Evidence map›Paper›PMID 31295808›Full record

ReviewInternational journal of molecular sciences2019

Cellular Responses to Proteasome Inhibition: Molecular Mechanisms and Beyond.

Nicolas Albornoz, Hianara Bustamante, Andrea Soza, Patricia Burgos

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.9field-weighted citation impact, top 8% of its field
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

41 citing papers in PubMed, 63 citations in OpenAlex.

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  11. P62 inhibits IL-1β release duringFrontiers in cellular and infection microbiology · 2025
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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

4 authors at 2 institutions in 1 country.

Nicolas AlbornozCentro de Biología Celular y Biomedicina (CEBICEM), Facultad de Medicina y Ciencia, Universidad San Sebastián, Lota 2465, Santiago 7510157, Chile.
Hianara BustamanteInstituto de Microbiología Clínica, Facultad de Medicina, Universidad Austral de Chile, Valdivia 5110566, Chile.
Andrea SozaCentro de Biología Celular y Biomedicina (CEBICEM), Facultad de Medicina y Ciencia, Universidad San Sebastián, Lota 2465, Santiago 7510157, Chile.
Patricia BurgosCentro de Biología Celular y Biomedicina (CEBICEM), Facultad de Medicina y Ciencia, Universidad San Sebastián, Lota 2465, Santiago 7510157, Chile. patricia.burgos@uss.cl.
San Sebastián University · CLAustral University of Chile · CL

Funding

Comisión Nacional de Investigación Científica y Tecnológica AFB-170005Comisión Nacional de Investigación Científica y Tecnológica PIA No. 172066Fondo Nacional de Desarrollo Científico, Tecnológico y de Innovación Tecnológica 1171649
6 · The paper itself

Abstract

Proteasome inhibitors have been actively tested as potential anticancer drugs and in the treatment of inflammatory and autoimmune diseases. Unfortunately, cells adapt to survive in the presence of proteasome inhibitors activating a variety of cell responses that explain why these therapies have not fulfilled their expected results. In addition, all proteasome inhibitors tested and approved by the FDA have caused a variety of side effects in humans. Here, we describe the different types of proteasome complexes found within cells and the variety of regulators proteins that can modulate their activities, including those that are upregulated in the context of inflammatory processes. We also summarize the adaptive cellular responses activated during proteasome inhibition with special emphasis on the activation of the Autophagic-Lysosomal Pathway (ALP), proteaphagy, p62/SQSTM1 enriched-inclusion bodies, and proteasome biogenesis dependent on Nrf1 and Nrf2 transcription factors. Moreover, we discuss the role of IRE1 and PERK sensors in ALP activation during ER stress and the involvement of two deubiquitinases, Rpn11 and USP14, in these processes. Finally, we discuss the aspects that should be currently considered in the development of novel strategies that use proteasome activity as a therapeutic target for the treatment of human diseases.

Indexed as

AnimalsAntineoplastic AgentsAutophagyEndoplasmic Reticulum StressHumansImmunomodulationLysosomesNeoplasmsProteasome Endopeptidase ComplexProteasome InhibitorsProtein Processing, Post-TranslationalSignal TransductionUnfolded Protein ResponseAntineoplastic AgentsProteasome Endopeptidase ComplexProteasome Inhibitorsautophagyimmunoproteasomeproteasome

Identifiers

PMID31295808
PMCPMC6678303
OpenAlexW2957150925

What OpenQuestion holds

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LicenceCC BY
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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.