Evidence map›Paper›PMID 18285463›Full record

ArticleMolecular and cellular biology2008

Phosphoinositide 3-kinases p110alpha and p110beta regulate cell cycle entry, exhibiting distinct activation kinetics in G1 phase.

Miriam Marqués, Amit Kumar, Isabel Cortés, Ana Gonzalez-García, Carmen Hernández, M Carmen Moreno-Ortiz, Ana C Carrera

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Signaling Pathways in Leukemic Stem Cells.Advances in experimental medicine and biology · 2019
    Review
  6. Class I Phosphoinositide 3-KinaseInternational journal of molecular sciences · 2018
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Nuclear PI3K signaling in cell growth and tumorigenesis.Frontiers in cell and developmental biology · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. MYC and the control of DNA replication.Cold Spring Harbor perspectives in medicine · 2014
    Review
  20. Downregulation of PI3Kcb utilizing adenovirus-mediated transfer of siRNA attenuates bone cancer pain.International journal of clinical and experimental pathology · 2014
    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

7 authors at 1 institution in 1 country.

Miriam MarquésDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, Darwin 3, Cantoblanco, Madrid E-28049, Spain.
Amit Kumar
Isabel Cortés
Ana Gonzalez-García
Carmen Hernández
M Carmen Moreno-Ortiz
Ana C Carrera
Centro Nacional de Biotecnología · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphoinositide 3-kinase (PI3K) is an early signaling molecule that regulates cell growth and cell cycle entry. PI3K is activated immediately after growth factor receptor stimulation (at the G(0)/G(1) transition) and again in late G(1). The two ubiquitous PI3K isoforms (p110alpha and p110beta) are essential during embryonic development and are thought to control cell division. Nonetheless, it is presently unknown at which point each is activated during the cell cycle and whether or not they both control S-phase entry. We found that p110alpha was activated first in G(0)/G(1), followed by a minor p110beta activity peak. In late G(1), p110alpha activation preceded that of p110beta, which showed the maximum activity at this time. p110beta activation required Ras activity, whereas p110alpha was first activated by tyrosine kinases and then further induced by active Ras. Interference with p110alpha and -beta activity diminished the activation of downstream effectors with different kinetics, with a selective action of p110alpha in blocking early G(1) events. We show that inhibition of either p110alpha or p110beta reduced cell cycle entry. These results reveal that PI3Kalpha and -beta present distinct activation requirements and kinetics in G(1) phase, with a selective action of PI3Kalpha at the G(0)/G(1) phase transition. Nevertheless, PI3Kalpha and -beta both regulate S-phase entry.

Indexed as

Cell CycleAnimalsCell LineCells, CulturedClass I Phosphatidylinositol 3-KinasesCyclinsEnzyme ActivationForkhead Box Protein O3Forkhead Transcription FactorsHumansIsoenzymesKineticsMicePhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-myc1-phosphatidylinositol 3-kinase p110 subunit, mouseClass I Phosphatidylinositol 3-KinasesCyclinsForkhead Box Protein O3Forkhead Transcription FactorsFoxO3 protein, mouseIsoenzymesMyc protein, mousePhosphatidylinositol 3-KinasesPIK3CB protein, humanProto-Oncogene Proteins c-myc

Identifiers

PMID18285463
PMCPMC2293125
OpenAlexW2049708945

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.