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Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing

ABSTRACT: Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing

PROVIDER: PRJNA1036226 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26686563_1.fastq.gz	Fastqsanger.gz
	SRR26686563_2.fastq.gz	Fastqsanger.gz
	SRR26686564_1.fastq.gz	Fastqsanger.gz
	SRR26686564_2.fastq.gz	Fastqsanger.gz
	SRR26686565_1.fastq.gz	Fastqsanger.gz

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Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing (HL60 RNA-seq)

Project description:The 21kD GTPase Rac is an evolutionarily ancient regulator of cell shape and behavior. Rac2 is predominantly expressed in hematopoietic cells where it is essential for survival and motility. The hyperactivating mutation Rac2E62K also causes human immunodeficiency, although the mechanism remains unexplained. Here we report that in Drosophila, hyperactivating Rac stimulates ovarian cells to cannibalize neighboring cells, destroying the tissue. We then show that hyperactive Rac2E62K stimulates human HL60-derived macrophage-like cells to engulf and kill living T cell leukemia cells. Primary mouse Rac2E62K/+ bone-marrow-derived macrophages also cannibalize primary Rac2E62K/+ T cells due to a combination of macrophage hyperactivity and T cell hypersensitivity to engulfment. Additionally, Rac2E62K/+ macrophages non-autonomously stimulate wild type macrophages to engulf T cells. Rac2E62K also enhances engulfment of target cancer cells by chimeric antigen receptor-expressing macrophages (CAR-M). We propose that Rac-mediated cell cannibalism may contribute to Rac2E62K/+ human immunodeficiency and enhance CAR-M cancer immunotherapy.

2023-11-13 | GSE247103 | GEO

Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing (BMDM RNA-seq)

2023-11-13 | GSE247104 | GEO

Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing (BMDM RNA-seq)

Project description:Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing (BMDM RNA-seq)

| PRJNA1036230 | ENA

Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing (HL60 RNA-seq)

Project description:Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing (HL60 RNA-seq)

| PRJNA1036231 | ENA

Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing.

Project description:The 21kD GTPase Rac is an evolutionarily ancient regulator of cell shape and behavior. Rac2 is predominantly expressed in hematopoietic cells where it is essential for survival and motility. The hyperactivating mutation Rac2E62K also causes human immunodeficiency, although the mechanism remains unexplained. Here, we report that in Drosophila, hyperactivating Rac stimulates ovarian cells to cannibalize neighboring cells, destroying the tissue. We then show that hyperactive Rac2E62K stimulates human HL60-derived macrophage-like cells to engulf and kill living T cell leukemia cells. Primary mouse Rac2+/E62K bone-marrow-derived macrophages also cannibalize primary Rac2+/E62K T cells due to a combination of macrophage hyperactivity and T cell hypersensitivity to engulfment. Additionally, Rac2+/E62K macrophages non-autonomously stimulate wild-type macrophages to engulf T cells. Rac2E62K also enhances engulfment of target cancer cells by chimeric antigen receptor-expressing macrophages (CAR-M) in a CAR-dependent manner. We propose that Rac-mediated cell cannibalism may contribute to Rac2+/E62K human immunodeficiency and enhance CAR-M cancer immunotherapy.

| S-EPMC10756302 | biostudies-literature

Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-13 | GSE247106 | GEO

The Rac-GEF Tiam1 controls integrin-dependent neutrophil responses

Project description:Rac GTPases are required for neutrophil adhesion and migration, and for the neutrophil effector responses that kill pathogens. These Rac-dependent functions are impaired when neutrophils lack the activators of Rac, Rac-GEFs from the Prex, Vav and Dock families. In this study, we demonstrate that Tiam1 is also expressed in neutrophils, governing focal complexes, actin cytoskeletal dynamics, polarisation and migration, in a manner depending on the integrin ligand to which the cells adhere. Tiam1 is dispensable for the generation of reactive oxygen species but mediates degranulation and NETs release in adherent neutrophils, as well as the killing of bacteria. In vivo, Tiam1 is required for neutrophil recruitment during aseptic peritonitis and for the clearance of Streptococcus pneumoniae during pulmonary infection. However, Tiam1 functions differently to other Rac-GEFs. Instead of promoting neutrophil adhesion to ICAM1 and stimulating β2 integrin activity as could be expected, Tiam1 restricts these processes. In accordance with these paradoxical inhibitory roles, Tiam1 limits the fMLP-stimulated activation of Rac1 and Rac2 in adherent neutrophils, rather than activating Rac as expected. Tiam1 promotes the expression of several regulators of small GTPases and cytoskeletal dynamics, including αPix, Psd4, Rasa3 and Tiam2. It also controls the association of Rasa3, and potentially αPix, Git2, Psd4 and 14‐3‐3ζ/δ, with Rac. We propose these latter roles of Tiam1 underlie its effects on Rac and β2 integrin activity and on cell responses. Hence, Tiam1 is a novel regulator of Rac-dependent neutrophil responses that functions differently to other known neutrophil Rac-GEFs.

2024-01-26 | PXD046791 | Pride

E. coli MG1655Î?rac treated (N340S/G324D Rho) vs control (WT Rho)

Project description:Transcription profiling of E. coli MG1655Î?rac, comparing the effect Rho mutants (SBS: N340S, G324D) with WT Rho Organism: Escherichia coli ,Agilent Custom Escherichia coli Gene Expression Microarray 8x15K (AMADID: 020304) designed by Genotypic Technology Private Limited.

2016-03-28 | E-GEOD-77177 | biostudies-arrayexpress

Key role for Rac in the early transcriptional response to ECM stiffness and the stiffness-dependent repression of ATF3

Project description:The Rho family GTPases, Rac and Rho, play critical roles in transmitting mechanical information contained within the extracellular matrix (ECM) to the cell. Rac and Rho have well described roles in regulating stiffness-dependent actin remodeling, proliferation and motility. However, much less is known about the relative roles of these GTPases in stiffness-dependent transcription, particularly at the genome-wide level. Here, we selectively inhibited Rac and Rho in mouse embryonic fibroblasts cultured on deformable substrata and used RNA sequencing to elucidate and compare the contribution of these GTPases to the early transcriptional response to ECM stiffness. Surprisingly, we found that the stiffness-dependent activation of Rac is dominant over Rho in the initial transcriptional response to ECM stiffness. We also identified Activating Transcription Factor 3 (ATF3) as a major target of stiffness/Rac-mediated signaling and show that ATF3 repression by ECM stiffness helps to explain how the stiffness-dependent activation of Rac results in the induction of cyclin D1.

2023-10-04 | GSE236266 | GEO

Identification of proteins precipitated by means of Acyl-RAC

Project description:The objective was to perform protein identification by ESI-LC-MSMS on a sample subjected to Acyl-RAC assay in order to study protein palmitoylation. The user transfected human paxillin (mCherry-paxillin-CAIL) into a mouse cell line and performed Acyl-RAC assay. The aim of this analysis was to determine whether human paxillin is palmitoylated and confirm the quality of the Acyl-RAC technique to detect palmitoylated proteins.

2021-03-30 | PXD023810 | Pride

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