Evidence map›Paper›PMID 31830556›Full record

ReviewCellular signalling2020

Proliferative signaling by ERBB proteins and RAF/MEK/ERK effectors in polycystic kidney disease.

Mitchell I Parker, Anna S Nikonova, Danlin Sun, Erica A Golemis

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Mitchell I ParkerProgram in Molecular Therapeutics, Fox Chase Cancer Center, 19111, USA; Molecular & Cell Biology & Genetics (MCBG) Program, Drexel University College of Medicine, 19102, USA.
Anna S NikonovaProgram in Molecular Therapeutics, Fox Chase Cancer Center, 19111, USA.
Danlin SunProgram in Molecular Therapeutics, Fox Chase Cancer Center, 19111, USA; Institute of Life Science, Jiangsu University, Jingkou District, Zhenjiang, Jiangsu 212013, China.
Erica A GolemisProgram in Molecular Therapeutics, Fox Chase Cancer Center, 19111, USA. Electronic address: Erica.Golemis@fccc.edu.
Fox Chase Cancer Center · USJiangsu University · CN

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
Interaction of protein-targeted therapeutics and ciliary dynamicsR01DK108195 · NIDDK · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2016 to 2020
$2.0M
Targeting asymmetric ciliary signaling in cancerR21CA228187 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2019 to 2020
$402k
Interaction of protein-targeted therapeutics and ciliary dynamicsR56DK108195 · NIDDK · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2015 to 2015
$116k
NCI NIH HHS P30 CA006927NCI NIH HHS R21 CA228187NIDDK NIH HHS R01 DK108195NIDDK NIH HHS R56 DK108195
6 · The paper itself

Abstract

A primary pathological feature of polycystic kidney disease (PKD) is the hyperproliferation of epithelial cells in renal tubules, resulting in formation of fluid-filled cysts. The proliferative aspects of the two major forms of PKD-autosomal dominant PKD (ADPKD), which arises from mutations in the polycystins PKD1 and PKD2, and autosomal recessive PKD (ARPKD), which arises from mutations in PKHD1-has encouraged investigation into protein components of the core cell proliferative machinery as potential drivers of PKD pathogenesis. In this review, we examine the role of signaling by ERBB proteins and their effectors, with a primary focus on ADPKD. The ERBB family of receptor tyrosine kinases (EGFR/ERBB1, HER2/ERBB2, ERBB3, and ERBB4) are activated by extracellular ligands, inducing multiple pro-growth signaling cascades; among these, activation of signaling through the RAS GTPase, and the RAF, MEK1/2, and ERK1/2 kinases enhance cell proliferation and restrict apoptosis during renal tubuloepithelial cyst formation. Characteristics of PKD include overexpression and mislocalization of the ERBB receptors and ligands, leading to enhanced activation and increased activity of downstream signaling proteins. The altered regulation of ERBBs and their effectors in PKD is influenced by enhanced activity of SRC kinase, which is promoted by the loss of cytoplasmic Ca

Indexed as

Signal TransductionCell ProliferationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHumansMitogen-Activated Protein Kinase KinasesPolycystic Kidney Diseasesraf KinasesErbB ReceptorsExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase Kinasesraf KinasesCiliaTargeted therapeuticsTubulogenesisTumorigenesis

Identifiers

PMID31830556
PMCPMC6957738
OpenAlexW2996555791

What OpenQuestion holds

Textmetadata
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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.