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β-Catenin Up-regulates Atoh1 Expression in Neural Progenitor Cells by Interaction with an Atoh1 3′ Enhancer

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TLDR
The authors found that β-catenin, the key mediator of the canonical Wnt pathway, increased expression of Atoh1 in mouse neuroblastoma cells and neural progenitor cells.
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This article is published in Journal of Biological Chemistry.The article was published on 2010-01-01 and is currently open access. It has received 119 citations till now. The article focuses on the topics: Enhancer & Mef2.

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Wnt Responsive Lgr5-Expressing Stem Cells Are Hair Cell Progenitors in the Cochlea

TL;DR: It is shown that Lgr5, a marker for adult stem cells, was expressed in a subset of supporting cells in the newborn and adult murine cochlea, and the responsiveness to Wnt of cells with a capacity for division and sensory cell formation suggests a potential route to new hair cell generation in the adult coChlea.
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Lgr5-positive supporting cells generate new hair cells in the postnatal cochlea.

TL;DR: The data suggest that the neonatal mammalian cochlea has some capacity for hair cell regeneration following damage alone and that Lgr5-positive cells act as hair cell progenitors in the coChlea.
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Opposing activities of Notch and Wnt signaling regulate intestinal stem cells and gut homeostasis

TL;DR: This work uses function-blocking antibodies against Notch receptors to demonstrate that Notch blockade perturbs intestinal stem cell function by causing a derepression of the Wnt signaling pathway, leading to misexpression of prosecretory genes and proposes that the interaction between Wnt and Notch signaling described here represents a common theme in adult stem cell biology.
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Generation of hair cells in neonatal mice by β-catenin overexpression in Lgr5-positive cochlear progenitors

TL;DR: The finding suggests that Wnt/β-catenin can drive Lgr5-positive cells to act as hair cell progenitors, even after their exit from the cell cycle and apparent establishment of cell fate.
Journal ArticleDOI

Molecular Mechanisms of Inner Ear Development

TL;DR: This chapter focuses on molecular mechanisms of inner ear development derived from studies of model organisms.
References
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Journal ArticleDOI

Wnt/beta-catenin signaling in development and disease.

TL;DR: A remarkable interdisciplinary effort has unraveled the WNT (Wingless and INT-1) signal transduction cascade over the last two decades, finding that Germline mutations in the Wnt pathway cause several hereditary diseases, and somatic mutations are associated with cancer of the intestine and a variety of other tissues.
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Notch/gamma-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells.

TL;DR: This work shows a rapid, massive conversion of proliferative crypt cells into post-mitotic goblet cells after conditional removal of the common Notch pathway transcription factor CSL/RBP-J and indicates that γ-secretase inhibitors, developed for Alzheimer's disease, might be of therapeutic benefit in colorectal neoplastic disease.
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Proneural genes and the specification of neural cell types

TL;DR: Parallel studies in Drosophila and vertebrates have revealed that proneural genes are key regulators of neurogenesis, coordinating the acquisition of a generic neuronal fate and of specific subtype identities that are appropriate for the location and time of neuronal generation.
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Regulation of Cerebral Cortical Size by Control of Cell Cycle Exit in Neural Precursors

TL;DR: Results show thatβ-catenin can function in the decision of precursors to proliferate or differentiate during mammalian neuronal development and suggest that β-catanin can regulate cerebral cortical size by controlling the generation of neural precursor cells.
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beta-Catenin controls hair follicle morphogenesis and stem cell differentiation in the skin.

TL;DR: It is shown that beta-catenin is required genetically downstream of tabby/downless and upstream of bmp and shh in placode formation and is essential for fate decisions of skin stem cells: in the absence of beta-Catenin, stem cells fail to differentiate into follicular keratinocytes, but instead adopt an epidermal fate.
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