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An engineered viral protein activates STAT5 to prevent T cell suppression

ABSTRACT: An engineered viral protein activates STAT5 to prevent T cell suppression

PROVIDER: PRJNA1221848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR32303064_1.fastq.gz	Fastqsanger.gz
	SRR32303064_2.fastq.gz	Fastqsanger.gz
	SRR32303066_1.fastq.gz	Fastqsanger.gz
	SRR32303066_2.fastq.gz	Fastqsanger.gz

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An engineered viral protein activates STAT5 to prevent T cell suppression

Project description:T cell therapy efficacy can be compromised if cytokine-induced Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling is dysregulated or insufficient to sustain functionality. Here, we demonstrate that LCK kinase activity can be recruited to non-canonical protein substrates to directly activate targeted STAT proteins in T cells. STAT activation was accomplished by engineering the Herpesvirus saimiri (HVS) tyrosine kinase interacting protein (TIP) to provide a platform for the enforced recruitment of LCK to STAT proteins. We determined that a minimal region of TIP that binds to LCK could be combined with STAT binding sites derived from endogenous cytokine receptors. These constructs activated targeted STAT proteins in a cytokine-independent manner. We identified a STAT5 activator that sustained CD8+ T cell survival and cytotoxic function ex vivo in the absence of IL-2. Tumor outgrowth was reduced in vivo due to enhanced T cell persistence and functionality. Single-cell transcriptomics revealed the STAT5 activator prevented the expression of genes associated with an exhausted T cell fate. Our findings demonstrate that signaling pathways can be rewired in T cells to sustain their function in solid tumors.

2025-05-19 | GSE289168 | GEO

An engineered viral protein activates STAT5 to prevent T cell suppression.

Project description: Not available

| S-EPMC12863462 | biostudies-literature

STAT5 inhibition abrogate TSLP-induced homeostatic maturation of human cDC2s

Project description:It has been reported that TSLP activates several downstream signalings including STAT5. To test whether TSLP triggers the homeostatic maturation program of human splenic cDC2 (DC2hm program) in a STAT5-dependant manner, we administrated TSLP to in-culture human splenic cDC2 with or without STAT5 inhibitor and performed RNA-seq. The results showed that TSLP-induced DC2hm-like profile was abrogated by STAT5 inhibition.

2026-02-23 | GSE282671 | GEO

Engineered cytokine-secreting cells to prevent foreign body response against implants

Project description:Engineered cytokine-secreting cells to prevent foreign body response against implants

| PRJNA1251884 | ENA

Murine Osteoclasts: Stat5 flox vs. Stat5 cKO

Project description:Transcriptional profiling of mouse osteoclasts comparing control osteoclasts from Stat5 flox mice with osteoclasts from Stat5 cKO mice. Two-condition experiment, Stat5 flox cells vs. Stat5 cKO cells

2013-12-09 | E-GEOD-51283 | biostudies-arrayexpress

Constitutively active STAT5 recruits p53 to alternative transcriptional targets in myeloid cancers

Project description:In several cancer types, STAT (Signal transducer and activator of transcription) transcription factors are constitutively activated. We previously identified a target gene, LPP/miR-28 (LIM domain containing preferred translocation partner in lipoma), induced by constitutive activation of STAT5, but not by transient cytokine-activated STAT5. Here, we demonstrate in transformed hematopoietic cells that binding of both STAT5B and p53 to chromatin is required for transcriptional activity of an alternative LPP/miR-28 promoter. Using a genome-wide approach, we identified 463 genomic positions at promoter regions where STAT5B and p53 are co-localized on the chromatin. At these positions, p53 chromatin binding is dependent on persistent STAT5B activation. The transcriptional activity of selected promoters bound by STAT5B and p53 was significantly changed upon STAT5 or p53 inhibition, and the transcription of these target genes is frequently altered in platelets of myeloproliferative neoplasm patients harboring mutations constitutively activating STAT5. These data suggest that the constitutive STAT5 activation recruits p53 in cancer cells and thereby activates oncogenic transcriptional programs. STAT5B and p53 ChIP-chip with or without JAK2 inhibition (ruxolitinib) to inhibit STAT5 phosphorylation and DNA binding.

2014-02-01 | E-GEOD-38143 | biostudies-arrayexpress

Engineered FGF19 promotes HDL biogenesis and transhepatic cholesterol efflux to prevent atherosclerosis

Project description:Engineered FGF19 promotes HDL biogenesis and transhepatic cholesterol efflux to prevent atherosclerosis

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Murine Osteoclasts: Stat5 flox vs. Stat5 cKO

Project description:Transcriptional profiling of mouse osteoclasts comparing control osteoclasts from Stat5 flox mice with osteoclasts from Stat5 cKO mice.

2013-12-09 | GSE51283 | GEO

Engineered transfer RNAs for suppression of premature termination codons

Project description:PTCs cause a multitude of human diseases and there are no established therapeutic options for their therapeutic management. Herein, we report the high-throughput cloning and identification, characterization and functional analysis of anticodon-edited tRNA which display efficacious PTC reversion in eukaryotic cells and mouse skeletal muscle. Notably, our screen identifies ACE-tRNA, in total, with the potential to repair a vast majority of known human disease-causing PTC, but this therapeutic will require overcoming tissue and delivery specific challenges. However, the engineered tRNA, once delivered, faithfully encode their cognate amino acid, thus abrogating spurious effects on downstream protein stability, folding, and trafficking, and consequently negating the need for tandem therapies involving protein folding or trafficking agents. When transfected as cDNA, ACE-tRNAs rescued multiple full-length proteins via PTC suppression; a NLuc luciferase reporter, a model protein HDH, and two disease nonsense mutations in CFTR.

2019-02-11 | PXD012581 | Pride

Critical functions for STAT5 tetramers in the maturation and survival of natural killer cells

Project description:Interleukin-15 (IL-15) is essential for the development and maintenance of natural killer (NK) cells. IL-15 activates STAT5 proteins, which can form dimers or tetramers. We previously found that NK cell numbers are decreased in Stat5a-Stat5b tetramer-deficient double knockin (DKI) mice, but the mechanism was not investigated. Here we show that STAT5 dimers are sufficient for NK cell development, whereas STAT5 tetramers mediate NK cell maturation and the expression of maturation-associated genes. Unlike the defective proliferation of Stat5 DKI CD8+ T cells, Stat5 DKI NK cells have normal proliferation to IL-15 but are susceptible to death upon cytokine withdrawal, with lower Bcl2 and increased active caspases. These findings underscore the importance of STAT5 tetramers in maintaining NK cell homeostasis. Moreover, defective STAT5 tetramer formation could represent a cause of NK cell immunodeficiency, and interrupting STAT5 tetramer formation might serve to control NK leukaemia.

2017-09-19 | GSE101470 | GEO

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