PuSH - Publikationsserver des Helmholtz Zentrums München: Missense mutation of POU domain class 3 transcription factor 3 in Pou3f3<sup>L423P</sup> mice causes reduced nephron number and impaired development of the thick ascending limb of the loop of Henle.

Informationen

Hinweise zu Qualitätskriterien von Zeitschriften

Open-Access-Richtlinie der Helmholtz-Gemeinschaft 2016

CC Licencences

Metriken für Publikationen

Navigation

Startseite

English

EVA: Veröffentlichen

Neuer EVA Antrag

Recherche

Erweiterte Suche

Durchblättern nach ...

... HMGU-Autoren/Konsortien

... Organisationsstruktur

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Arbeitsgruppen

... Erscheinungsjahr

Publikationen im Überblick

Statistik

HGF Fortschrittsbericht

OA Publikationen

Eintragen

Neue Publikation eintragen

Neue Publikation holen aus...

...EVA

Fehlende Publikation melden

Highlights

Suche

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmholtz Open Science

Bibliometrische Indikatoren

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Rieger, A.* ; Kemter, E.* ; Kumar, S.* ; Popper, B.* ; Aigner, B.* ; Wolf, E. ; Wanke, R.* ; Blutke, A.*

Missense mutation of POU domain class 3 transcription factor 3 in Pou3f3^L423P mice causes reduced nephron number and impaired development of the thick ascending limb of the loop of Henle.

PLoS ONE 11:e0158977 (2016)

Verlagsversion

Forschungsdaten

DOI

PMC

	Open Access Gold

Abstract
Metriken
Zusatzinfos

During nephrogenesis, POU domain class 3 transcription factor 3 (POU3F3 aka BRN1) is critically involved in development of distinct nephron segments, including the thick ascendinglimb of the loop of Henle (TAL). Deficiency of POU3F3 in knock-out mice leads to underdevelopmentof the TAL, lack of differentiation of TAL cells, and perinatal death due to renal failure. Pou3f3L423P mutant mice, which were established in the Munich ENU Mouse MutagenesisProject, carry a recessive point mutation in the homeobox domain of POU3F3. Homozygous Pou3f3L423P mutants are viable and fertile. The present study used functional, as well as qualitative and quantitative morphological analyses to characterize the renal phenotypeof juvenile (12 days) and aged (60 weeks) homo- and heterozygous Pou3f3L423Pmutant mice and age-matched wild-type controls. In both age groups, homozygous mutants vs. control mice displayed significantly smaller kidney volumes, decreased nephron numbersand mean glomerular volumes, smaller TAL volumes, as well as lower volume densitiesof the TAL in the kidney. No histological or ultrastructural lesions of TAL cells or glomerular cells were observed in homozygous mutant mice. Aged homozygous mutants displayed increased serum urea concentrations and reduced specific urine gravity, but no evidence of glomerular dysfunction. These results confirm the role of POU3F3 in developmentand function of the TAL and provide new evidence for its involvement in regulation of the nephron number in the kidney. Therefore, Pou3f3L423P mutant mice represent a valuableresearch model for further analyses of POU3F3 functions, or for nephrological studies examining the role of congenital low nephron numbers.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

3.057

0.000

PuSH - Publikationsserver des Helmholtz Zentrums München

Missense mutation of POU domain class 3 transcription factor 3 in Pou3f3L423P mice causes reduced nephron number and impaired development of the thick ascending limb of the loop of Henle.

Missense mutation of POU domain class 3 transcription factor 3 in Pou3f3^L423P mice causes reduced nephron number and impaired development of the thick ascending limb of the loop of Henle.