Evidence map›Paper›PMID 42149316›Full record

ReviewNeurochemical research2026

Unfolded Protein Response in Glioblastoma: Mechanisms of Proteostasis, Tumor Adaptation, and Therapeutic Relevance.

Hasan Onur Caglar

Abstract readReview
In one paragraph

Review in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Hasan Onur CaglarDepartment of Molecular Biology and Genetics, Science Faculty, Erzurum Technical University, Erzurum, 25050, Turkey. hasan.caglar@erzurum.edu.tr.ORCID http://orcid.org/0000-0002-3637-4755

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is an aggressive brain tumor that rapidly develops resistance to standard clinical therapies. The tumor microenvironment of GBM is highly hostile, characterized by hypoxia, elevated reactive oxygen species, and severe metabolic stress. These conditions promote protein misfolding, particularly in the endoplasmic reticulum (ER), thereby triggering ER stress. The unfolded protein response (UPR) is an adaptive signaling pathway that mitigates ER stress, restores proteostasis, and promotes cellular survival. Activation of UPR signaling provides a survival advantage to GBM cells under these adverse conditions. This signaling is closely associated with drug resistance and malignant progression in GBM. Furthermore, inhibition of UPR sensors exhibits anticancer effects, highlighting their potential as therapeutic targets in GBM. This review describes the biological functions of UPR sensors and their roles in GBM pathogenesis and treatment response.

Indexed as

Adaptation, PhysiologicalBrain NeoplasmsGlioblastomaProteostasisUnfolded Protein ResponseAnimalsEndoplasmic Reticulum StressHumansSignal TransductionTumor MicroenvironmentATF6Endoplasmic reticulum stressGlioblastomaIRE1PERKUnfolded protein response

Identifiers

PMID42149316
PMCPMC13183704

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.