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- W3126459384 abstract "Significance The Hedgehog signaling pathway is fundamental in animal development, controlling the size, morphology, and differentiation of tissues and organs. How Hedgehog signaling is evolutionarily tuned to produce different outputs is poorly understood. We use cell biology, mathematical modeling, and analysis of mutations causing birth defects to demonstrate that ultrasensitivity is a key signal-processing feature of the Hedgehog pathway, which can lead to different outputs. We explain ultrasensitivity by a mathematical model of Hedgehog signaling whereby the tumor-suppressor membrane protein Patched catalyzes the deactivation of the GPCR-like transducer Smoothened in primary cilia. The Sonic Hedgehog ligand binds and inhibits Patched, causing switch-like Smoothened activation. Our results clarify the regulation of the Patched–Smoothened module in normal signaling and in disease." @default.
- W3126459384 created "2021-02-15" @default.
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- W3126459384 date "2021-02-01" @default.
- W3126459384 modified "2023-09-23" @default.
- W3126459384 title "Mechanism and ultrasensitivity in Hedgehog signaling revealed by Patched1 disease mutations" @default.
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- W3126459384 doi "https://doi.org/10.1073/pnas.2006800118" @default.
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