Linked Life Data

10774739

Source:http://linkedlifedata.com/resource/pubmed/id/10774739

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-6-26
pubmed:abstractText
For embryos that have small pancreas and lack brain, eyes and thymus, the defects are caused by mutation of a single gene, Hes1. Hes1 encodes a basic helix-loop-helix (bHLH) transcriptional repressor and functionally antagonizes positive bHLH genes such as the neuronal determination gene, Mash1. Misexpression of Hes1 inhibits cell differentiation and keeps cells at the precursor stage or proliferative stage. Conversely, in the absence of Hes1, the expression of positive bHLH genes is upregulated and cells differentiate prematurely without sufficient cell growth. As a result, the development of many tissues such as the brain, eye and pancreas is severely affected. Thus, Hes1 regulates tissue morphogenesis by maintaining undifferentiated cells. In the case of T cell development, Hes1 mutation leads to defects of expansion of early T cell precursors and thereby suppresses T cell fate specification. Thus, Hes1 promotes differentiation of some cell types in addition to maintenance of the undifferentiated state. Interestingly, Hes1 expression is controlled by the transmembrane protein Notch, which is activated by the ligands expressed on the surface of neighboring cells. Taken together, these results indicate that the Notch-Hes1 pathway, which is controlled by cell-cell interaction, plays an essential role in differentiation of many cell types.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1016-8478
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-7
pubmed:dateRevised
2006-11-28
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
The bHLH gene Hes1 regulates differentiation of multiple cell types.
pubmed:affiliation
Institute for Virus Research, Kyoto University, Japan. rkageyam@virus.kyoto-u.ac.jp
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't