Evidence map›Paper›PMID 23900679›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013

The protein p17 signaling pathways in cancer.

Klaus Heese

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  4. Expression and Function of FAM72A Gene in Multiple MyelomaFAM72A.Current pharmaceutical biotechnology · 2025
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  15. Review
  16. Lead discovery and in silico 3D structure modeling of tumorigenic FAM72A (p17).Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 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

1 author at 1 institution in 1 country.

Klaus HeeseGraduate School of Biomedical Science and Engineering, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul, 133-791, Republic of Korea, klaus@hanyang.ac.kr.
Hanyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P17 is a novel neuronal protein expressed under physiological conditions only at very low levels in other tissues. Accumulating data indicate its crucial involvement in tumorigenic effects. Using molecular, cellular, and biocomputational methods, the current study unraveled p17 mode of action. Data indicate that mitochondria-associated p17 interacts with the proteins TMEM115, YPEL3, ERP44, CDK5RAP, and NNAT. Moreover, p17 drives the cell cycle into the G0/G1 phase and enhances survival of proliferating cells. Interference with p17 activities thus might become a novel option to influence also the tumor suppressor protein p53 signaling pathways for the treatment of tumors.

Indexed as

Amino Acid SequenceAnimalsApoptosis Regulatory ProteinsCarrier ProteinsCell LineCell SurvivalG1 PhaseHEK293 CellsHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsMCF-7 CellsMembrane ProteinsMicroscopy, FluorescenceMitochondriaMitochondrial ProteinsApoptosis Regulatory ProteinsCarrier ProteinsCDK5RAP1 protein, humanERP44 protein, humanFAM72A protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsMitochondrial ProteinsMolecular ChaperonesNeoplasm ProteinsNerve Tissue ProteinsNNAT protein, humanp17 amyloid-beta peptide-induced protein, humanSulfur Group TransferasesTMEM115 protein, humanTumor Suppressor ProteinsYPEL3 protein, human

Identifiers

PMID23900679
OpenAlexW1976387435

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.