Inactivation of TGFβ signaling in neural crest stem cells leads to multiple defects reminiscent of DiGeorge syndrome

Clicks: 40
ID: 274649
2005
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #184 of 206 articles by views in genes & development

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 206 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Specific inactivation of TGFβ signaling in neural crest stem cells (NCSCs) results in cardiovascular defects and thymic, parathyroid, and craniofacial anomalies. All these malformations characterize DiGeorge syndrome, the most common microdeletion ...
Reference Key
sommer2005genesinactivation Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Heiko Wurdak, Lars M. Ittner, Karl S. Lang, Per Leveen, Ueli Suter, Jan A. Fischer, Stefan Karlsson, Walter Born, Lukas Sommer;Heiko Wurdak;Lars M. Ittner;Karl S. Lang;Per Leveen;Ueli Suter;Jan A. Fischer;Stefan Karlsson;Walter Born;Lukas Sommer;
Journal genes & development
Year 2005
DOI
10.1101/gad.317405
URL
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC551573/?report=classic
Keywords

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.