README-for-EGAS00001004884-reused-WGS-files-via-link - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001007669 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:This dataset contains 318 Tumor and Control WGS files submitted in another EGA box for samples for Gerhauser et al.,Cancer Cell, 2018, 34:996-1011. WGS and sequencing protocol was earlier described in Weischenfeldt et al, Cancer Cell, 2013.
| EGAD00001007861 | EGA
Project description:This dataset contains 538 Tumor and Control WGS and WES files for samples already submitted and published in study EGAS00001004276
| EGAD00001007817 | EGA
Project description:While DNA methylation is an important gene regulatory mechanism in mammals (Razin and Riggs 1980; Moore, Le, and Fan 2013), its function in arthropods remains poorly understood. Studies in eusocial insects have argued for its role in caste development by regulating gene expression and splicing (Elango et al. 2009; Lyko et al. 2010; Bonasio et al. 2012; Flores et al. 2012; Foret et al. 2012; Li-Byarlay et al. 2013; Marshall, Lonsdale, and Mallon 2019; Shi et al. 2013)(Alvarado et al. 2015; Kucharski et al. 2008). However, such findings are not always consistent across studies, and have therefore remained controversial (Arsenault, Hunt, and Rehan 2018; Cardoso-Junior et al. 2021; Harris et al. 2019; Herb et al. 2012; Libbrecht et al. 2016; Oldroyd and Yagound 2021b; Patalano et al. 2015). Here we use CRISPR/Cas9 to mutate the maintenance DNA methyltransferase DNMT1 in the clonal raider ant, Ooceraea biroi. Mutants have greatly reduced DNA methylation but no obvious developmental phenotypes, demonstrating that, unlike mammals (Brown and Robertson 2007; En Li, Bestor, and Jaenisch 1992; Jackson-Grusby et al. 2001; Panning and Jaenisch 1996), ants can undergo normal development without DNMT1 or DNA methylation. Additionally, we find no evidence of DNA methylation regulating caste development. However, mutants are sterile, while in wildtypes, DNMT1 is localized to the ovaries and maternally provisioned into nascent oocytes. This supports the idea that DNMT1 plays a crucial but unknown role in the insect germline (Amukamara et al. 2020; Arsala et al. 2021; Bewick et al. 2019; Schulz et al. 2018; Ventós-Alfonso et al. 2020; Washington et al. 2020).
2023-03-23 | GSE182212 | GEO
Project description:differential RNA sequencing (dRNA-seq) (Sharma et al., 2010; Dugar et al., 2013) was used to differentially map 5' ends in Campylobacter jejuni NCTC11168 wildtype and RNase III (rnc, Cj1635c) deletion.
2024-05-16 | GSE230836 | GEO
Project description:Canonical auxin signalling starts with auxin binding to the receptor complex, followed by modulation of gene transcription and protein abundance (Tan et al., 2007; Chapman and Estelle, 2009; Slade et al., 2017). However, recent studies also showed an alternative mechanism in roots involving intra-cellular auxin perception, but not transcriptional reprogramming (Fendrych et al., 2018). Despite knowledge on effects of auxin on Arabidopsis root growth at the protein and phosphorylation level is increasing (Zhang et al., 2013; Mattei et al., 2013; Slade et al., 2017), it still remains incomplete. To address this gap in our knowledge, we explored the impact of auxin on the root tip proteome and phosphoproteome.
