Evidence map›Paper›PMID 30733337›Full record

ArticleThe Journal of biological chemistry2019

Loss of the tumor suppressor BIN1 enables ATM Ser/Thr kinase activation by the nuclear protein E2F1 and renders cancer cells resistant to cisplatin.

Watson P Folk, Alpana Kumari, Tetsushi Iwasaki, Slovénie Pyndiah, Joanna C Johnson, Erica K Cassimere, Amy L Abdulovic-Cui, Daitoku Sakamuro

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Dementia and metabolic syndrome: a bibliometric analysis.Frontiers in aging neuroscience · 2024
    Article
  5. Article
  6. BIN1 in cancer: biomarker and therapeutic target.Journal of cancer research and clinical oncology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Lower expression ofJournal of Alzheimer's disease reports
    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

8 authors.

Watson P FolkFrom the Biochemistry and Cancer Biology Graduate Program, Augusta University, Augusta, Georgia 30912.
Alpana Kumarithe Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, Georgia 30912.
Tetsushi Iwasakithe Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, Georgia 30912.
Slovénie Pyndiahthe Molecular Signaling Program, Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112.
Joanna C Johnsonthe Medicinal Chemistry and Molecular Pharmacology Graduate Program, Purdue University, West Lafayette, Indiana 47907, and.
Erica K Cassimerethe Molecular Signaling Program, Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112.
Amy L Abdulovic-Cuithe Department of Biological Sciences, College of Science and Mathematics, Augusta University, Augusta, Georgia 30904.
Daitoku SakamuroFrom the Biochemistry and Cancer Biology Graduate Program, Augusta University, Augusta, Georgia 30912, dsakamuro@augusta.edu.

Funding

Role of Bin1 in Cancer ChemosensitizationR01CA140379 · NCI · LSU HEALTH SCIENCES CENTER · PI SAKAMURO, DAITOKU · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA140379
6 · The paper itself

Abstract

The tumor suppressor bridging integrator 1 (BIN1) is a corepressor of the transcription factor E2F1 and inhibits cell-cycle progression. BIN1 also curbs cellular poly(ADP-ribosyl)ation (PARylation) and increases sensitivity of cancer cells to DNA-damaging therapeutic agents such as cisplatin. However, how BIN1 deficiency, a hallmark of advanced cancer cells, increases cisplatin resistance remains elusive. Here, we report that BIN1 inactivates ataxia telangiectasia-mutated (ATM) serine/threonine kinase, particularly when BIN1 binds E2F1. BIN1 + 12A (a cancer-associated

Indexed as

Drug Resistance, NeoplasmTranscription, GeneticAcid Anhydride HydrolasesAdaptor Proteins, Signal TransducingAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorCisplatinDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA, NeoplasmDNA RepairDNA Repair EnzymesE2F1 Transcription FactorHistonesHumansAcid Anhydride HydrolasesAdaptor Proteins, Signal TransducingAtaxia Telangiectasia Mutated ProteinsATM protein, humanBIN1 protein, humanCell Cycle ProteinsCisplatinDNA-Binding ProteinsDNA, NeoplasmDNA Repair EnzymesE2F1 protein, humanE2F1 Transcription FactorH2AX protein, humanHistonesMRE11 Homologue ProteinMRE11 protein, humanNBN protein, humanNuclear ProteinsRAD50 protein, humanTumor Suppressor Proteinsataxia telangiectasiaBIN1cancerchemoresistanceDNA damage responsedouble-stranded DNA breaksE2F transcription factorgenomic instabilityMRN complexp53tumor suppressor gene

Identifiers

PMID30733337
PMCPMC6462522

What OpenQuestion holds

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Registered trials

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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.