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ABSTRACT: WC/KC/KS

PROVIDER: PRJNA748942 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15215103_1.fastq.gz	Fastqsanger.gz
	SRR15215103_2.fastq.gz	Fastqsanger.gz
	SRR15215104_1.fastq.gz	Fastqsanger.gz
	SRR15215104_2.fastq.gz	Fastqsanger.gz
	SRR15215105_1.fastq.gz	Fastqsanger.gz

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Metabolomic Profiling of the Striatum in Shank3 Knockout ASD Rats: Effects of Early Swimming Regulation

Project description:OBJECTIVE: This study aimed to investigate the regulatory impact of early swimming intervention on striatal metabolism in Shank3 gene knockout ASD model rats. METHODS: Shank3 gene knockout exon 11-21 male 8-day-old SD rats were used as experimental subjects and randomly divided into three groups: Shank3 knockout control group (KC), wild-type control group (WC) from the same litter and Shank3 knockout swimming group (KS). Rats in the exercise group received early swimming intervention for 8 weeks starting at 8 days old. GC-MS metabolism was employed to detect the changes of metabolites in striatum. RESULTS: There were 17 differential metabolites (14 down-regulated) between the KC and WC groups, 19 differential metabolites (18 up-regulated) between the KS and KC groups and 22 differential metabolites (18 up-regulated) between the KS and WC groups. CONCLUSION: The metabolism of striatum in Shank3 knockout ASD model rats is disrupted, involving metabolites related to synaptic morphology, Glu and GABAergic synapses are abnormal. Early swimming intervention regulated the striatal metabolome group of ASD model rats, with differential metabolites primarily related to nerve development, synaptic membrane structure and synaptic signal transduction.

2024-09-27 | MTBLS8577 | MetaboLights

Cross species hybridization of human cancer cells xenografted into different mouse organ sites

Project description:To test gene expression changes of human cancer cells and mouse surrounding tissue cells during tumor progression, 4 different types of cancer cells (MDA-MB231Br3, PC14Br4, KM12M, A375SM) were injected into mouse brain, skin and orthotopic sites. RNAs containing human cancer cells and mouse surrounding tissue cells were extracted and hybridized into human and mouse arrays at the same times and it revealed the brain microenvironment induced complete reprogramming of metasized cancer cells, resulting in a gain of neuronal cell characteristic , mimicking neurogenesis during development. Human in vivo: 4 KB, 4 KS, 3 KC, 5 MB, 5 MF, 4 MS, 3 PB, 3 PL, 4 PS, 5 AB, 5 AS , 1 BR_N_PC Mouse in vivo: 4 KB, 4 KS, 3 KC, 5 MB, 5 MF, 4 MS, 3 PB, 3 PL, 4 PS, 5 AB, 5 AS , 3 BR, 3 PC_BRM, 1 BR_PCM

2011-09-23 | E-GEOD-19184 | biostudies-arrayexpress

PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [ChIP-seq]

Project description:Kaposi’s sarcoma (KS) is an AIDS-defining cancer caused by the KS-associated herpesvirus (KSHV). Unanswered questions regarding KS are its cellular ontology and the conditions conducive to viral oncogenesis. We identify PDGFRA(+)/SCA-1(+) bone marrow-derived mesenchymal stem cells (Pα(+)S MSCs) as KS spindle-cell progenitors and found that pro-angiogenic environmental conditions typical of KS are critical for KSHV sarcomagenesis. This is because growth in KS-like conditions generates a de-repressed KSHV epigenome allowing oncogenic KSHV gene expression in infected Pα(+)S MSCs. Furthermore, these growth conditions allow KSHV-infected Pα(+)S MSCs to overcome KSHV-driven oncogene-induced senescence and cell cycle arrest via a PDGFRA-signaling mechanism; thus identifying PDGFRA not only as a phenotypic determinant for KS-progenitors but also as a critical enabler for viral oncogenesis.

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Project description:Kabuki syndrome (KS) is a rare multiple congenital anomalies/mental retardation (MCA/MR) syndrome described in 19811,2. In 2010, exome sequencing identified MLL2 mutations in patients with KS3. Since then, 5 studies identified a mutation in MLL2 in 56-75,6% of KS patients3-7. Here, we describe 2 KS and 1 KS-like patient with a de novo partial or complete deletion of UTX, a histone demethylase interacting with MLL2 in gene regulation. UTX locates on the X chromosome and we showed that the X chromosome with the deleted copy of UTX is preferentially inactivated despite the fact that UTX escapes X-inactivation. This study unveiled deletion of UTX as a second cause of KS and highlights the growing role of histone methylase/demethylase in MCA/MR syndrome.

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Genome-wide expression analysis of dikaryotic colonies of Schizophyllum commune under various conditions: wild-type, delta-wc2, delta-wc2 hsp3(pr)-wc2

Project description:The blue light receptor WC-2 was shown to be involved in mushroom development in the basidiomycete Schizophyllum commune. When the gene encoding WC-2 was deleted, no mushrooms formed and colony morphology was radial. This phenotype was similar to the wild-type colony grown in the dark. This phenotype could be complemented by transforming the wc-2 deletion strain with a construct encompassing the wc-2 coding sequence under the control of the heat inducible promoter hsp3. A daily heat shock of 1 hour at 42 degrees Celsius resulted in mushroom development and an asymmetrical colony. In this study we performed a genome-wide expression analysis on dikaryons of wild-type (not heat shocked), delta-wc2 (heat shocked or not heat shocked) and the complemented strain delta-wc2 hsp3-wc2 (heat shocked or not heat shocked).

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Proteomic Analysis of Tear Fluid from the Offspring of Keratoconus Patients Toward Novel Biomarkers and Pathways Associated with Corneal Biomechanical Weakness and Disease Susceptibility.

Project description:Keratoconus (KC) is a chronic and degenerative condition marked by pathological weakening, thinning, and protrusion of the corneal tissue. Corneal biomechanical weakness constitutes a hallmark of early keratoconus (KC) stages, which has underlined the importance of the study of biomechanical response in the early clinical screening of KC. In this line, the family history of KC is consistently identified as the leading risk factor for KC development, and the first-order pediatric relatives of KC patients are considered the most vulnerable population for KC development. On the other hand, tear fluid has become an attractive and accessible source that could be useful in identifying the molecular targets of several ocular diseases, such as corneal ectasias and more specifically KC disease. So, based on the vulnerability of first-order pediatric KC relatives to develop the disease, as well as the potential of tear fluid as a biomarker source, the purpose of this study was to analyze quantitatively and qualitatively the tear proteome of young KC offspring using micro–liquid chromatography coupled to tandem mass spectrometry, trying to get closer to the molecular drivers underlying the alterations in corneal biomechanical properties at at-risk stages of KC and to provide new insights into the molecular mechanisms involved in the earlier stages of the disease.

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