All

What are you looking for?

All
Projects
Results
Organizations

Quick search

  • Projects supported by TA ČR
  • Excellent projects
  • Projects with the highest public support
  • Current projects

Smart search

  • That is how I find a specific +word
  • That is how I leave the -word out of the results
  • “That is how I can find the whole phrase”

NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F23%3A00576977" target="_blank" >RIV/86652036:_____/23:00576977 - isvavai.cz</a>

  • Alternative codes found

    RIV/00023001:_____/23:00084167

  • Result on the web

    <a href="https://www.nature.com/articles/s41467-023-41306-6" target="_blank" >https://www.nature.com/articles/s41467-023-41306-6</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/s41467-023-41306-6" target="_blank" >10.1038/s41467-023-41306-6</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development

  • Original language description

    NEUROD1 is a transcription factor that helps maintain a mature phenotype of pancreatic & beta, cells. Disruption of Neurod1 during pancreatic development causes severe neonatal diabetes, however, the exact role of NEUROD1 in the differentiation programs of endocrine cells is unknown. Here, we report a crucial role of the NEUROD1 regulatory network in endocrine lineage commitment and differentiation. Mechanistically, transcriptome and chromatin landscape analyses demonstrate that Neurod1 inactivation triggers a downregulation of endocrine differentiation transcription factors and upregulation of non-endocrine genes within the Neurod1-deficient endocrine cell population, disturbing endocrine identity acquisition. Neurod1 deficiency altered the H3K27me3 histone modification pattern in promoter regions of differentially expressed genes, which resulted in gene regulatory network changes in the differentiation pathway of endocrine cells, compromising endocrine cell potential, differentiation, and functional properties.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2023

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Nature Communications

  • ISSN

    2041-1723

  • e-ISSN

    2041-1723

  • Volume of the periodical

    14

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    20

  • Pages from-to

    5554

  • UT code for WoS article

    001066679400001

  • EID of the result in the Scopus database