Evidence map›Paper›PMID 37529255›Full record

ArticleTurkish journal of biology = Turk biyoloji dergisi2022

p110α activity at the M-to-G1 transition is critical for cellular proliferation and reentry into the cell cycle.

Onur Çizmecioğlu

Abstract read
In one paragraph

Article in Turkish journal of biology = Turk biyoloji dergisi, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

1 author.

Onur ÇizmecioğluDepartment of Molecular Biology and Genetics, Science Faculty, İhsan Doğramacı Bilkent University, Ankara, Turkey.ORCID https://orcid.org/0000-0002-7608-6950

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphoinositide 3-kinase (PI3K) signaling pathway is essential for normal physiology and is impaired in diseases such as premalignant hyperproliferative disorders, primary immunodeficiency, metabolic disorders, and cancer. Although the core PI3K pathway components are known today, a long-standing gap in our knowledge of PI3K signaling concerns how distinct PI3K isoforms and their activity patterns contribute to the functional consequences of pathway upregulation. In order to address this issue, we devised a molecular genetic cell model, which allowed temporal regulation of the indispensable PI3K isoform, p110α in distinct stages of the cell cycle. We found that late M and early G1 presence of p110α is key for proper cell cycle progression, whereas its S-phase abundance was redundant. Our results also emphasize a critical dependence of cell cycle reentry on early G1 activity of p110α. Collectively, our findings provide a temporal perspective to p110α activation and offer insight into which wave of PI3K activity could be essential for cell cycle progression.

Indexed as

Cell cyclep110αphosphoinositide 3-kinase pathwaysignal transductiontemporal regulation

Identifiers

PMID37529255
PMCPMC10388040

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.