Nextpresso: Next Generation Sequencing Expression Analysis Pipeline

Graña, Osvaldo; Rubio-Camarillo, Miriam; Fdez-Riverola, Florentino; Pisano, David G.; Glez-Peña, Daniel

doi:10.2174/1574893612666170810153850

Cited by 60 publications

(54 citation statements)

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“…The resulting purified cDNA library was applied to an Illumina flow cell for cluster generation and sequenced on an Illumina HiSeq 2500 following manufacturer's protocols. Fifty‐one base single‐end sequencing reads were analyzed with the nextpresso pipeline (Grana et al , ), as follows: Sequencing quality was checked with FastQC v0.11.0 (http://www.bioinformatics.babraham.ac.uk/projects/fastqc/). Reads were aligned to the mouse genome (NCBI37/mm9) with TopHat‐2.0.10 (Trapnell et al , ) using Bowtie 1.0.0 (Langmead et al , ) and SAMtools 0.1.19 (Li et al , ), allowing two mismatches and 20 multihits.…”

Section: Methodsmentioning

confidence: 99%

Role of bulge epidermal stem cells and TSLP signaling in psoriasis

et al. 2019

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Psoriasis is a common inflammatory skin disease involving a cross‐talk between epidermal and immune cells. The role of specific epidermal stem cell populations, including hair follicle stem cells (HF‐SCs) in psoriasis is not well defined. Here, we show reduced expression of c‐JUN and JUNB in bulge HF‐SCs in patients with scalp psoriasis. Using lineage tracing in mouse models of skin inflammation with inducible deletion of c‐Jun and JunB, we found that mutant bulge HF‐SCs initiate epidermal hyperplasia and skin inflammation. Mechanistically, thymic stromal lymphopoietin (TSLP) was identified in mutant cells as a paracrine factor stimulating proliferation of neighboring non‐mutant epidermal cells, while mutant inter‐follicular epidermal (IFE) cells are lost over time. Blocking TSLP in psoriasis‐like mice reduced skin inflammation and decreased epidermal proliferation, VEGFα expression, and STAT5 activation. These findings unravel distinct roles of HF‐SCs and IFE cells in inflammatory skin disease and provide novel mechanistic insights into epidermal cell interactions in inflammation.

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Section: Methodsmentioning

confidence: 99%

Role of bulge epidermal stem cells and TSLP signaling in psoriasis

et al. 2019

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“…D" kit. The adapter-ligated library was completed by PCR with Illumina PE primers (8-11 cycles) and the resulting directional cDNA libraries were sequenced for 50 bases in a single-read format (Illumina HiSeq2000) and analyzed with nextpresso (Graña, Rubio-Camarillo et al, 2018). Reads were quality-checked with FastQC (http://www.bioinformatics.babraham.ac.uk/projects/fastqc) and aligned to the mouse genome (GRCm38/mm10) with TopHat-2.0.10 (Trapnell, Roberts et al, 2012), using Bowtie 1.0.0 (Langmead, Trapnell et al, 2009) and Samtools 0.1.19 (Li & Durbin, 2009), allowing two mismatches and five multihits.…”

Section: Analysis Of Mrna and Microrna Levelsmentioning

confidence: 99%

miR-203 imposes an intrinsic barrier during cellular reprogramming by targeting NFATC2

Salazar

Martı́nez-Martı́nez

Graña‐Castro

et al. 2020

Preprint

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Cellular reprogramming from somatic to pluripotent cells is the basis for multiple applications aimed to replace damaged tissues in regenerative medicine. However, this process is limited by intrinsic barriers that are induced in response to reprogramming factors. In this manuscript we report that miR-203, a microRNA with multiple functions in differentiation and tumor suppression, acts as an endogenous barrier to reprogramming.Genetic ablation of miR-203 results in enhanced reprogramming whereas its expression prevents the formation of pluripotent cells both in vitro and in vivo. Mechanistically, this effect correlates with the direct repression of NFATC2, a transcription factor involved in the early phases of reprogramming. Inhibition of NFATC2 mimics miR-203 effects whereas NFATC2 overexpression rescues inducible cell pluripotency in miR-203overexpressing cultures. These data suggest that miR-203 repression may favor the efficiency of reprogramming in a variety of cellular models.

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“…Library construction and sequencing were done as described previously (22). Alignment to human genome hg19 transcript assembly and differential expression was carried out using Nextpresso (23). Genes were considered as differentially expressed if FDR < 0.05.…”

Section: Rna-seqmentioning

confidence: 99%

CREBBP/EP300 Bromodomain Inhibition Affects the Proliferation of AR-Positive Breast Cancer Cell Lines

García-Carpizo

Ruiz‐Llorente

Sarmentero

et al. 2019

Molecular Cancer Research

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Inhibitors that prevent the binding of bromodomains to acetylated histones hold therapeutic potential. However, the effects of targeting most of the 60 different bromodomains found in the human proteome remain unexplored. Here, we investigate the molecular mechanisms responsible for the antiproliferative properties of CREBBP/EP300 bromodomain inhibition in ER-negative breast cancer cell lines. We show using genetic and chemical approaches that CREBBP/ EP300 bromodomains are critical to support the proliferation of the triple-negative breast cancer cell line MDA-MB-453. Analysis of the transcriptional pathways affected by CREBBP/EP300 bromodomain inhibitors reveals that the expression of genes associated with super-enhancers is downregulated, which in turn are occupied by very high levels of androgen receptor (AR) in MDA-MB-453 cells.Treatment of MDA-MB-453 with CREBBP/EP300 bromodomain inhibitors downregulates the expression of an ARdependent signature distinctive of breast cancer tumors that express AR and causes a decrease in H3K27ac levels at ARbinding sites. In accordance, in prostate cancer cell lines that express AR CREBBP/EP300 bromodomain inhibitors downregulate the expression of genes bound by AR and associated with super-enhancers. In summary, we report that triplenegative breast cancer cell lines that express AR are particularly sensitive to CREBBP/EP300 bromodomain inhibitors and consequently these inhibitors hold potential to treat this type of cancer.Implications: AR-dependent cancer cell lines are sensitive to CREBBP/EP300 bromodomain inhibitors. Materials and Methods Cell lines and reagentsHuman cancer cell lines MDA-MB-231, MDA-MB-453, SKBR3, DU145, PC3, LNCaP, VCaP, and 22RV1 were purchased from ATCC. CAL148 and MFM223 were purchased from DSMZ. SUM185PE was purchased from Asterand Bioscience. The identity

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Nextpresso: Next Generation Sequencing Expression Analysis Pipeline

Cited by 60 publications

References 0 publications

Role of bulge epidermal stem cells and TSLP signaling in psoriasis

Role of bulge epidermal stem cells and TSLP signaling in psoriasis

miR-203 imposes an intrinsic barrier during cellular reprogramming by targeting NFATC2

CREBBP/EP300 Bromodomain Inhibition Affects the Proliferation of AR-Positive Breast Cancer Cell Lines

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