ArticleCell death discovery2021
OASIS/CREB3L1 is a factor that responds to nuclear envelope stress.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- New Roles of bZIP-Containing Membrane-Bound Transcription Factors in Chromatin Tethering and Karyoptosis.International journal of molecular sciences · 2025Review
- Decreased DNA density is a better indicator of a nuclear bleb than lamin B loss.Journal of cell science · 2025Article
- Lack of Nuclear Localization of the Creb3l1 Transcription Factor Causes Defects in Caudal Fin Bifurcation in Zebrafish Danio rerio.Cells, tissues, organs · 2025Article
- VPS4B orchestrates response to nuclear envelope stress by regulating ESCRT-III dynamics in glioblastoma.Nucleus (Austin, Tex.) · 2024Article
- Revealing the crucial roles of suppressive immune microenvironment in cardiac myxoma progression.Signal transduction and targeted therapy · 2024Article
- Dysregulated CREB3 cleavage at the nuclear membrane induces karyoptosis-mediated cell death.Experimental & molecular medicine · 2024Article
- DNA density is a better indicator of a nuclear bleb than lamin B loss.bioRxiv : the preprint server for biology · 2024Article
- Molecular Mechanisms for the Regulation of Nuclear Membrane Integrity.International journal of molecular sciences · 2023Review
- Epigenomic response to albuterol treatment in asthma-relevant airway epithelial cells.Clinical epigenetics · 2023Article
- Impact of cell cycle on repair of ruptured nuclear envelope and sensitivity to nuclear envelope stress in glioblastoma.Cell death discovery · 2023Article
- Nuclear softening mediated by Sun2 suppression delays mechanical stress-induced cellular senescence.Cell death discovery · 2023Article
- Impact of Nuclear Envelope Stress on Physiological and Pathological Processes in Central Nervous System.Neurochemical research · 2022Review
- Pan-cancer analysis of CREB3L1 as biomarker in the prediction of prognosis and immunotherapeutic efficacy.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear envelope (NE) safeguards the genome and is pivotal for regulating genome activity as the structural scaffold of higher-order chromatin organization. NE had been thought as the stable during the interphase of cell cycle. However, recent studies have revealed that the NE can be damaged by various stresses such as mechanical stress and cellular senescence. These types of stresses are called NE stress. It has been proposed that NE stress is closely related to cellular dysfunctions such as genome instability and cell death. Here, we found that an endoplasmic reticulum (ER)-resident transmembrane transcription factor, OASIS, accumulates at damaged NE. Notably, the major components of nuclear lamina, Lamin proteins were depleted at the NE where OASIS accumulates. We previously demonstrated that OASIS is cleaved at the membrane domain in response to ER stress. In contrast, OASIS accumulates as the full-length form to damaged NE in response to NE stress. The accumulation to damaged NE is specific for OASIS among OASIS family members. Intriguingly, OASIS colocalizes with the components of linker of nucleoskeleton and cytoskeleton complexes, SUN2 and Nesprin-2 at the damaged NE. OASIS partially colocalizes with BAF, LEM domain proteins, and a component of ESCRT III, which are involved in the repair of ruptured NE. Furthermore, OASIS suppresses DNA damage induced by NE stress and restores nuclear deformation under NE stress conditions. Our findings reveal a novel NE stress response pathway mediated by OASIS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.