Evidence map›Paper›PMID 18820703›Full record

ArticleOncogene2009

Polo-like kinase 1 phosphorylates and regulates Bcl-x(L) during pironetin-induced apoptosis.

Y Tamura, S Simizu, M Muroi, S Takagi, M Kawatani, N Watanabe, H Osada

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Targeting polo-like kinase 1 in acute myeloid leukemia.Therapeutic advances in hematology · 2015
    Review
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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

7 authors at 1 institution in 1 country.

Y TamuraAntibiotics Laboratory and Chemical Biology Department, Advanced Science Institute, RIKEN, Wako, Saitama, Japan.
S Simizu
M Muroi
S Takagi
M Kawatani
N Watanabe
H Osada
RIKEN Advanced Science Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bcl-x(L), an anti-apoptotic Bcl-2 family member protein, contributes to the resistance against chemotherapies such as tubulin-binder treatment in many human tumors. Although Bcl-x(L) is phosphorylated after tubulin-binder treatment, the role of the phosphorylation and its responsible kinase(s) are poorly understood. Here, we identified Plk1 (polo-like kinase 1) as a Bcl-x(L) kinase. Same location of Bcl-x(L) and Plk1 was revealed by immunocytochemical analyses at M-phase in situ. Plk1 phosphorylates Bcl-x(L) in vitro, and we identified Plk1 phosphorylation sites in Bcl-x(L). When all of these phosphorylation sites were substituted to alanines, the anti-apoptotic activity of the Bcl-x(L) mutant against the apoptosis induced by pironetin, but not against ultraviolet-induced apoptosis, was increased. These observations suggest that Plk1 is a regulator of Bcl-x(L) phosphorylation and controls the anti-apoptotic activity of Bcl-x(L) during pironetin-induced apoptosis.

Indexed as

ApoptosisAlaninebcl-X ProteinCell Cycle ProteinsCell Line, TumorHumansMutationPhosphorylationPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsPyronesSerineAlaninebcl-X ProteinCell Cycle ProteinspironetinPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsPyronesSerine

Identifiers

PMID18820703
OpenAlexW2046009879

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.