Evidence map›Paper›PMID 30374841›Full record

ArticleThe journal of physiological sciences : JPS2019

The class II phosphoinositide 3-kinases PI3K-C2α and PI3K-C2β differentially regulate clathrin-dependent pinocytosis in human vascular endothelial cells.

Khin Thuzar Aung, Kazuaki Yoshioka, Sho Aki, Kazuhiro Ishimaru, Noriko Takuwa, Yoh Takuwa

Open access · goldAbstract read
In one paragraph

Article in The journal of physiological sciences : JPS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Advances in PSMA theranostics.Translational oncology · 2022
    Article
  12. Internalization of benzylisoquinoline alkaloids by resting and activated bone marrow-derived mast cells utilizes energy-dependent mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  13. An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022
    Article
  14. 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

6 authors at 2 institutions in 1 country.

Khin Thuzar AungDepartment of Physiology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan.
Kazuaki YoshiokaDepartment of Physiology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan.
Sho AkiDepartment of Physiology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan.
Kazuhiro IshimaruDepartment of Physiology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan.
Noriko TakuwaDepartment of Physiology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan.
Yoh TakuwaDepartment of Physiology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan. ytakuwa@med.kanazawa-u.ac.jp.
Kanazawa University · JPIshikawa Prefectural University · JP

Funding

Japan International Cooperation Agency J-14-10306Japan Society for the Promotion of Science 15H04673Japan Society for the Promotion of Science 16K15409Japan Society for the Promotion of Science 16K18988Japan Society for the Promotion of Science 17K08532Japan Society for the Promotion of Science 17K08542Ministry of Education, Culture, Sports, Science and Technology 25116711
6 · The paper itself

Abstract

Pinocytosis is an important fundamental cellular process that is used by the cell to transport fluid and solutes. Phosphoinositide 3-kinases (PI3Ks) regulate a diverse array of dynamic membrane events. However, it is not well-understood which PI3K isoforms are involved in specific mechanisms of pinocytosis. We performed knockdown studies of endogenous PI3K isoforms and clathrin heavy chain (CHC) mediated by small interfering RNA (siRNA). The results demonstrated that the class II PI3K PI3K-C2α and PI3K-C2β, but not the class I or III PI3K, were required for pinocytosis, based on an evaluation of fluorescein-5-isothiocyanate (FITC)-dextran uptake in endothelial cells. Pinocytosis was partially dependent on both clathrin and dynamin, and both PI3K-C2α and PI3K-C2β were required for clathrin-mediated-but not clathrin-non-mediated-FITC-dextran uptake at the step leading up to its delivery to early endosomes. Both PI3K-C2α and PI3K-C2β were co-localized with clathrin-coated pits and vesicles. However, PI3K-C2β, but not PI3K-C2α, was highly co-localized with actin filament-associated clathrin-coated structures and required for actin filament formation at the clathrin-coated structures. These results indicate that PI3K-C2α and PI3K-C2β play differential, indispensable roles in clathrin-mediated pinocytosis.

Indexed as

Actin CytoskeletonAnimalsCells, CulturedClass II Phosphatidylinositol 3-KinasesClathrinEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsPhosphatidylinositol 3-KinasesPinocytosisRNA, Small InterferingClass II Phosphatidylinositol 3-KinasesClathrinPhosphatidylinositol 3-KinasesPIK3C2A protein, humanPIK3C2B protein, humanRNA, Small InterferingClass II PI3KClathrinEndothelial cellPI3K-C2αPI3K-C2βPinocytosis

Identifiers

PMID30374841
PMCPMC10717547
OpenAlexW2898660663

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.