Evidence map›Paper›PMID 29679048›Full record

ArticleScientific reports2018

Disruption of Hox9,10,11 function results in cellular level lineage infidelity in the kidney.

Keri A Drake, Mike Adam, Robert Mahoney, S Steven Potter

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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  7. Single-Cell Chromatin and Gene-Regulatory Dynamics of Mouse Nephron Progenitors.Journal of the American Society of Nephrology : JASN · 2022
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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 1 institution in 1 country.

Keri A DrakeDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Mike AdamDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Robert MahoneyDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
S Steven PotterDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA. Steve.Potter@cchmc.org.ORCID 0000-0003-0726-0350
Cincinnati Children's Hospital Medical Center · US

Funding

Pediatric Scientist Development Program (PSDP) [K12]K12HD000850 · NICHD · YALE UNIVERSITY · PI Sallie R. Permar · 1987 to 2026
$44.1M
Proteomics CoreP50DK096418 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI DEVARAJAN, PRASAD · 2012 to 2021
$8.4M
Recombineering based analysis of Hox function in kidney developmentR01DK099995 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI POTTER, S. STEVEN · 2014 to 2017
$1.4M
NICHD NIH HHS K12 HD000850NIDDK NIH HHS P50 DK096418NIDDK NIH HHS R01 DK099995
6 · The paper itself

Abstract

Hox genes are important regulators of development. The 39 mammalian Hox genes have considerable functional overlap, greatly confounding their study. In this report, we generated mice with multiple combinations of paralogous and flanking Abd-B Hox gene mutations to investigate functional redundancies in kidney development. The resulting mice developed a number of kidney abnormalities, including hypoplasia, agenesis, and severe cysts, with distinct Hox functions observed in early metanephric kidney formation and nephron progenitor maintenance. Most surprising, however, was that extensive removal of Hox shared function in these kidneys resulted in cellular level lineage infidelity. Strikingly, mutant nephron tubules consisted of intermixed cells with proximal tubule, loop of Henle, and collecting duct identities, with some single cells expressing markers associated with more than one nephron segment. These results indicate that Hox genes are required for proper lineage selection/maintenance and full repression of genes involved in cell fate restriction in the developing kidney.

Indexed as

AnimalsCell DifferentiationCell LineageFemaleGenes, HomeoboxHomeodomain ProteinsKidneyKidney TubulesLoop of HenleMaleMiceMice, KnockoutMutationNephronsOrganogenesisTranscription FactorsHomeodomain ProteinsTlx1 protein, mouseTranscription Factors

Identifiers

PMID29679048
PMCPMC5910417
OpenAlexW2807288807

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.