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Debra J. Morrison

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  7
Citations -  893

Debra J. Morrison is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Transcription factor & Receptor tyrosine kinase. The author has an hindex of 7, co-authored 7 publications receiving 866 citations. Previous affiliations of Debra J. Morrison include Northwestern University.

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Sprouty proteins: multifaceted negative-feedback regulators of receptor tyrosine kinase signaling

TL;DR: New biochemical and genetic evidence indicates specific roles of the Spry genes in development and multiple modes of action of theSpry proteins in regulation of the RTK-induced response.
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Tyrosine Phosphorylation of Sprouty Proteins Regulates Their Ability to Inhibit Growth Factor Signaling: A Dual Feedback Loop

TL;DR: It is found that tyrosine phosphorylation of Sprouty2 affected neither its subcellular localization nor its interaction with Grb2, FRS2/SNT, or otherSprouty proteins, which highlights a novel negative and positive regulatory loop that allows for the controlled, homeostatic inhibition of RTK signaling.
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WT1 Activates a Glomerular-Specific Enhancer Identified from the Human Nephrin Gene

TL;DR: The Wilms tumor suppressor gene (WT1) is a zinc-finger-containing transcription factor that is coexpressed with NPHS1 in differentiated podocytes; gel shift binding assays demonstrate that a recombinant WT1 protein can bind and activate the 186-bp NPHS 1 fragment in a sequence-specific manner.
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The receptor tyrosine kinase regulator Sprouty1 is a target of the tumor suppressor WT1 and important for kidney development.

TL;DR: Sprouty1 represents a physiologically relevant target gene of WT1 during kidney development, including a homologue of the Drosophila receptor tyrosine kinase regulator, sprouty, which plays a key role in the early steps of glomerulus formation.
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WT1 Induces Apoptosis through Transcriptional Regulation of the Proapoptotic Bcl-2 Family Member Bak

TL;DR: The hypothesis that Wilms' tumors arise, in part, because WT1 mutant proteins fail to promote programmed cell death during kidney development is supported.