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Jennifer H. Kong

Researcher at Stanford University

Publications -  25
Citations -  1418

Jennifer H. Kong is an academic researcher from Stanford University. The author has contributed to research in topics: Smoothened & Hedgehog signaling pathway. The author has an hindex of 12, co-authored 24 publications receiving 1070 citations. Previous affiliations of Jennifer H. Kong include University of California, Los Angeles.

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Gli protein activity is controlled by multisite phosphorylation in vertebrate Hedgehog signaling.

TL;DR: A program of multisite phosphorylation that regulates the conversion of Gli proteins into transcriptional activators is described, suggesting aosphorylation-based mechanism for how agradient of Hh signaling in a morphogenetic field can be converted into a gradient of transcriptional activity.
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Cholesterol activates the G-protein coupled receptor Smoothened to promote Hedgehog signaling.

TL;DR: The results show that cholesterol can initiate signaling from the cell surface by engaging the extracellular domain of a GPCR and suggest that SMO activity may be regulated by local changes in cholesterol abundance or accessibility.
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Biochemical mechanisms of vertebrate hedgehog signaling.

TL;DR: This review discusses the mechanisms by which the HH signal is received by patched on target cells, transduced across the cell membrane by smoothened, and transmitted to the nucleus by GLI proteins to influence gene-expression programs.
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Transcription factor Olig2 defines subpopulations of retinal progenitor cells biased toward specific cell fates

TL;DR: Clonal lineage analysis was used to investigate the progeny of a subset of RPCs, those that express the basic helix–loop–helix transcription factor, Olig2, and indicated that the multipotent progenitor pool is made up of distinctive types of RPC, which have biases toward producing subsets of retinal neurons in a terminal division, with the types of neurons produced varying over time.
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Netrin1 Produced by Neural Progenitors, Not Floor Plate Cells, Is Required for Axon Guidance in the Spinal Cord

TL;DR: Genetic approaches in mice are used to selectively remove netrin from different regions of the spinal cord and show that the FP is not the source of netrin1 directing axons to the ventral midline, while local VZ-suppliedNetrin1 is required for this step.