muscle atrophy induced by diseases such as cancer or drugs such as dexamethasone are largely unknown. We would therefore like to determine the proteomic signature of atrophying muscle caused by tumor burden (LLC cell injected mice) and dexamethasone treatment in order to examine possible biomarkers and regulators of muscle atrophy. We would also like to compared the proteomic signature of different modes of muscle atrophy to determine similarities and differences in the possible biomarkers and regulators.
Project description:Analyzing and comparing proteome and phosphoproteome profiling between CD8+ DC and CD8- DC not only will be very helpful to understand the molecular mechanisms regulating CD8+/- DC differentiation and function but also can screen CD8+ or CD8- DC specific regulatory pathways or molecules.
Project description:The molecular networks underlying Alzheimer’s disease (AD) are not well-defined. We present temporal profiling of >14,000 proteins and >34,000 phosphosites at the asymptomatic and symptomatic stages of AD, deep proteomics analysis of transgenic mouse models.
Project description:The molecular networks underlying Alzheimer’s disease (AD) are not well-defined. We present temporal profiling of >14,000 proteins and >34,000 phosphosites at the asymptomatic and symptomatic stages of AD, deep proteomics analysis of transgenic mouse models.
Project description:The molecular networks underlying Alzheimer’s disease (AD) are not well-defined. We present temporal profiling of >14,000 proteins and >34,000 phosphosites at the asymptomatic and symptomatic stages of AD, deep proteomics analysis of transgenic mouse models.
Project description:Skeletal muscle atrophy is a debilitating condition that occurs with aging and disease but the underlying mechanisms are incompletely understood. Previous work determined that common transcriptional changes occur in muscle during atrophy induced by different stimuli. However, whether this holds true at the proteome level remains largely unexplored. Here, we find that, contrary to this earlier model, distinct atrophic stimuli (corticosteroids, cancer, and aging) induce largely different mRNA and protein changes during muscle atrophy in mice. Moreover, there is widespread transcriptome-proteome disconnect. Consequently, atrophy markers (atrogenes) identified in earlier microarray-based studies do not emerge from these proteomic surveys as the most relevantly associated with atrophy in all conditions. Rather, we identify proteins that are distinctly modulated by different types of atrophy (herein defined as “atroproteins”) such as the myokine CCN1/Cyr61, which regulates myofiber type switching during sarcopenia. Altogether, these integrated analyses indicate that different catabolic stimuli induce muscle atrophy via largely distinct mechanisms.