Evidence map›Paper›PMID 17486078›Full record

ArticleOncogene2007

The autophagic inducer smARF interacts with and is stabilized by the mitochondrial p32 protein.

S Reef, O Shifman, M Oren, A Kimchi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  9. Review
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  11. Review
  12. Small mitochondrial Arf (smArf) protein corrects p53-independent developmental defects ofProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. Article
  14. Elevated expression of HABP1 is a novel prognostic indicator in triple-negative breast cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
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  19. Physiologic functions of cyclophilin D and the mitochondrial permeability transition pore.Circulation journal : official journal of the Japanese Circulation Society · 2013
    Review
  20. 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

4 authors at 1 institution in 1 country.

S ReefDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
O Shifman
M Oren
A Kimchi
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alternative reading frame (ARF) mRNA encodes two pro-death proteins, the nucleolar p19ARF and a shorter mitochondrial isoform, named smARF (hsmARF in human). While p19ARF can inhibit cell growth by causing cell cycle arrest or type I apoptotic cell death, smARF is able to induce type II autophagic cell death. Inappropriate proliferative signals generated by proto-oncogenes, such as c-Myc and E2F1, can elevate both p19ARF and smARF proteins. Here, we reveal a novel means of regulation of smARF protein steady state levels through its interactions with the mitochondrial p32. The p32 protein physically interacts with both human and murine smARF, and colocalizes with these short isoforms to the mitochondria. Remarkably, knocking down p32 protein levels significantly reduced the steady state levels of smARF by increasing its turn over. As a consequence, the ability of ectopically expressed smARF to induce autophagy and to cause mitochondrial membrane dissipation was significantly reduced. In contrast, the protein levels of full-length p19ARF, which mainly resides in the nucleolus, were not influenced by p32 depletion, suggesting that p32 exclusively stabilizes the mitochondrial smARF protein. Thus the interaction with p32 provides a means of specifically regulating the expression of the recently identified autophagic inducer, smARF, and adds yet another layer of complexity to the multifaceted regulation of the ARF gene.

Indexed as

AutophagyAnimalsCarrier ProteinsCyclin-Dependent Kinase Inhibitor p16HumansMiceMitochondrial ProteinsProtein IsoformsTumor Suppressor Protein p14ARFC1QBP protein, humanCarrier ProteinsCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16Mitochondrial ProteinsProtein IsoformsTumor Suppressor Protein p14ARF

Identifiers

PMID17486078
OpenAlexW1970867404

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.