Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide pooled CRISPR knockout screen for novel regulators of macrophage efferocytosis.

ABSTRACT: Genome-wide pooled CRISPR knockout screen for novel regulators of macrophage efferocytosis.

PROVIDER: PRJNA873271 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21221208.fastq.gz	Fastqsanger.gz
	SRR21221209.fastq.gz	Fastqsanger.gz
	SRR21221210.fastq.gz	Fastqsanger.gz
	SRR21221211.fastq.gz	Fastqsanger.gz
	SRR21221212.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Genome-wide pooled CRISPR knockout screen for novel regulators of macrophage efferocytosis.

Project description:We performed a FACS-based genome-wide CRISPR knockout screen in primary murine macrophages to identify regulators of efferocytosis, the phagocytic clearance of dying cells. The screen identified known and novel regulators of macrophage efferocytosis. More broadly, the screen approach can be applied to interrogate complex functional phenotypes in primary macrophages.

2022-11-23 | GSE212008 | GEO

CRISPR screen for NMD regulators

Project description:CRISPR screen for NMD regulators

| PRJNA602918 | ENA

CRISPR screen to identify regulators of neuronal differentiation

Project description:To search for factors regulating neuronal differentiation, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of depletion of their mutant clones within a pooled loss-of-function library upon neuronal differentiation.

2024-01-12 | E-MTAB-11944 | biostudies-arrayexpress

CRISPR screen for regulators of cadherin based cell to cell adhesion

Project description:Pooled Crispr based genome wide screen to find potential (transcriptional) regulators and pathways underlying the regulation of cadherin based cell to cell adhesion.

2024-07-03 | GSE244919 | GEO

Identify proinsulin regulators using CRISPR screen and mouse genetics [CRISPR screen]

Project description:Identify proinsulin regulators using CRISPR screen and mouse genetics [CRISPR screen]

| PRJNA1030057 | ENA

Genome-wide CRISPR screen to identify CD58 regulators

Project description:Genome-wide CRISPR screen to identify CD58 regulators

| PRJNA934388 | ENA

CRISPR screen to identify regulators of neuronal differentiation

Project description:CRISPR screen to identify regulators of neuronal differentiation

| PRJEB54698 | ENA

Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

2021-12-01 | E-MTAB-8885 | biostudies-arrayexpress

Identify proinsulin regulators using CRISPR screen and mouse genetics [CRISPR screen]

Project description:Proinsulin is the precursor of insulin in pancreatic beta cells. Altered proinsulin and proinsulin to insulin ratio mark beta cell dysfunction, predictuing disease progression into type 1 and type 2 diabetes. Of essential role for beta cell function, knowledge about proinsulin production and its role in disease are currently very limited. Using genome wide CRISPR screen, we identified 84 proinsulin regulators including classical protein convertases Pcsk1 and Cpe, and novel factors like Pdia6. Among the list 29 proinsulin regulators were trajectory genes involved in disease progression in obesity and type 2 diabetes in humans. In vivo mouse genetics study revealed unique genetic architecture and quantitative trait loci (QTLs) modulating plasma proinsulin levels. Integrative analyzing and mapping of the QTL signals directly pinpointed to proinsulin regulators identified from the CRISPR screen, which in return greatly improved resolution of the mouse genetic study. 4 out of 5 overlapped genes can be individually validated. Knocking down the leading hits Pdia6 leads to decreased proinsulin content and remarkable loss of proinsulin granules in beta cells. Consequently, proinsulin secretion was greatly decreased. Mechanistically, protein translation rate was greatly impaired after knocking down Pdia6. Our study demonstrated the power of combining in vitro functional genomics with in vivo mouse genetics study to identify proinsulin regulatory network in pancreatic beta cells.

2023-11-15 | GSE245845 | GEO

Identify proinsulin regulators using CRISPR screen and mouse genetics

Project description:Identify proinsulin regulators using CRISPR screen and mouse genetics

| PRJNA1030049 | ENA