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Proteomics on mdxmTR Mice

ABSTRACT: Label free proteomics of skeletal muscle from mdxmTR mice.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Skeletal Muscle

DISEASE(S): Muscular Dystrophy

SUBMITTER: Brian McDonagh

LAB HEAD: Brian McDonagh

PROVIDER: PXD010507 | Pride | 2022-03-01

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	Control_1.mgf	Mgf
	Control_1.msf	Msf
	Control_1.raw	Raw
	Control_2.mgf	Mgf
	Control_2.msf	Msf

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1 - 5 of 36

Publications

Multiomics analysis of the mdx/mTR mouse model of Duchenne muscular dystrophy.

Van Pelt Douglas W DW Kharaz Yalda A YA Sarver Dylan C DC Eckhardt Logan R LR Dzierzawski Justin T JT Disser Nathaniel P NP Piacentini Alex N AN Comerford Eithne E McDonagh Brian B Mendias Christopher L CL

Connective tissue research 20200715 1

<h4>Purpose/aim</h4>Duchenne muscular dystrophy (DMD) is a progressive neuromuscular disease characterized by extensive muscle weakness. Patients with DMD lack a functional dystrophin protein, which transmits force and organizes the cytoskeleton of skeletal muscle. Multiomic studies have been proposed as a way to obtain novel insight about disease processes from preclinical models, and we used this approach to study pathological changes in dystrophic muscles.<h4>Materials and methods</h4>We eval ...[more]

PMID: 32664808

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Proteome of Young and Old Murine Diaphragm and Associaated Changes in Contractile Properties

Project description:Proteomic analysis of young and old murine diaphragm and associated changed in contractile aproperties. Redox sensitive Cysteine residues from both adult and old diaphragm tissues examined.

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Defective Mitochondrial Lipid Oxidation Results in the Pathological Accumulation of Fat After Rotator Cuff Tear

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2020-04-15 | PXD009034 | Pride

A novel phosphate-starvation response in fission yeast requires the endocytic function of Myosin I (ChIP-seq)

Project description:S. pombe Myosin I (MyoI) plays a key role in cytoskeletal functions, in particular it is part of the endocytotic machinery. Here we show a novel role for MyoI in regulating the response to low phosphate stress. Deletion of MyoI led to an increased proliferation in low phosphate media when compared to a control strain; mutations in other proteins involved in the early steps of endocytosis, such as ARP2 and Sla2/END4, led to the same phenotype. We show that once cells are deprived of phosphate they undergo clear morphological changes, slow down growth but retain viability. This is reminiscent of a quiescence response, and it is completely abolished when MyoI is absent. Transcriptomic analysis revealed a wide perturbation of gene expression upon phosphate starvation, with rapid induction of stress-regulated genes. However, Æmyo1 cells displayed little or negligible effects at gene expression level when they were phosphate-starved. Using a combination of super resolution microscopy and genetic approaches we pinpointed the specific function of MyoI in endocytosis as critical for the response to low phosphate stress. Furthermore, introduction of point-mutated MyoI (with ablated endocytic function) into a ÆmyoI background failed to restore phosphate stress response. Taken together, our data indicate how endocytosis, and in particular MyoI, play a pivotal role in mediating cellular response to nutrients, bridging the external environment and internal molecular functions of the cells. ChIP-seq analysis of Myo1-GFP genomic binding in control or low phosphate condition

2015-09-15 | E-GEOD-67105 | biostudies-arrayexpress

Expression profiling of cisplatin resistant cells derived from H460 lung cell line.

Project description:Combination of platinum-based chemotherapy and radiation is currently the standard treatment for locally advanced lung cancer patients. However, therapeutic resistance to these therapies may arise from the presence of cancer stem cells (CSCs). To investigate the CSCs hypothesis of chemo-radiation resistance, we used microarray assay to profile CSCs-like cisplatin-resistant lung cancer cells (CDDP-R) versus its parental cells. CDDP-R cells were established by exposing H460 lung cancer cells to 3¬µM cisplatin for 7 days, followed by 0.8% methylcellulose selection over 14 consecutive days.¬†We found that CDDP-R cells expressed higher levels of stem cell markers, including CD133 and ALDH. They are more resistant to cisplatin- and etoposide-induced apoptosis and to high radiation dose (20Gy). Clonogenic assays suggest that CDDP-R cells were more resistant to radiation than parental H460 cells (DER=1.21, p<0.01). Xenograft studies suggest that CDDP-R cells were more tumorigenic (p<0.001). Microarray and comprehensive protein interaction networks analyses revealed IGFBP3 as a highly ranked hub protein which plays an important role in the mechanism of cisplatin resistance. We found reduced level of IGFBP3 and enhanced IGFR-1 activation upon IGF stimulation in CDDP-R cells. The specific targeting of IGF-1R using siRNA resulted in significant sensitization of CDDP-cells (DER=1.17, p<0.05) to radiation compared with the parental H460 cells. Our findings suggest that CDDP-R cells have the characteristics of CSCs and constitute a ‚Äúsuitable‚Äù model to study lung CSCs. Profiling of CSCs-like H460 cells led to the identification of IGF as an important pathway for chemo- and radiotherapy resistance in lung cancer. gene expression comparison of two groups

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Regulation of Gamma globin gene expression by AT2 and its associated proteins through the cAMP response element.

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PAT-seq - a high-throughput polyadenylation assay for the Illumina platform

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A new phosphate-starvation response in fission yeast requires the endocytic function of myosin I

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Time-course microarray study of Cryptococcus neoformans var. neoformans (JEC20xJEC21) sexual development

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