Evidence map›Paper›PMID 10822387›Full record

ArticleOncogene2000

Caspases and mitochondria in c-Myc-induced apoptosis: identification of ATM as a new target of caspases.

A Hotti, K Järvinen, P Siivola, E Hölttä

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Identification and characterization of the human inhibitor of caspase-activated DNase gene promoter.Apoptosis : an international journal on programmed cell death · 2008
    Article
  13. Article
  14. ATM and ATR: sensing DNA damage.World journal of gastroenterology · 2004
    Review
  15. A decade of caspases.Oncogene · 2003
    Review
  16. Article
  17. Article
  18. The c-Myc target gene PRDX3 is required for mitochondrial homeostasis and neoplastic transformation.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  19. Article
  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.

A HottiHaartman Institute, Department of Pathology, University of Helsinki, Finland.
K Järvinen
P Siivola
E Hölttä
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanism(s) of c-Myc transcription factor-induced apoptosis is still obscure. The activation of c-Myc has been found to lead into the processing/activation of caspases (caspase-3), but the significance of this for the cell demise is debatable. Here we report that several targets of caspases (PKCdelta, MDM2, PARP, replication factor C, 70 kDa U1snRNP, fodrin and lamins) are cleaved during c-Myc-induced apoptosis in Rat-1 MycER cells, indicating an important role for caspases in the apoptotic process. We further found that the ATM (ataxia telangiectasia mutated)--protein is a novel key substrate of caspases. In in vitro assays, purified recombinant ATM protein was found to be cleaved by the effector caspases 3 and 7. The functional significance of the ATM cleavage is supported by the finding that ectopic expression of ATM protected in part against apoptosis. We also show that c-Myc-induced apoptosis involves loss of mitochondrial transmembrane potential, release of cytochrome c from mitochondria into the cytosol and subsequent processing of caspase-9. The cleavage of caspase-9 is, however, minimal and a much later event than the processing/activation of caspase-3, suggesting that it is not the apical caspase. Evidence is provided that there is, nevertheless, an upstream caspase(s) regulating the functions of caspase-3 and mitochondria. Additionally, it was found that p53 becomes upregulated, together with its transcriptional targets MDM2 and p21, upon c-Myc induction, but this occurs also at a later time than the activation of caspase-3.

Indexed as

Genes, mycAmino Acid Chloromethyl KetonesAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCarrier ProteinsCaspase 3Caspase 7Caspase InhibitorsCaspasesCell Cycle ProteinsCells, CulturedCysteine Proteinase InhibitorsCytochrome c GroupDNA-Binding ProteinsEnzyme ActivationAmino Acid Chloromethyl KetonesAtaxia Telangiectasia Mutated ProteinsATM protein, humanbenzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketonebenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCarrier ProteinsCASP3 protein, humanCasp3 protein, ratCASP7 protein, humanCaspase 3Caspase 7Caspase InhibitorsCaspasesCell Cycle ProteinsCysteine Proteinase InhibitorsCytochrome c GroupDNA-Binding ProteinsIsoenzymesLaminsMicrofilament ProteinsNuclear ProteinsOligopeptidesPoly(ADP-ribose) PolymerasesPRKCD protein, humanPrkcd protein, ratProtein Kinase CProtein Kinase C-deltaProtein Serine-Threonine KinasesRecombinant ProteinsSpectrinTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID10822387
OpenAlexW2320890190

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.