Nonmyocytic androgen receptor regulates the sexually dimorphic development of the embryonic bulbocavernosus muscle

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F14%3A10272412" target="_blank" >RIV/00216208:11110/14:10272412 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1210/en.2014-1008" target="_blank" >http://dx.doi.org/10.1210/en.2014-1008</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1210/en.2014-1008" target="_blank" >10.1210/en.2014-1008</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Nonmyocytic androgen receptor regulates the sexually dimorphic development of the embryonic bulbocavernosus muscle

Popis výsledku v původním jazyce

The bulbocavernosus (BC) is a sexually dimorphic muscle observed only in males. Androgen receptor knockout mouse studies show the loss of BC formation. This suggests that androgen signaling plays a vital role in its development. Androgen has been known to induce muscle hypertrophy through satellite cell activation and myonuclei accretion during muscle regeneration and growth. To identify the mechanism of sexual dimorphism during BC embryonic development, the timing of morphological differences was firstestablished. The BC was morphologically different between male and female mice at embryonic day (E) 16.5. Differences in the myogenic process were detected at E15.5. The male BC possesses a higher number of proliferating undifferentiated myoblasts. To identify the role of androgen signaling, muscle-specific androgen receptor (AR) mutation was introduced, which resulted in no observable phenotypes. Hence, the expression of AR in the BC was examined and found that the AR did not colocaliz

Název v anglickém jazyce

Nonmyocytic androgen receptor regulates the sexually dimorphic development of the embryonic bulbocavernosus muscle

Popis výsledku anglicky

The bulbocavernosus (BC) is a sexually dimorphic muscle observed only in males. Androgen receptor knockout mouse studies show the loss of BC formation. This suggests that androgen signaling plays a vital role in its development. Androgen has been known to induce muscle hypertrophy through satellite cell activation and myonuclei accretion during muscle regeneration and growth. To identify the mechanism of sexual dimorphism during BC embryonic development, the timing of morphological differences was firstestablished. The BC was morphologically different between male and female mice at embryonic day (E) 16.5. Differences in the myogenic process were detected at E15.5. The male BC possesses a higher number of proliferating undifferentiated myoblasts. To identify the role of androgen signaling, muscle-specific androgen receptor (AR) mutation was introduced, which resulted in no observable phenotypes. Hence, the expression of AR in the BC was examined and found that the AR did not colocaliz

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EA - Morfologické obory a cytologie

OECD FORD obor

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Projekt

—

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Endocrinology

ISSN

0013-7227

e-ISSN

—

Svazek periodika

155

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

15

Strana od-do

2467-2479

Kód UT WoS článku

000342343400015

EID výsledku v databázi Scopus

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