Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Myeloid-specific ablation of Pdcd1 alters fate comittment of tumor-associated macrophages and induces anti-tumor immunity

ABSTRACT: Myeloid-specific ablation of Pdcd1 alters fate comittment of tumor-associated macrophages and induces anti-tumor immunity

PROVIDER: PRJNA849613 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19664368_1.fastq.gz	Fastqsanger.gz
	SRR19664368_2.fastq.gz	Fastqsanger.gz
	SRR19664369_1.fastq.gz	Fastqsanger.gz
	SRR19664369_2.fastq.gz	Fastqsanger.gz
	SRR19664370_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Myeloid-specific SHP-2 ablation alters the fate commitment of myeloid cells and induces anti-tumor immunity

Project description:Myeloid-specific SHP-2 ablation alters the fate commitment of myeloid cells and induces anti-tumor immunity

| PRJNA777536 | ENA

Myeloid-specific ablation of Pdcd1 alters fate comittment of tumor-associated macrophages and induces anti-tumor immunity

Project description:We generated mice with conditional targeting of the Pdcd1 gene (encoding for PD-1) in myeloid cells (Pdcd1-2fl/flLysMCre). Pdcd1-2fl/flLysMCre mice had significantly diminished tumor growth. As revealed by RNA-seq, myeloid-specific Pdcd1 ablation was paralleled by generation of myeloid cells with monocytic dominance, and activated macrophages with molecular signatures of enhanced myeloid cell differentiation, macrophage activation, phagocytosis, TLR and NF-kB signaling, chemokine and cytokine production, and expression of immunostimulatory molecules.

2022-10-26 | GSE206207 | GEO

Myeloid-specific SHP-2 ablation alters the fate commitment of myeloid cells and induces anti-tumor immunity

Project description:We generated mice with conditional targeting of the Ptpn11 gene (encoding for Shp-2) in T cells (Shp-2fl/flLckCre) or myeloid cells (Shp-2fl/flLysMCre). Although no difference in tumor growth was observed between Shp-2fl/flLckCre and control mice and both groups were similarly benefitted by PD-1 blockade, Shp-2fl/flLysMCre mice had significantly diminished tumor growth that was not further decreased by anti-PD-1 treatment. As revealed by RNA-seq, myeloid-specific Shp-2 ablation was paralleled by expansion of activated myeloid cells and macrophages with molecular signatures of enhanced neutrophil and macrophage differentiation, phagocytosis, antigen-presenting function, TLR and type I IFN signaling, chemokine production, and expression of immunostimulatory molecules, which promoted T cell recruitment and activation.

2022-10-26 | GSE187394 | GEO

LSD1 ablation stimulates anti-tumor immunity and enables checkpoint blockade

Project description:LSD1 ablation stimulates anti-tumor immunity and enables checkpoint blockade

| PRJNA445303 | ENA

LSD1 ablation stimulates anti-tumor immunity and enables checkpoint blockade

Project description:Chromatin regulators play a broad role in regulating gene expression, and when gone awry, can lead to cancer. Here we demonstrate that ablation of the histone demethylase LSD1 in cancer cells increases repetitive element expression, including ERVs, and decreases expression of RNA-induced silencing complex (RISC) components. Significantly, this leads to dsRNA stress and activation of type 1 interferon, which stimulates anti-tumor T cell immunity and restrains tumor growth. Furthermore, LSD1 depletion enhances tumor immunogenicity and T cell infiltration in poorly immunogenic tumors, and elicits significant responses of checkpoint blockade-refractory mouse melanoma to anti-PD-1 therapy. Consistently, TCGA data analysis shows an inverse correlation between LSD1 expression and CD8+ T cell infiltration in various human cancers. Our study identifies LSD1 as a potent inhibitor of anti-tumor immunity and responsiveness to immunotherapy, and suggests LSD1 inhibition combined with PD-(L)1 blockade as a novel cancer treatment strategy.

2018-06-21 | GSE112230 | GEO

TREM1 deficiency alters the tumor myeloid landscape

Project description:TREM1 deficiency alters the tumor myeloid landscape

| PRJEB65047 | ENA

Ablation of coactivator Med1 switches the cell fate of dental epithelia to that generating hair [mixed stage]

Project description:Cell fate is defined by specific transcriptional program. Here, we provide evidence that the transcriptional coactivator, Mediator 1 (MED1), is critical in determining the cell fate of ectodermal epithelia. MED1 ablation disrupted enamel formation and generated hair adjacent to the incisors. Deletion of MED1 altered the differentiation of dental epithelia to one expressing epidermal and hair genes similar to the skin. The cellular switch from dental to epidermal/hair lineage was characterized by abnormalities in MED1 deficient dental epithelial stem cells residing in cervical loop. MED1 deficiency caused a failure of dental epithelial stem cells to commit to the dental stratum intermedium regulated by Notch signaling. Instead, MED1 deficient cells retained stem cell potentials expressing Sox2. These cells were eventually adopted an epidermal fate probably through calcium provided through capillary networks, which is originally utilized for enamel formation. Our results demonstrate that MED1 regulates Sox2/Notch1 regulated cell lineage determination in dental epithelia. Our study also shows a potential to regenerate hairs by using genetically engineered dental tissues or cells outside of the skin. n=3 WT and KO (each sample contain dissected dental tissues from 3 mice combined)

2013-09-23 | E-GEOD-50503 | biostudies-arrayexpress

Ablation of coactivator Med1 switches the cell fate of dental epithelia to that generating hair [maturation stage]

Project description:Cell fate is defined by specific transcriptional program. Here, we provide evidence that the transcriptional coactivator, Mediator 1 (MED1), is critical in determining the cell fate of ectodermal epithelia. MED1 ablation disrupted enamel formation and generated hair adjacent to the incisors. Deletion of MED1 altered the differentiation of dental epithelia to one expressing epidermal and hair genes similar to the skin. The cellular switch from dental to epidermal/hair lineage was characterized by abnormalities in MED1 deficient dental epithelial stem cells residing in cervical loop. MED1 deficiency caused a failure of dental epithelial stem cells to commit to the dental stratum intermedium regulated by Notch signaling. Instead, MED1 deficient cells retained stem cell potentials expressing Sox2. These cells were eventually adopted an epidermal fate probably through calcium provided through capillary networks, which is originally utilized for enamel formation. Our results demonstrate that MED1 regulates Sox2/Notch1 regulated cell lineage determination in dental epithelia. Our study also shows a potential to regenerate hairs by using genetically engineered dental tissues or cells outside of the skin. n=4 WT and KO (each group contains dissected dental tissues from 3 mice combined)

2013-09-23 | E-GEOD-50502 | biostudies-arrayexpress

Ablation of coactivator Med1 switches the cell fate of dental epithelia to that generating hair [CL stage]

2013-09-23 | E-GEOD-50501 | biostudies-arrayexpress

Loss of Asxl1 Alters Mesenchymal Stem Cell Fate through H3K4me3

Project description:Loss of Asxl1 Alters Mesenchymal Stem Cell Fate through H3K4me3

| PRJNA305426 | ENA