Evidence map›Paper›PMID 16857581›Full record

ReviewMolecular cell2006

H2AX is a target of the JNK signaling pathway that is required for apoptotic DNA fragmentation.

Hayla K Sluss, Roger J Davis

Open access · bronzeAbstract readReviewComment
PubMed Publisher
In one paragraph

Review in Molecular cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

31 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  12. The Anti-Cancer Effect ofAntioxidants (Basel, Switzerland) · 2019
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  18. Benzylidenetetralones, cyclic chalcone analogues, induce cell cycle arrest and apoptosis in HCT116 colorectal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Hayla K SlussDepartment of Cancer Cell Biology and University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Roger J Davis
Howard Hughes Medical Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanism of apoptotic signaling by JNK is incompletely understood. In the July 7 issue of Molecular Cell, Lu et al. (2006) report that JNK phosphorylation of H2AX at a noncanonical site is required for caspase-induced DNA fragmentation.

Indexed as

DNA FragmentationApoptosisHistonesJNK Mitogen-Activated Protein KinasesPhosphorylationSignal TransductionH2AX protein, humanHistonesJNK Mitogen-Activated Protein Kinases

Identifiers

PMID16857581
OpenAlexW2040426803

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.