Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8741610_1.fastq.gz | Fastqsanger.gz | |||
| SRR8741610_2.fastq.gz | Fastqsanger.gz | |||
| SRR8741620_1.fastq.gz | Fastqsanger.gz | |||
| SRR8741620_2.fastq.gz | Fastqsanger.gz | |||
| SRR8741611_1.fastq.gz | Fastqsanger.gz |
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Project description:We affinity-purified VEX1GFP-associated proteins using cryomilling and high-affinity nanobodies. The procedure was carried out initially in insect-stage T. brucei, for which protocols were established, and then in bloodstream-form T. brucei. Quantitative proteomic analysis revealed tag-dependent enrichment of GFP and the same set of five proteins in four independent experiments; VEX1 was enriched, as expected, but also Tb927.11.13380, an ortholog of the nonsense-mediated mRNA-decay (NMD) ATP-dependent superfamily 1-type helicases, UPF1/SMG2/NAM7/Rent1 19), now designated VEX2 (predicted 224-kDa, 2026 residues). The other three proteins that displayed tag-dependent enrichment were all three components of chromatin assembly factor 1 (CAF-1; CAF-1a, Tb927.8.3980; CAF-1b, Tb927.10.7050, CAF-1c, Tb927.11.4970a), the evolutionary conserved hetero-trimeric replication-associated histone chaperone.
2019-05-31 | PXD013304 | Pride
Project description:RNA-seq following knockdown of VEX2, VEX1/VEX2 or CAF-1b
| PRJEB21615 | ENA
Project description:Senescence of stromal fibroblasts has been linked to establishment of cancer associated fibroblasts (CAF) and aging-associated increase of tumors. However, in clinically occurring carcinomas, density and proliferation of CAFs are frequently increased rather than decreased. We previously showed that genetic deletion or down-modulation of the canonical Notch effector CSL/RBP-J? in skin dermal fibroblasts is sufficient for CAF activation with consequent development of multifocal keratinocyte tumors. We now show that CSL deletion or knockdown induces senescence of primary fibroblasts derived from dermis, oral mucosa, breast and lung. CSL functions in these cells as a constitutive direct repressor of multiple senescence- and CAF-effector genes. At the same time, it physically interacts with p53, repressing its activity, and p53 activation provides a failsafe mechanism against compromised CSL function. Concomitant loss of CSL and p53 overcomes fibroblast senescence, enhances expression of CAF effector genes and, in vivo, promotes tumour and stromal cell expansion. Together, the findings support a CAF activation/stromal evolution model under convergent CSL/p53 control. Examination of genome-wide CSL binding sites in primary human dermal fibroblasts usinf two different antibodies against CSL
2015-08-24 | E-GEOD-59942 | biostudies-arrayexpress
Project description:During development, specialized cell lineages are generated through the establishment of cell type-specific transcriptional patterns and epigenetic programs. However, the precise mechanisms and regulators that maintain these specialized cell states remain largely elusive. To identify molecules that safeguard somatic cell identity, we performed two comprehensive RNAi screens targeting known and predicted chromatin regulators during transcription factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPSCs). Remarkably, subunits of the chromatin assembly factor-1 (CAF-1) complex emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation, DNA methylation and heterochromatin maintenance. Suppression of CAF-1 increased reprogramming efficiencies by several orders of magnitude and generated iPSCs two to three times faster compared to controls without affecting cell proliferation. We demonstrate that suppression of CAF-1 leads to a more accessible chromatin structure specifically at enhancer elements early during reprogramming. These changes were accompanied by increased binding of the reprogramming factor Sox2 to ESC-specific regulatory elements and earlier activation of pluripotency-associated genes. Notably, suppression of CAF-1 also enhanced iPSC formation from blood progenitors as well as the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 as an unanticipated regulator of somatic cell identity and provide a potential strategy to modulate cellular plasticity in a regenerative setting. Keywords: Genome binding/occupancy profiling by high throughput sequencing Chromatin accessibility and Sox2 bindings in CAF-1 knockdown and Renilla control during early OKSM reprogramming by high throughput sequencing
2015-12-10 | E-GEOD-72744 | biostudies-arrayexpress
Project description:Gene expression profiling of CAF co-cultured with human oral squamous cell carcinoma (OSCC) cells compared with mono-cultured CAF. To identify key molecular regulators expressed by carcinoma-associated fibroblasts (CAF) that promote cancer cell invasion, microarrays were performed by comparing co-cultured OSCC cells and CAF with monoculture controls. comparison 1: CAF co-cultured with OSCC vs. mono-cultured CAF comparison 2: OSCC co-cultured with CAF vs. mono-cultured OSCC 1.7X10(5) YD-10B OSCC cells and 1.7X10(5) CAF were seeded in the upper chamber and lower chamber, respectively, of 6-transwell plates containing collagen-coated 1 micrometer pore transmembrane filters (Becton Dickinson, Franklin Lakes, NJ, USA). Monoculture control samples were generated by culturing only CAF or OSCC on the same side of the filter as in the co-culture design.
