Evidence map›Paper›PMID 24813709›Full record

ArticleMolecular cell2014

Akt-ing up on SRPK1: oncogene or tumor suppressor?

Alex Toker, Y Rebecca Chin

Open access · bronzeAbstract readComment
In one paragraph

Article in Molecular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Rap1 Activity Is Essential for Focal Adhesion and Slit Diaphragm Integrity.Frontiers in cell and developmental biology · 2022
    Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. The influence of SRPK1 on glioma apoptosis, metastasis, and angiogenesis through the PI3K/Akt signaling pathway under normoxia.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  8. Article
  9. Article
  10. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Alex TokerDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: atoker@bidmc.harvard.edu.
Y Rebecca ChinDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: rchin1@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · US

Funding

Novel regulation of PI3K/Akt to direct targeted breast cancer therapiesR01CA177910 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2013 to 2023
$3.9M
Akt isoform-specific signaling in breast cancer metastasisR00CA157945 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CHIN, YUET MING REBECCA · 2014 to 2016
$711k
NCI NIH HHS R00 CA157945NCI NIH HHS R01 CA177910
6 · The paper itself

Abstract

In this issue of Molecular Cell, Wang et al. (2014) report that the splicing kinase SRPK1 can function as both an oncogene and a tumor suppressor by modulating the activation state of the protein kinase Akt. This is shown to be mediated by the ability of SRPK1 to bind to the Akt phosphatase PHLPP1.

Indexed as

Protein Processing, Post-TranslationalAnimalsCarcinogenesisFemaleHumansMaleNuclear ProteinsPhosphoprotein PhosphatasesProtein Serine-Threonine KinasesNuclear ProteinsPHLPP1 protein, mousePhosphoprotein PhosphatasesProtein Serine-Threonine KinasesSrpk1 protein, mouse

Identifiers

PMID24813709
PMCPMC4089875
OpenAlexW2073261165

What OpenQuestion holds

Textmetadata
LicenceTDM
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.