Evidence map›Paper›PMID 30910772›Full record

ReviewCold Spring Harbor perspectives in biology2020

Proteome-Scale Mapping of Perturbed Proteostasis in Living Cells.

Isabel Lam, Erinc Hallacli, Vikram Khurana

Abstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Cell-Nonautonomous Regulation of Proteostasis in Aging and Disease.Cold Spring Harbor perspectives in biology · 2020
    Review
  6. Review
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

3 authors.

Isabel Lam *Ann Romney Center for Neurologic Disease, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115.
Erinc Hallacli *Ann Romney Center for Neurologic Disease, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115.
Vikram KhuranaAnn Romney Center for Neurologic Disease, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteinopathies are degenerative diseases in which specific proteins adopt deleterious conformations, leading to the dysfunction and demise of distinct cell types. They comprise some of the most significant diseases of aging-from Alzheimer's disease to Parkinson's disease to type 2 diabetes-for which not a single disease-modifying or preventative strategy exists. Here, we survey approaches in tractable cellular and organismal models that bring us toward a more complete understanding of the molecular consequences of protein misfolding. These include proteome-scale profiling of genetic modifiers, as well as transcriptional and proteome changes. We describe assays that can capture protein interactomes in situ and distinct protein conformational states. A picture of cellular drivers and responders to proteotoxicity emerges from this work, distinguishing general alterations of proteostasis from cellular events that are deeply tied to the intrinsic function of the misfolding protein. These distinctions have consequences for the understanding and treatment of proteinopathies.

Indexed as

Disease Models, AnimalProteostasisAnimalsHumansProteomicsProteostasis Deficiencies

Identifiers

PMID30910772
PMCPMC6996455

What OpenQuestion holds

Textmetadata
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.