scispace - formally typeset
M

Miranda van Triest

Researcher at Utrecht University

Publications -  13
Citations -  1817

Miranda van Triest is an academic researcher from Utrecht University. The author has contributed to research in topics: Transcription factor & Regulation of gene expression. The author has an hindex of 11, co-authored 11 publications receiving 1720 citations. Previous affiliations of Miranda van Triest include University Medical Center Utrecht.

Papers
More filters
Journal ArticleDOI

A novel Epac-specific cAMP analogue demonstrates independent regulation of Rap1 and ERK.

TL;DR: A novel cAMP analogue is developed, 8CPT-2Me-cAMP, which activates Epac, but not PKA, both in vitro and in vivo, and tests the widespread model that Rap1 mediates cAMP-induced regulation of the extracellular signal-regulated kinase (ERK).
Journal ArticleDOI

FOXO4 transcriptional activity is regulated by monoubiquitination and USP7/HAUSP.

TL;DR: It is shown that FOXO becomes monoubiquitinated in response to increased cellular oxidative stress, resulting in its re-localization to the nucleus and an increase in its transcriptional activity.
Journal ArticleDOI

Redox-sensitive cysteines bridge p300/CBP-mediated acetylation and FoxO4 activity

TL;DR: It is shown that reactive oxygen species induce the formation of cysteine-thiol disulfide-dependent complexes of FoxO and the p300/CBP acetyltransferase, and that modulation of Fox O biological activity by p300 /CBP-mediated acetylation is fully dependent on theformation of this redox-dependent complex.
Journal ArticleDOI

Genome-wide analysis of FOXO3 mediated transcription regulation through RNA polymerase II profiling.

TL;DR: Together, the data elucidate how FOXOs regulate gene transcription and provide insight into mechanisms by which FOXOs can induce different gene expression programs depending on chromatin architecture.
Journal ArticleDOI

Sequential regulation of the small GTPase Rap1 in human platelets.

TL;DR: It is shown that in platelets, α-thrombin induces Rap1 activation first by a calcium-mediated pathway independently of PKC and then by a second activation phase mediated byPKC and, in part, integrin αIIbβ3.