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• W2091268459 startingPage "136" @default.
• W2091268459 abstract "Neuronal apoptosis is a key component in the sculpting of tissues during embryonic and postnatal development and is driven largely by the action of caspases. In the mouse olfactory system, caspase-3 and -9 are expressed in olfactory receptor neurons (ORNs) of adult mice, and their selective retrograde activation drives ORN apoptosis following ablation of their target, the olfactory bulb (OB). Here, we show that both of these caspases are expressed at the earliest stages of ORN embryonic development, and their expression is concentrated in outgrowing ORN axons. The retention, in null mice for both caspases, of a population of ORNs that would normally undergo developmental apoptosis beginning at E13 of development, results in a permanently expanded population of ORNs. In turn, in some caspase-3 null mice, the ORN target organ, the OB, also develops abnormally, resulting in the formation of secondary, apparently functional, extracranial ectopic OBs." @default.
• W2091268459 created "2016-06-24" @default.
• W2091268459 creator A5061980316 @default.
• W2091268459 creator A5090758782 @default.
• W2091268459 date "2004-01-01" @default.
• W2091268459 modified "2023-09-29" @default.
• W2091268459 title "Caspase-3 and caspase-9 mediate developmental apoptosis in the mouse olfactory system" @default.
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• W2091268459 doi "https://doi.org/10.1002/cne.20120" @default.
• W2091268459 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15156583" @default.
• W2091268459 hasPublicationYear "2004" @default.
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