Evidence map›Paper›PMID 38197533›Full record

ArticleCurrent protocols2024

Histodenz Separation of Lysosomal Subpopulations for Analysis of Chaperone-mediated Autophagy.

Calvin M Burns, Richard A Miller, S Joseph Endicott

Open access · hybridAbstract read
In one paragraph

Article in Current protocols, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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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

3 authors at 1 institution in 1 country.

Calvin M BurnsDepartment of Pathology, University of Michigan, Ann Arbor, Michigan.
Richard A MillerDepartment of Pathology, University of Michigan, Ann Arbor, Michigan.
S Joseph EndicottDepartment of Pathology, University of Michigan, Ann Arbor, Michigan.ORCID https://orcid.org/0000-0002-8237-9784
University of Michigan · US

Funding

Systems BiologyU19AG023122 · NIA · TRANSLATIONAL GENOMICS RESEARCH INST · PI Thomas Girke, NICHOLAS Joseph SCHORK · 2004 to 2026
$102.6M
Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
Laboratory for Anti-Geric Testing, Evaluation and ResearchU01AG022303 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RICHARD A MILLER · 2003 to 2026
$25.4M
Integrative Omics to enhance therapeutics development for healthy agingUH3AG064706 · NIA · TRANSLATIONAL GENOMICS RESEARCH INST · PI MILLER, RICHARD A, SCHORK, NICHOLAS JOSEPH · 2021 to 2024
$3.3M
NIA NIH HHS P30 AG024824NIA NIH HHS U01 AG022303NIA NIH HHS U19 AG023122NIA NIH HHS UH3 AG064706
6 · The paper itself

Abstract

Chaperone-mediated autophagy (CMA) is the most selective form of lysosomal proteolysis, in which proteins are individually selected for lysosomal degradation. CMA degradation targets bear a pentapeptide consensus motif that is recognized by the cytosolic chaperone HSPA8 (Hsc70), which participates in the trafficking of the target to the lysosomal surface. From there, it is translocated into the lysosomal lumen, independent of vesicle fusion, in a process dependent upon the lysosomal transmembrane protein LAMP2A. There are limited tools for studying CMA in whole cells and tissues, and many of the best techniques for studying CMA rely on the preparation of lysosome enriched fractions. Such experiments include (1) the in vitro evaluation of CMA substrate uptake activity, (2) the characterization of changes to lysosomal resident and CMA regulatory proteins, and (3) lysosomal targetomics, i.e., the use of quantitative proteomics to characterize lysosomal degradation targets. Previous studies using discontinuous metrizamide gradients have shown that a subpopulation of liver lysosomes is responsible for the majority of CMA activity ("CMA

Indexed as

Chaperone-Mediated AutophagyAnimalsbeta-N-AcetylhexosaminidasesBiological AssayLysosomesMetrizamideMicebeta-N-AcetylhexosaminidasesMetrizamideautophagydensity purificationlysosomesorganelle isolation

Identifiers

PMID38197533
PMCPMC10874119
OpenAlexW4390696010

What OpenQuestion holds

Textmetadata
LicenceTDM
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.