Evidence map›Paper›PMID 11687952›Full record

ArticleNeoplasia (New York, N.Y.)

Blocking Chk1 expression induces apoptosis and abrogates the G2 checkpoint mechanism.

Y Luo, S K Rockow-Magnone, P E Kroeger, L Frost, Z Chen, E K Han, S C Ng, R L Simmer, V L Giranda

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 50 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Y LuoDepartment 47S AP9A, Cancer Research, Pharmaceutical Products Division, Abbott Laboratories, 100 Abbott Park Road, Abbott Park, IL 60064, USA. yan.luo@abbott.com
S K Rockow-Magnone
P E Kroeger
L Frost
Z Chen
E K Han
S C Ng
R L Simmer
V L Giranda
Abbott Fund · USAbbott (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Checkpoint kinase 1 (Chk1) is a checkpoint gene that is activated after DNA damage. It phosphorylates and inactivates the Cdc2 activating phosphatase Cdc25C. This in turn inactivates Cdc2, which leads to G2/M arrest. We report that blocking Chk1 expression by antisense or ribozymes in mammalian cells induces apoptosis and interferes with the G2/M arrest induced by adriamycin. The Chk1 inhibitor UCN-01 also blocks the G2 arrest after DNA damage and renders cells more susceptible to adriamycin. These results indicate that Chk1 is an essential gene for the checkpoint mechanism during normal cell proliferation as well as in the DNA damage response.

Indexed as

ApoptosisOxazinesProtein Kinase InhibitorsXanthenesAlkaloidsAntineoplastic AgentsAntineoplastic Agents, PhytogenicBlotting, WesternCaspasesCell CycleCheckpoint Kinase 1Coloring AgentsDNA, AntisenseDNA PrimersDoxorubicinDrug Resistance7-hydroxystaurosporineAlkaloidsAntineoplastic AgentsAntineoplastic Agents, PhytogenicCaspasesCheckpoint Kinase 1CHEK1 protein, humanColoring AgentsDNA, AntisenseDNA PrimersDoxorubicinEnzyme InhibitorsEtoposideOxazinesProtein Kinase InhibitorsProtein KinasesresazurinRNA, CatalyticStaurosporineXanthenes

Identifiers

PMID11687952
PMCPMC1506209
OpenAlexW1979986967

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.