Evidence map›Paper›PMID 18434386›Full record

ArticleAmerican journal of physiology. Renal physiology2008

Src regulates cell cycle protein expression and renal epithelial cell proliferation via PI3K/Akt signaling-dependent and -independent mechanisms.

Jingping Xing, Zhu Zhang, Haiping Mao, Rick G Schnellmann, Shougang Zhuang

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. p57International journal of molecular sciences · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Hyperhomocysteinemia Exacerbates Cisplatin-induced Acute Kidney Injury.International journal of biological sciences · 2017
    Article
  10. Article
  11. Enhanced CaJournal of nanomaterials · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Hsp27 inhibits sublethal, Src-mediated renal epithelial cell injury.American journal of physiology. Renal physiology · 2009
    Article
  19. 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

5 authors at 1 institution in 1 country.

Jingping XingDepartment of Medicine, Brown University School of Medicine, Rhode Island Hospital Middle, Providence, RI 02903, USA.
Zhu Zhang
Haiping Mao
Rick G Schnellmann
Shougang Zhuang
Rhode Island Hospital · US

Funding

Histone deacetylases as novel therapeutic targets for kidney fibrosisR01DK085065 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2010 to 2017
$2.8M
Dedifferentiation Following Renal Cell InjuryR01DK071997 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2006 to 2009
$1.1M
NIDDK NIH HHS DK-071997NIDDK NIH HHS R01 DK085065
6 · The paper itself

Abstract

Our recent studies showed that Src family kinases (SFKs) are important mediators of proliferation in renal proximal tubular cells (RPTC). In this study, we elucidate the signaling mechanisms that mediate SFK regulation of cell proliferation and cycle protein expression, and identify the SFK member responsible for these responses in a mouse RPTC line. Akt, a target of phosphoinositide-3-kinase (PI3K), and ERK1/2 were constitutively phosphorylated in RPTC cultured in the presence of serum. While treatment of cells with PP1, a specific SFK inhibitor, completely blocked phosphorylation of ERK1/2 and Akt, only inhibition of PI3K/Akt resulted in decreased RPTC proliferation. Incubation of cells with PP1 decreased cyclin D1 expression, decreased p27 and p57 phosphorylation, and increased p27 and p57 expression, two cyclin-dependent kinase inhibitors. Inhibition of the PI3K pathway decreased expression of cyclin D1 without altering expression of p27 and p57. In contrast, PP1 and PI3K inhibition had no effect on cyclin E and p21. Although RPTC expressed Src, Fyn, and Lyn, only siRNA-mediated knockdown of Src decreased RPTC proliferation, decreased cyclin D1 expression, and increased p27 and p57 expression. These data reveal that Src is a crucial mediator of RPTC proliferation and Src-mediated proliferation is associated with PI3K-dependent upregulation of cyclin D1 and PI3K-independent downregulation of p27 and p57.

Indexed as

Cell LineCell ProliferationChromonesCyclin D1Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent Kinase Inhibitor p57Epithelial CellsHydrazinesKidneyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazinesQuinolines2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneCdkn1c protein, mouseChromonesCyclin D1Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent Kinase Inhibitor p57HydrazinesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazinesQU663 compoundQuinolinessrc-Family Kinases

Identifiers

PMID18434386
PMCPMC2494517
OpenAlexW2097233438

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.