Evidence map›Paper›PMID 35253003›Full record

ArticleJournal of cellular signaling2022

c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease.

Abigail O Smith, Julie A Jonassen, Kenley M Preval, Roger J Davis, Gregory J Pazour

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

Article in Journal of cellular signaling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

5 citing papers in PubMed, 1 citations in OpenAlex.

  1. Review
  2. Article
  3. Cilia Structure and Function in Human Disease.Current opinion in endocrine and metabolic research · 2024
    Article
  4. Review
  5. Illumination of understudied ciliary kinases.Frontiers in molecular biosciences · 2024
    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

5 authors at 1 institution in 1 country.

Abigail O SmithProgram in Molecular Medicine, University of Massachusetts Medical School, Biotech II, Suite 213, 373 Plantation Street, Worcester, MA, USA 01605.
Julie A JonassenDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA, USA 01655.
Kenley M PrevalProgram in Molecular Medicine, University of Massachusetts Medical School, Biotech II, Suite 213, 373 Plantation Street, Worcester, MA, USA 01605.
Roger J DavisProgram in Molecular Medicine, University of Massachusetts Medical School, Biotech II, Suite 213, 373 Plantation Street, Worcester, MA, USA 01605.
Gregory J PazourProgram in Molecular Medicine, University of Massachusetts Medical School, Biotech II, Suite 213, 373 Plantation Street, Worcester, MA, USA 01605.
University of Massachusetts Chan Medical School · US

Funding

Metabolic Stress SignalingR01DK107220 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2016 to 2023
$3.6M
Trafficking of Cystoproteins to the Primary CiliumR01DK103632 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI PAZOUR, GREGORY J · 2015 to 2019
$1.9M
NIDDK NIH HHS R01 DK103632NIDDK NIH HHS R01 DK107220
6 · The paper itself

Abstract

Polycystic kidney disease is an inherited degenerative disease in which the uriniferous tubules are replaced by expanding fluid-filled cysts that ultimately destroy organ function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common form, afflicting approximately 1 in 1,000 people and is caused by mutations in the transmembrane proteins polycystin-1 (Pkd1) and polycystin-2 (Pkd2). The mechanisms by which polycystin mutations induce cyst formation are not well understood, however pro-proliferative signaling must be involved for tubule epithelial cell number to increase over time. We recently found that the stress-activated mitogen-activated protein kinase (MAPK) pathway c-Jun N-terminal kinase (JNK) pathway is activated in cystic disease and genetically removing JNK reduces cyst growth driven by a loss of Pkd2. This review covers the current state of knowledge of signaling in ADPKD with an emphasis on the JNK pathway.

Indexed as

CiliaJun N Terminal kinaseMitogen-activated protein kinase signalingMus musculusPolycystic kidney diseasePolycystin-1Polycystin-2

Identifiers

PMID35253003
PMCPMC8896658
OpenAlexW4213418413

What OpenQuestion 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 OpenQuestion graph.