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MTORC1 inhibition activates the integrated stress response (ISR) in TALL-1 cell line

ABSTRACT: mTORC1 inhibition activates the integrated stress response (ISR) in TALL-1 cell line

PROVIDER: PRJNA1142566 | ENA |

REPOSITORIES: ENA

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mTORC1 inhibition activates the integrated stress response (ISR) in TALL-1 cell line

Project description:mTOR sensitized T-ALL cell lines and patient-derived xenografts (PDX) from patients with R/R T-ALL to the BCL-2 inhibitor Venetoclax.

2025-07-09 | GSE273650 | GEO

Functional translatome proteomics reveal converging regulation by mTORC1 and eIF2α

Project description:Regulation of the translatome is essential during stress. However, the precise sets of translational targets regulated by the key translational stress responses –integrated stress response (ISR) and mTORC1 – remain elusive. We developed multiplexed enhanced protein dynamics (mePROD) proteomics, combining dynamic SILAC, multiplexing, and signal amplification, to enable measuring acute changes in protein synthesis. Treating cells with ISR/mTORC1-modulating stressors, we showed extensive translatome modulation and ~20% of proteins synthesized at highly reduced rates. Comparing translation-deficient sub-proteomes revealed an extensive overlap demonstrating that target specificity is achieved on protein level and not by pathway activation. Titrating inhibition of cap-dependent translation confirmed that synthesis of individual proteins is controlled by intrinsic properties responsive to global translation inhibition. This study reports a method to measure translation rates at the nascent chain level and provides insight into how the ISR and mTORC1, two key cellular pathways, regulate the translatome to guide cellular survival upon stress.

2019-12-06 | PXD014377 | Pride

Functional Translatome Proteomics Reveal Converging and Dose-Dependent Regulation by mTORC1 and eIF2α

2019-12-09 | PXD015438 | Pride

Disruption of the Integrator complex triggers the Integrated Stress Response through formation of double-stranded RNA [48h_INTS8_RNAseq]

Project description:Acute loss of INT induces transcription factors that initiate stress-responses like the Integrated Stress Response (ISR). Inefficient elongation upon INT loss enables termination in introns and dsRNA formation. dsRNA is recognized by PKR, which persistently activates the ISR in samples from patients with INT mutations

2025-04-16 | GSE283862 | GEO

Disruption of the Integrator complex triggers the Integrated Stress Response through formation of double-stranded RNA [RIPseq]

2025-04-16 | GSE267044 | GEO

Disruption of the Integrator complex triggers the Integrated Stress Response through formation of double-stranded RNA [PROseq]

2025-04-16 | GSE267042 | GEO

Disruption of the Integrator complex triggers the Integrated Stress Response through formation of double-stranded RNA [TTseq]

2025-04-16 | GSE267040 | GEO

Disruption of the Integrator complex triggers the Integrated Stress Response through formation of double-stranded RNA [RNAseq]

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ISR target genes revealed by comprehensive microarray network study using Perk -/-, Atf4 -/-, eIF2a S51A mutant, Fv2E-PERK

Project description:To identify the target genes of integrated stress reponse (ISR), we have employed whole genome microarray expression in MEF cells. ISR gene setimation under ER stress condition using Perk -/-, Atf4 -/-, eIF2a S51A mutant, Fv2E-PERK MEF cells

2015-09-01 | E-GEOD-49598 | biostudies-arrayexpress

Uncovering the Role of PIM2 in Modulating MCL1 Dependency and Activation of ISR-Mediated NOXA Expression

Project description:Our study delves into the intricate dynamics of the integrated stress response (ISR) axis, focusing on the pivotal role of PIM2 kinase and its interaction with the BCL2 family of proteins, revealing crucial mechanisms governing cell survival and tumor progression. Elevated PIM2 expression is a hallmark of various cancers, often correlating with disease aggressiveness. Using a model of normal and malignant plasma cells, we unveil that inhibiting PIM2 kinase triggers not only the production of phosphorylated BAD but also activates ISR-mediated NOXA expression. This shift towards heightened dependence on MCL1 underscores the synergy achieved through combined PIM/MCL1 inhibition, largely propelled by ISR-mediated NOXA expression. In mouse xenograft models, dual targeting of PIM2 and MCL1 effectively controls tumor growth, a response reversed by ISR-specific inhibition, concomitant with the upregulation of genes associated with tumor cell dissemination. These findings illuminate the molecular intricacies of PIM2 inhibition and its implications for cancer therapy, particularly in tumors marked by elevated PIM2 expression.

2024-11-29 | GSE266112 | GEO

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