- Home
- Search Results
- Page 1 of 1
Search for: All records
-
Total Resources2
- Resource Type
-
00020
- Availability
-
20
- Author / Contributor
- Filter by Author / Creator
-
-
Gebelein, Brian (2)
-
Kopan, Raphael (2)
-
Kuang, Yi (2)
-
Preusse, Kristina (2)
-
Sprinzak, David (2)
-
Yuan, Zhenyu (2)
-
Brunskill, Eric W. (1)
-
Cain, Brittany (1)
-
Campbell, Ian (1)
-
Chaturvedi, Praneet (1)
-
Christensen, Collin J (1)
-
Dai, Quanhui (1)
-
Eafergan, Nathanel (1)
-
Eafergen, Natanel (1)
-
Golan, Ohad (1)
-
Hass, Matthew R (1)
-
Hass, Matthew R. (1)
-
Kobia, Francis M. (1)
-
Kovall, Rhett A (1)
-
Kovall, Rhett A. (1)
-
- Filter by Editor
-
-
Koo, Bon-Kyoung (1)
-
& Spizer, S. M. (0)
-
& . Spizer, S. (0)
-
& Ahn, J. (0)
-
& Bateiha, S. (0)
-
& Bosch, N. (0)
-
& Brennan K. (0)
-
& Brennan, K. (0)
-
& Chen, B. (0)
-
& Chen, Bodong (0)
-
& Drown, S. (0)
-
& Ferretti, F. (0)
-
& Higgins, A. (0)
-
& J. Peters (0)
-
& Kali, Y. (0)
-
& Ruiz-Arias, P.M. (0)
-
& S. Spitzer (0)
-
& Spitzer, S. (0)
-
& Spitzer, S.M. (0)
-
(submitted - in Review for IEEE ICASSP-2024) (0)
-
-
Have feedback or suggestions for a way to improve these results?
!
Note: When clicking on a Digital Object Identifier (DOI) number, you will be taken to an external site maintained by the publisher.
Some full text articles may not yet be available without a charge during the embargo (administrative interval).
What is a DOI Number?
Some links on this page may take you to non-federal websites. Their policies may differ from this site.
-
Kuang, Yi ; Golan, Ohad ; Preusse, Kristina ; Cain, Brittany ; Christensen, Collin J ; Salomone, Joseph ; Campbell, Ian ; Okwubido-Williams, FearGod V ; Hass, Matthew R ; Yuan, Zhenyu ; et al ( , eLife)Notch pathway haploinsufficiency can cause severe developmental syndromes with highly variable penetrance. Currently, we have a limited mechanistic understanding of phenotype variability due to gene dosage. Here, we unexpectedly found that inserting an enhancer containing pioneer transcription factor sites coupled to Notch dimer sites can induce a subset of Notch haploinsufficiency phenotypes in Drosophila with wild type Notch gene dose. Using Drosophila genetics, we show that this enhancer induces Notch phenotypes in a Cdk8-dependent, transcription-independent manner. We further combined mathematical modeling with quantitative trait and expression analysis to build a model that describes how changes in Notch signal production versus degradation differentially impact cellular outcomes that require long versus short signal duration. Altogether, these findings support a ‘bind and discard’ mechanism in which enhancers with specific binding sites promote rapid Cdk8-dependent Notch turnover, and thereby reduce Notch-dependent transcription at other loci and sensitize tissues to gene dose based upon signal duration.more » « less