Evidence map›Paper›PMID 35468900›Full record

ArticleNature communications2022

Transcription factors AP-2α and AP-2β regulate distinct segments of the distal nephron in the mammalian kidney.

Joseph O Lamontagne, Hui Zhang, Alia M Zeid, Karin Strittmatter, Alicia D Rocha, Trevor Williams, Sheryl Zhang, Alexander G Marneros

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

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. 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 2 institutions in 1 country.

Joseph O LamontagneCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Hui ZhangCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.ORCID 0000-0002-4936-4791
Alia M ZeidCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Karin StrittmatterCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Alicia D RochaCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Trevor WilliamsDepartment of Craniofacial Biology, University of Colorado, Anschutz Medical Campus, Aurora, CO, 80045, USA.
Sheryl ZhangCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Alexander G MarnerosCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA. amarneros@mgh.harvard.edu.ORCID 0000-0003-3866-020X
Harvard University · USUniversity of Colorado Anschutz Medical Campus · US

Funding

Functional characterization of a novel key regulator of the distal nephron whose deficiency leads to renal fibrosis and cyst formationR01DK118134 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MARNEROS, ALEXANDER GEORG · 2019 to 2023
$1.7M
Mechanisms controlling distal nephron maturationR01DK121178 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MARNEROS, ALEXANDER GEORG · 2019 to 2022
$1.4M
Role of KCTD1 for primary hyperparathyroidismR21AG063377 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI MARNEROS, ALEXANDER GEORG · 2019 to 2020
$436k
NIA NIH HHS R21 AG063377NIDDK NIH HHS R01 DK118134NIDDK NIH HHS R01 DK121178
6 · The paper itself

Abstract

Transcription factors AP-2α and AP-2β have been suggested to regulate the differentiation of nephron precursor populations towards distal nephron segments. Here, we show that in the adult mammalian kidney AP-2α is found in medullary collecting ducts, whereas AP-2β is found in distal nephron segments except for medullary collecting ducts. Inactivation of AP-2α in nephron progenitor cells does not affect mammalian nephrogenesis, whereas its inactivation in collecting ducts leads to defects in medullary collecting ducts in the adult. Heterozygosity for AP-2β in nephron progenitor cells leads to progressive distal convoluted tubule abnormalities and β-catenin/mTOR hyperactivation that is associated with renal fibrosis and cysts. Complete loss of AP-2β in nephron progenitor cells caused an absence of distal convoluted tubules, renal cysts, and fibrosis with β-catenin/mTOR hyperactivation, and early postnatal death. Thus, AP-2α and AP-2β have non-redundant distinct spatiotemporal functions in separate segments of the distal nephron in the mammalian kidney.

Indexed as

beta CateninTranscription Factor AP-2AnimalsKidney Tubules, DistalMammalsNephronsTOR Serine-Threonine Kinasesbeta CateninTOR Serine-Threonine KinasesTranscription Factor AP-2

Identifiers

PMID35468900
PMCPMC9038906
OpenAlexW4224923648

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.