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Plasticity of the Mammalian Integrated Stress Response [eIF2B5]

ABSTRACT: Plasticity of the Mammalian Integrated Stress Response [eIF2B5]

PROVIDER: PRJNA1114733 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29130907_1.fastq.gz	Fastqsanger.gz
	SRR29130907_2.fastq.gz	Fastqsanger.gz
	SRR29130908_1.fastq.gz	Fastqsanger.gz
	SRR29130908_2.fastq.gz	Fastqsanger.gz
	SRR29130909_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Plasticity of the Mammalian Integrated Stress Response [eIF2B5]

Project description:Decreased nucleotide exchange activity of the eukaryotic translation initiation factor eIF2B coupled with increased phosphorylation of eIF2alpha (eIF2alpha-p) is a hallmark of the “canonical” integrated stress response (c-ISR). In mammals, however, it is unclear whether decreased eIF2B activity in absence of alterations in eIF2alpha-p which occurs in human disease including leukodystrophies, is synonymous to c-ISR. Herein, we describe a previously unknown mechanism of adaptation to decreased eIF2B activity, distinct from c-ISR, which we term “split” ISR (s-ISR). We demonstrate that s-ISR comprises translation reprogramming of only a subset of c-ISR mRNA targets which is accompanied by distinct transcriptomes. In contrast to c-ISR, s-ISR requires eIF4E-dependent translation of the upstream open reading frame 1 and subsequent stabilization of ATF4 mRNA. This is followed by altered expression of a subset of metabolic genes (e.g., PCK2), resulting in metabolic adaptations to maintain cellular bioenergetics under conditions of low eIF2B activity. Overall, these data demonstrate hitherto-unappreciated plasticity of the mammalian ISR, whereby the loss of eIF2B activity in the absence of increased eIF2-p, activates an eIF4E/ATF4/PCK2 axis to maintain energy homeostasis.

2025-01-22 | GSE268130 | GEO

Plasticity of the Mammalian Integrated Stress Response [atf4]

Project description:Plasticity of the Mammalian Integrated Stress Response [atf4]

| PRJNA1114729 | ENA

Plasticity of the Mammalian Integrated Stress Response [eIF2B5_eIF4E]

Project description:Plasticity of the Mammalian Integrated Stress Response [eIF2B5_eIF4E]

| PRJNA1114731 | ENA

Plasticity of the Mammalian Integrated Stress Response [eIF2B5_eIF4E]

2025-01-22 | GSE268132 | GEO

Plasticity of the Mammalian Integrated Stress Response [atf4]

2025-01-22 | GSE268127 | GEO

Plasticity of the mammalian integrated stress response.

Project description: Not available

| S-EPMC12119373 | biostudies-literature

Epidermal basal cell-specific in vivo ribosome profiling to describe the translation landscape of HrasG12V and Eif2b5

Project description:eIF2B5 is necessary for HrasG12V hyperplastic growth. Ribosome profiling was used to describe HrasG12V and WT dependence on eIF2B5-mediated translation.

2020-06-10 | GSE126660 | GEO

OMA1, DELE1 and HRI relay mitochondrial stress to the mammalian integrated stress response

Project description:OMA1, DELE1 and HRI relay mitochondrial stress to the mammalian integrated stress response

| PRJNA557038 | ENA

RNA-seq of cerebellum from Eif2b5[R191H] mice

Project description:The integrated stress response (ISR) is a conserved signaling pathway triggered by a variety of insults that include ER stress, mitochondrial stress, amino acid deprivation, and viral infection. The essential stress sensor and key effector of this pathway is eIF2B, and loss-of-function mutations in any of its 5 subunits can lead to Vanishing White Matter disease (VWM) in humans. We generated and characterized mouse models harboring different pathogenic mutations to model VWM and to understand the impact of chronic ISR activation on organismal and cellular physiology. Here, we performed bulk RNA-seq on the cerebellum from 5-month-old homozygous Eif2b5[R191H] (n=4) and WT mice (n=5).

2025-06-30 | E-MTAB-15246 | biostudies-arrayexpress

Targeting the epigenome and the integrated stress response to normalize colorectal cancer subclonal plasticity and progression

Project description:Despite therapeutic advances, metastatic colorectal cancer remains a therapeutic challenge as most patients will develop resistance to therapy and will progress. Epigenetic mechanisms are implicated in enabling the acquisition of new phenotypic traits as drivers of colorectal cancer progression, rather than new genetic mutations or expansion of existing mutant clones. It remains unclear, however, which epigenetic mechanisms sustain colorectal cancer plasticity, how they are induced, and how this plasticity generates subclonal diversity that drives the aggressive cancer phenotype. Here we identify the integrated stress response as an inducer of colorectal cancer cell plasticity, subclonal diversity, and tumor progression in the stress-surviving cells. Combined analysis of chromatin accessibility and gene transcription profiling in these cells found the emergence of an endogenous interferon response as a key phenotypic trait associated with subclonal colorectal cancer cell diversity, treatment resistance and heightened aggressiveness. We unveil a new experimental approach to successfully prevent treatment-resistant colorectal cancer progression by combining epigenetic modulators with a cereblon-dependent degrader of GSPT1, a regulator of protein synthesis, to normalize chromatin accessibility and induce colorectal cancer cell death. Collectively, our study identifies the integrated stress response as an inducer of epigenetic and transcriptional plasticity in colorectal cancer cells and highlights a successful approach to therapeutic intervention.

2026-04-06 | GSE312823 | GEO

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