2010-06-21 | E-GEOD-18532 | biostudies-arrayexpress
Project description:Cancer associated fibroblasts (CAFs) are integral to the solid tumor microenvironment. Once thought to be a relatively uniform population of matrix-producing cells, the arrival of single cell RNA sequencing has revealed diverse CAF phenotypes. Here, we further probe CAF heterogeneity with a comprehensive multiome approach. Using paired, same-cell chromatin accessibility and transcriptome analysis, we provide an integrated analysis of CAF subpopulations over a complex spatial transcriptomic and proteomic landscape to identify three superclusters – steady state-like (SSL), mechanoresponsive (MR) and immunomodulatory (IM) CAFs. These superclusters are recapitulated across multiple tissue types and species. Selective disruption of underlying mechanical force or immune checkpoint inhibition therapy results in shifts in CAF subpopulation distributions and impacts tumor growth. As such, the balance among CAF superclusters may have considerable translational implications. Collectively, this research expands our understanding of CAF biology, identifying regulatory pathways in CAF differentiation and elucidating novel therapeutic targets in a species- and tumor-agnostic manner.
2022-10-21 | GSE212481 | GEO
Project description:Carcinoma-associated fibroblasts (CAF) are key players in the tumor microenvironment. By combining 6 well-known stromal markers, we identify four CAF subsets (CAF-S1 to CAF-S4) in human breast and ovarian cancers.
| EGAS00001003344 | EGA
Project description:Compare the difference between pairwise aNOF and CAF samples for two patients patient #225: aNOF #225 vs CAF #225 patient #248: aNOF #248 vs CAF #248
2012-01-27 | E-GEOD-35249 | biostudies-arrayexpress
Project description:OsDDM1 and OsDRM2 display functional specificities that define distinct DNA methylation pathways in the bulk of DNA methylation of the rice genome Cr_DJ.CG.bw: Cr_DJ CG methylation Cr_DJ.CHG.bw: Cr_DJ CHG methylation Cr_DJ.CHH.bw: Cr_DJ CHH methylation ddm1ab.CG.bw: ddm1a/1b CG methylation ddm1ab.CHG.bw: ddm1a/1b CHG methylation ddm1ab.CHH.bw: ddm1a/1b CHH methylation S706.CG.bw: osdrm2 CG methylation S706.CHG.bw: osdrm2 CHG methylation S706.CHH.bw: osdrm2 CHH methylation H3k9me2_macs_peaks.xls: CrDJ H3K9me2 modification peaks H3k9me2_macs_treat_afterfiting.wig: CrDJ H3K9me2 modification wig CrDJ_K27_macs_peaks.xls: CrDJ H3K27me3 modification peaks CrDJ_K27_macs_treat_afterfiting.wig: CrDJ H3K27me3 modification wig DJvsddm1a1b_DESeq2_treated_results.xls: CrDJ and osddm1a1b different expression genes DJvsS706_DEseq2_treated.results.xls: CrDJ and osdrm2 different expression genes smRNA24nt.gff: CrDJ 24nt smRNA smRNA24nt.706.gff: osdrm2 24nt smRNA
2016-06-13 | E-GEOD-81436 | biostudies-arrayexpress