Unknown

Dataset Information

0

Deletion of retinoic acid receptor ? (RAR?) impairs pancreatic endocrine differentiation.


ABSTRACT: All-trans retinoic acid (RA) signals via binding to retinoic acid receptors (RARs ?, ?, and ?). RA directly influences expression of Pdx1, a transcription factor essential for pancreatic development and beta-cell (?-cell) maturation. In this study we follow the differentiation of cultured wild-type (WT) vs. RAR? knockout (KO) embryonic stem (ES) cells into pancreatic islet cells. We found that RAR? KO ES cells show greatly reduced expression of some important endocrine markers of differentiated islet cells, such as glucagon, islet amyloid polypeptide (Iapp), and insulin 1 (Ins1) relative to WT. We conclude that RAR? activity is essential for proper differentiation of ES cells to pancreatic endocrine cells.

SUBMITTER: Perez RJ 

PROVIDER: S-EPMC3821387 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature

altmetric image

Publications

Deletion of retinoic acid receptor β (RARβ) impairs pancreatic endocrine differentiation.

Pérez Ronald J RJ   Benoit Yannick D YD   Gudas Lorraine J LJ  

Experimental cell research 20130610 14


All-trans retinoic acid (RA) signals via binding to retinoic acid receptors (RARs α, β, and γ). RA directly influences expression of Pdx1, a transcription factor essential for pancreatic development and beta-cell (β-cell) maturation. In this study we follow the differentiation of cultured wild-type (WT) vs. RARβ knockout (KO) embryonic stem (ES) cells into pancreatic islet cells. We found that RARβ KO ES cells show greatly reduced expression of some important endocrine markers of differentiated  ...[more]

Similar Datasets

| S-EPMC1900023 | biostudies-literature
| S-EPMC2962525 | biostudies-literature
| S-EPMC2475501 | biostudies-literature
| S-EPMC6947571 | biostudies-literature
| S-EPMC4197984 | biostudies-literature
| S-EPMC5031550 | biostudies-literature
2014-01-23 | E-GEOD-53736 | biostudies-arrayexpress
| S-EPMC7190832 | biostudies-literature
| S-EPMC5651880 | biostudies-other
| S-EPMC7328135 | biostudies-literature