Evidence map›Paper›PMID 32474911›Full record

ArticleJournal of cellular physiology2020

Cre/loxP approach-mediated downregulation of Pik3c3 inhibits the hypertrophic growth of renal proximal tubule cells.

Ting Liu, Jialing Yuan, Caihong Dai, Jinxian Xu, Shude Li, Benjamin D Humphreys, Daniel T Kleven, Jian-Kang Chen

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

8 authors at 3 institutions in 2 countries.

Ting LiuDepartments of Cellular Biology & Anatomy and Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia.
Jialing YuanDepartments of Cellular Biology & Anatomy and Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia.
Caihong DaiDepartments of Cellular Biology & Anatomy and Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia.
Jinxian XuDepartments of Cellular Biology & Anatomy and Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia.
Shude LiDepartment of Biochemistry & Molecular Biology, School of Basic Medical Sciences, Kunming Medical University, Kunming, Yunnan, China.
Benjamin D HumphreysDivision of Nephrology, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri.
Daniel T KlevenDepartment of Pathology, Medical College of Georgia, Augusta University, Augusta, Georgia.
Jian-Kang ChenDepartments of Cellular Biology & Anatomy and Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia.ORCID 0000-0001-9490-5588
Augusta University · USKunming Medical University · CNWashington University in St. Louis · US

Funding

Resource Based Center for Musculoskeletal Biology and Medicine (Overall Application)P30AR074992 · NIAMS · WASHINGTON UNIVERSITY · PI MATTHEW J SILVA · 2019 to 2026
$6.8M
Mechanisms Underlying the Susceptibility and Severity of Acute Kidney InjuryR01DK114328 · NIDDK · AUGUSTA UNIVERSITY · PI CHEN, JIAN-KANG · 2017 to 2021
$1.7M
Mechanism of Compensatory Renal HypertrophyR01DK083575 · NIDDK · VANDERBILT UNIVERSITY · PI CHEN, JIAN-KANG · 2011 to 2015
$1.7M
NIAMS NIH HHS P30 AR074992NIDDK NIH HHS R01 DK083575NIDDK NIH HHS R01 DK114328
6 · The paper itself

Abstract

Nephron loss stimulates residual functioning nephrons to undergo compensatory growth. Excessive nephron growth may be a maladaptive response that sets the stage for progressive nephron damage, leading to kidney failure. To date, however, the mechanism of nephron growth remains incompletely understood. Our previous study revealed that class III phosphatidylinositol-3-kinase (Pik3c3) is activated in the remaining kidney after unilateral nephrectomy (UNX)-induced nephron loss, but previous studies failed to generate a Pik3c3 gene knockout animal model. Global Pik3c3 deletion results in embryonic lethality. Given that renal proximal tubule cells make up the bulk of the kidney and undergo the most prominent hypertrophic growth after UNX, in this study we used Cre-loxP-based approaches to demonstrate for the first time that tamoxifen-inducible SLC34a1 promoter-driven CreER

Indexed as

AnimalsClass III Phosphatidylinositol 3-KinasesExtracellular Matrix ProteinsGene Expression Regulation, DevelopmentalHumansIntegrasesKidneyKidney Tubules, ProximalMechanistic Target of Rapamycin Complex 1MiceNephrectomyNephronsPhosphorylationProtein-Lysine 6-OxidaseRibosomal Protein S6 Kinases, 90-kDaSignal TransductionClass III Phosphatidylinositol 3-KinasesCre recombinaseExtracellular Matrix ProteinsIntegrasesLox protein, mouseMechanistic Target of Rapamycin Complex 1PIK3C3 protein, mouseProtein-Lysine 6-OxidaseRibosomal Protein S6 Kinases, 90-kDaRps6ka1 protein, mouseSirolimusSlc34a1 protein, mouseSodium-Phosphate Cotransporter Proteins, Type IIaclass III phosphatidylinositol-3 kinase (Pik3c3)compensatory nephron hypertrophy (CNH)mammalian target of rapamycin complex 1 (mTORC1)renal proximal tubule cells (RPTC)ribosomal protein S6 (rpS6) phosphorylationunilateral nephrectomy (UNX)

Identifiers

PMID32474911
PMCPMC8205307
OpenAlexW3031726712

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.