2021-09-09 | PXD021267 | Pride
Project description:DNAseq of Batrachochytrium dendrobatidis (Farrer et al PLoS Genet 2013)
| PRJNA174849 | ENA
Project description:CD47 is a transmembrane glycoprotein that is ubiquitously expressed in different organs and tissues (Barclay and Van den Berg 2014; Liu, et al. 2017). In the human immune system, CD47 interacts with some integrins, two counter-receptor signal regulator protein (SIRP) family members, and the secreted thrombospondin-1 (TSP1) (Barclay and Van den Berg 2014; Gao, et al. 2016; Kaur, et al. 2013; Oldenborg, et al. 2000). CD47 has two established roles in the immune system. The CD47-SIRPα interaction was identified as a critical innate immune checkpoint, which delivers an antiphagocytic signal to macrophages and inhibits neutrophil cytotoxicity (Martínez- Sanz, et al. 2021). Its interaction with inhibitory SIRPα is a physiological anti-phagocytic “don’t eat me” signal on circulating red blood cells that is co-opted by cancer cells (Matlung, et al. 2017). Many malignant cells overexpress CD47 (Betancur, et al. 2017; Chao, et al. 2011; Jaiswal, et al. 2009; Majeti, et al. 2009; Oronsky, et al. 2020; Petrova, et al. 2017). CD47/SIRPα-targeted therapeutics have been developed to overcome this immune checkpoint for cancer treatment (Kaur, et al. 2020; Matlung, et al. 2017). Secondly, engagement of CD47 on T cells by TSP1 regulates their differentiation and survival (Grimbert, et al. 2006; Lamy, et al. 2007) and inhibits T cell receptor signaling and antigen presentation by dendritic cells (DCs) (Kaur, et al. 2014; Li, et al. 2002; Liu, et al. 2015; Miller, et al. 2013; Soto-Pantoja, et al. 2014; Weng, et al. 2014). TSP1/CD47 signaling has similar inhibitory functions to limit NK cell activation (Kim, et al. 2008; Nath, et al. 2018; Nath, et al. 2019; Schwartz, et al. 2019) and IL1β production by macrophages (Stein, et al. 2016). CD47 is therefore a checkpoint that regulates both innate and adaptive immunity. The recent understanding of CD47 antagonism associated with increased antigen presentation by DCs (Liu, et al. 2016) and natural killer cell cytotoxicity (Nath, et al. 2019) contributes to the heightened interest in CD47 as a therapeutic target (Kaur, et al. 2020).
2022-09-21 | GSE198820 | GEO
Project description:DNA damage can promote altered RNA splicing and decreased gene expression (Gregersen and Svejstrup, 2018; Milek et al., 2017; Munoz et al., 2009; Shkreta and Chabot, 2015), and aberrant splicing is implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Fragile X syndrome and spinal muscular atrophy (SMA) (Conlon et al., 2016; Jia et al., 2012; Loomis et al., 2014; Qiu et al., 2014; Scotti and Swanson, 2016). Therefore, we used RNA-seq data to assess RNA-splicing in double-mutant brain tissue using multivariate analysis of transcriptional splicing (rMATS) (Shen et al., 2014) and a splicing deficiency score algorithm (Bai et al., 2013) to assess intron retention.
2021-12-14 | GSE174841 | GEO
Project description:The present study extends the analysis initiated in a previous report in the popular HD transgenic mouse strain N171-82Q (82Q) (Valor et al., 2013), to other diverse mHtt-expressing animal and cellular models. We show that bulk histone hypoacetylation is not a general rule. Moreover, examination of other histone post-traslational modifications led to a detailed study of the trimethylation of lysine 4 of histone H3 (H3K4me3), which is tightly associated with active genes (Lopez-Atalaya et al., 2013), by combining both single-gene and genome-wide approaches. Comparison of the 82Q and another animal model, the R6/1 strain, revealed that changes in the levels of bulk H3K4me3 may be correlated with the degree of methylation impairment for specific genes. Yet, these changes are restricted to few genomic positions. In any case, and reminiscent of the situation with histone acetylation (Valor et al., 2013; McFarland et al., 2012), deficits in histone H3 methylation do not follow a straight relationship with transcriptional dysregulation.
2015-12-31 | GSE63675 | GEO
Project description:Several intracellular pathogens target the host miRNA to modulate the expression of host proteins for their successful infection and survival. For example, S. typhimurium (Schulte et al., 2011) and Mycobacterium tuberculosis (Kumar et al., 2015) downregulate miRNAs of let-7 family to modulate immune response in host; H. pylori infection induces the expression of miR-155 to inhibit the release of IL-8 (Xiao et al., 2009); L. monocytogens triggers the expression of anti- inflammatory cytokine IFN-β by downregulation of miR-145 (Izar et al., 2012). Similarly, Leishmania infection also modulates the expression of various miRNA in macrophages (Lemaire et al., 2013). Consequently, it has been shown that L. donovani infection downregulates miR-122 expression which lowers serum cholesterol to facilitate infection (Ghosh et al., 2013). Whereas, Leishmania significantly enhances the miR30A- 3p expression and modulates autophagic pathway in macrophages (Singh et al., 2016). To understand how Leishmania modulate the expression of various genes in infected macrophages, we have compared the miRNA profile of uninfected and infected macrophages.
2017-06-19 | GSE89529 | GEO