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Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features [L-NICD]

ABSTRACT: Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features [L-NICD]

PROVIDER: PRJNA646662 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12235456_1.fastq.gz	Fastqsanger.gz
	SRR12235456_2.fastq.gz	Fastqsanger.gz
	SRR12235457_1.fastq.gz	Fastqsanger.gz
	SRR12235457_2.fastq.gz	Fastqsanger.gz
	SRR12235458_1.fastq.gz	Fastqsanger.gz

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Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features

Project description:Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features

| PRJNA646654 | ENA

Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features [Venus]

Project description:Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features [Venus]

| PRJNA646661 | ENA

Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features [L-NICD]

Project description:Hepatocellular carcinoma (HCC) is the predominant primary liver cancer and an increasing cause of cancer-related deaths worldwide, due in part through increased obesity-associated nonalcoholic steatohepatitis (NASH) and associated fibrosis. The Notch signaling pathway is inappropriately “reactivated” in hepatocytes in obesity and plays an active role in the pathogenesis of NASH-associated fibrosis. We aimed to understand the involvement of Notch in the pathogenesis of mouse and human HCC.

2020-09-28 | GSE154551 | GEO

Notch activity determines a common hepatocellular carcinoma subtype with unique molecular and clinicopathologic features [Venus]

2020-09-28 | GSE154550 | GEO

Modeling Notch-induced tumor cell survival in the Drosophila ovary identifies cellular and transcriptional response to nuclear NICD accumulation

Project description:Notch is a conserved developmental signaling pathway that is dysregulated in many cancer types, most often through constitutive activation. Tumor cells with nuclear accumulation of the active Notch receptor, NICD, generally exhibit enhanced survival while patients experience poorer outcomes. To understand the impact of NICD accumulation during tumorigenesis, we developed a tumor model using the Drosophila ovarian follicular epithelium. Using this system we demonstrated that NICD accumulation contributed to larger tumor growth, reduced apoptosis, increased nuclear size, and fewer incidents of DNA damage without altering ploidy. Using bulk RNA sequencing we identified the key Notch-induced targets involved in cell survival and DNA damage repair which were alternatively regulated prior to tumor formation. Finally, using single-cell RNA sequencing we demonstrated that genes contributing to many pathways are altered following tumor formation in a cell-type-specific manner. Ectopically expressing NICD produced dysregulated expression of genes involved in cell death regulation, immune and stress response, JAK/STAT signaling, cytoskeletal binding, adhesion, polarity, and growth regulation. This valuable tumor model for nuclear NICD accumulation in adult Drosophila follicle cells has allowed us to better understand the specific role of nuclear NICD accumulation in tumor cells in tumor cell survival and tumor progression.

2021-09-19 | GSE182505 | GEO

HEK NICD AP-MS - Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs)

Project description:Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs). Tight quantitative and temporal control of Notch activity is essential for vascular development, yet the details of Notch regulation in ECs are incompletely understood. We found that ubiquitin-specific peptidase 10 (USP10) interacted with the NOTCH1 intracellular domain (NICD1) to slow the ubiquitin-dependent turnover of this short-lived form of the activated NOTCH1 receptor. Accordingly, inactivation of USP10 reduced NICD1 abundance and stability, and diminished Notch-induced target gene expression in ECs. In mice, loss of endothelial Usp10 increased vessel sprouting and partially restored the patterning defects caused by ectopic expression of NICD1. Thus, USP10 functions as an NICD1 deubiquitinase, which fine-tunes endothelial Notch responses during angiogenic sprouting.

2019-04-11 | PXD013192 | Pride

Gene expression changes in Nicd induced wing disc hyperplasia

Project description:The outcome of Notch proliferation on proliferation depends on the context. In Drosophila wing imaginal discs Notch activation causes hyperplasia despite having localized inhibitory effects on proliferation. To understand te underlying mechanisms we have used genomic strategies to identify the Notch-Su(H) target genes during wing discs hyperplasis. these data are the results from expression profiling the RNAs from hyperplastic wing discs overexpressing Nicd. Direct comparison of third instar lavae wing imaginal disc Nicd (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with UAS-Nicd; FRT82B) vs control (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with FRT82B ). 4 Biological replicates, the 2nd replicate was performed as a dye-swap.

2013-12-31 | E-GEOD-41428 | biostudies-arrayexpress

Su(H) bound regions in Nicd induced wing-disc hyperplasia

Project description:The outcome of Notch activation on proliferation depends on cellular context. In Drosophila wing discs Notch activation causes hyperplasia despite having localized inhibitory effects on proliferation. To understand the underlying mechanisms we have used genomic strategies to identify the Notch-Su(H) target genes directly activated during wing disc hyperplasia. These data are the results from ChIP-Chip experiments to identify genomic regions occupied by Su(H) in hyperplastic Nicd-expressing Drosophila wing discs. 2 independent replicates; Immunoprecipitation perfomed with Su(H) antibody on chromatin isolated from wing discs overexpressing Nicd (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with UAS-Nicd; FRT82B) and compared to the total input DNA.

2013-12-31 | E-GEOD-41426 | biostudies-arrayexpress

Transcriptome profiling of Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed intestinal progenitor cells

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of intestinal progenitor cells in Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed midguts Methods: mRNA profiles of intestinal progenitor cells isolated from 7-day-old wild-type (Ctrl) and ttk-RNAi, dpn overexpressed(dpn OE), Nicd overexpressed(Nicd OE) and seq&Nicd overexpressed(seq&Nicd OE) Drosophila midgut were generated by deep sequencing using Illumina HiSeq 2500. Results: ttk-RNAi in intestinal progenitor cells induces the expression of many neural-specific genes, including dpn and seq. Dpn ectopic expresion explains most of the ttk-RNAi expression profile change. Seq ectopic expression explains the expression of neural-specific Notch targets in the ttk-RNAi intestinal progenitor cells.

2021-02-23 | GSE130942 | GEO

Histone variant H2A.Z deposition and acetylation directs the canonical Notch signaling response

Project description:The study deals with the elucidation of potential interaction partners of the intracellular domain of the transmembrane receptor Notch1, termed NICD. The NICD is released from the cytoplasmic tail of the Notch receptor by gamma-secretase treatment and translocated as a transcription factor to the nucleus. Here, virally transduced recombinant NICD constructs (wild-type and deltaEP hyperactive mutant) were employed for AP-MS with the aim of identifying novel NICD interactors in a murine T cell leukemia cell line.

2018-06-25 | PXD008747 | Pride

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