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HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5

ABSTRACT: HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5

PROVIDER: PRJNA993230 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25194940_1.fastq.gz	Fastqsanger.gz
	SRR25194940_2.fastq.gz	Fastqsanger.gz
	SRR25194941_1.fastq.gz	Fastqsanger.gz
	SRR25194941_2.fastq.gz	Fastqsanger.gz
	SRR25196468_1.fastq.gz	Fastqsanger.gz

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HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [4T1]

Project description:HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [4T1]

| PRJNA993232 | ENA

HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [4T1 tumors]

Project description:HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [4T1 tumors]

| PRJNA992504 | ENA

HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [MDA-MB-231]

Project description:HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [MDA-MB-231]

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HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [4T1 tumors]

Project description:Breast cancer cells or tumors underwent RNA-sequencing or single cell RNA-sequencing to study the role of HSF1 in tumor-immune interactions.

2023-07-11 | GSE236830 | GEO

HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [4T1]

Project description:Breast cancer cells or tumors underwent RNA-sequencing or single cell RNA-sequencing to study the role of HSF1 in tumor-immune interactions.

2023-07-11 | GSE236836 | GEO

HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5 [MDA-MB-231]

Project description:Breast cancer cells or tumors underwent RNA-sequencing or single cell RNA-sequencing to study the role of HSF1 in tumor-immune interactions.

2023-07-11 | GSE236835 | GEO

HSF1 excludes CD8+ T cells from breast tumors via suppression of CCL5

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

2023-07-11 | GSE236972 | GEO

Yeast HSF1 vs hsf1-ba1

Project description:Upon heat shock, Hsf1 protein is extensively phosphorylated, however, this modification is inhibited by an hsf1-bal mutation. To get genome-wide effect of the hyperphosphorylation on Hsf1-regulated transcription, the heat-induced gene expression profiles in HSF1 and hsf1-bal cells were compared. Keywords: stress response

2005-09-27 | GSE3361 | GEO

Caravagna2010 - Tumour suppression by immune system

Project description:Tumour suppression by immune system through stochastic oscillations GiulioCaravagnaa Albertod’Onofriob PaoloMilazzoa RobertoBarbutia https://doi.org/10.1016/j.jtbi.2010.05.013 Abstract The well-known Kirschner–Panetta model for tumour–immune System interplay [Kirschner, D., Panetta, J.C., 1998. Modelling immunotherapy of the tumour–immune interaction. J. Math. Biol. 37 (3), 235–252] reproduces a number of features of this essential interaction, but it excludes the possibility of tumour suppression by the immune system in the absence of therapy. Here we present a hybrid–stochastic version of that model. In this new framework, we show that in reality the model is also able to reproduce the suppression, through stochastic extinction after the first spike of an oscillation.

2024-09-02 | BIOMD0000000912 | BioModels

Mitochondrial HSF1 triggers mitochondrial dysfunction and neurodegeneration in Huntington’s disease

Project description:Aberrant localization of proteins to mitochondria disturbs mitochondrial function and contributes to the pathogenesis of Huntington’s disease (HD). However, the crucial factors and the molecular mechanisms remain elusive. Here, we found that heat shock transcription factor 1 (HSF1) accumulates in the mitochondria of HD cell cultures, a YAC128 mouse model, and human striatal organoids derived from HD induced pluripotent stem cells (iPSCs). Overexpression of mitochondria-targeting HSF1 (mtHSF1) in the striatum causes neurodegeneration and HD-like behavior. Mechanistically, mtHSF1 facilitates mitochondrial fission by activating dynamin-related protein 1 (Drp1) phosphorylation at S616. Moreover, mtHSF1 suppresses single-stranded DNA binding protein 1 (SSBP1) oligomer formation, which results in mitochondrial DNA (mtDNA) deletion. Suppression of HSF1 mitochondrial localization by DH1, a unique peptide inhibitor, abolishes HSF1-induced mitochondrial abnormalities and ameliorates deficits in an HD animal model and human striatal organoids. Altogether, our findings describe an unsuspected role of HSF1 in contributing to mitochondrial dysfunction, which may provide a promising therapeutic target for HD.

2022-04-13 | GSE198927 | GEO

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