Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2014 Jun 19;10(6):e1003655. doi: 10.1371/journal.pcbi.1003655

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2014 Chen et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

PMC Copyright notice

Notch signaling regulates the differentiation and patterning of each of the sensory cell types shown. Sensory cell expression for each of the miRNAs listed was shown previously (see text for references). miRNA canonical target sites in the UTRs of Notch and Hes homologs were found using our previously described target prediction algorithm [33]. Some of these targets have been experimentally verified (V) (human: [65]; sea squirt: [33]; fruit fly: [9]). In Drosophila, miR-2, miR-6 and miR-7 overexpression (O) have all been previously shown to cause a phenotype indicative of suppressed Notch signaling activity and loss of lateral inhibition, such as increased density or clustering of microchaetes [9]. In human airway epithelial tissue, knockdown (K) of miR-449 has been shown to cause a decreased rate of ciliated cells indicative of Notch signaling gain-of-function [65].

Inline graphic — Notch signaling regulates the differentiation and patterning of each of the sensory cell types shown. Sensory cell expression for each of the miRNAs listed was shown previously (see text for references). miRNA canonical target sites in the UTRs of Notch and Hes homologs were found using our previously described target prediction algorithm [33]. Some of these targets have been experimentally verified (V) (human: [65]; sea squirt: [33]; fruit fly: [9]). In Drosophila, miR-2, miR-6 and miR-7 overexpression (O) have all been previously shown to cause a phenotype indicative of suppressed Notch signaling activity and loss of lateral inhibition, such as increased density or clustering of microchaetes [9]. In human airway epithelial tissue, knockdown (K) of miR-449 has been shown to cause a decreased rate of ciliated cells indicative of Notch signaling gain-of-function [65].