Evidence map›Paper›PMID 25105300›Full record

ArticleMolecular medicine (Cambridge, Mass.)2014

Regulation of autophagy by α1-antitrypsin: "a foe of a foe is a friend".

Michal G Shapira, Boris Khalfin, Eli C Lewis, Abraham H Parola, Ilana Nathan

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Humanin Derivatives Inhibit Necrotic Cell Death in Neurons.Molecular medicine (Cambridge, Mass.) · 2015
    Article
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

5 authors at 1 institution in 1 country.

Michal G ShapiraDepartment of Chemistry, Faculty of Natural Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Boris KhalfinDepartment of Chemistry, Faculty of Natural Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel Department of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel New York University Shanghai, People's Republic of China.
Eli C LewisDepartment of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Abraham H ParolaDepartment of Chemistry, Faculty of Natural Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel New York University Shanghai, People's Republic of China.
Ilana NathanDepartment of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel Soroka University Medical Center, Beer-Sheva, Israel.
Ben-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is involved in both the cell protective and the cell death process but its mechanism is largely unknown. The present work unravels a novel intracellular mechanism by which the serpin α1-antitrypsin (AAT) acts as a novel negative regulator of autophagic cell death. For the first time, the role of intracellularly synthesized AAT, other than in liver cells, is demonstrated. Autophagic cell death was induced by N-α-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and tamoxifen. By utilizing a fluorescently tagged TPCK analog, AAT was "fished out" (pulled out) as a TPCK intracellular protein target. The interaction was further verified by competition binding experiments. Both inducers caused downregulation of AAT expression associated with activation of trypsin-like proteases. Furthermore, silencing AAT by siRNA induced autophagic cell death. Moreover, AAT administration to cultured cells prevented autophagic cell death. This new mechanism could have implications in the treatment of diseases by the regulation of AAT levels in which autophagy has a detrimental function. Furthermore, the results imply that the high synthesis of endogenous AAT by cancer cells could provide a novel resistance mechanism of cancer against autophagic cell death.

Indexed as

alpha 1-AntitrypsinAutophagyCell CycleHT29 CellsHumansMCF-7 CellsProtein Synthesis InhibitorsRNA, Small InterferingTamoxifenTosylphenylalanyl Chloromethyl KetoneTrypsinalpha 1-AntitrypsinProtein Synthesis InhibitorsRNA, Small InterferingTamoxifenTosylphenylalanyl Chloromethyl KetoneTrypsin

Identifiers

PMID25105300
PMCPMC4212011
OpenAlexW2193747679

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.