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• W2096290989 abstract "The p75 neurotrophin receptor (p75NTR) regulates neuronal survival, apoptosis, and growth. Recent studies have reported that disruption of Exon IV produces a null mouse lacking all p75NTR gene products (p75NTR ExonIV-/- ), whereas mice lacking p75NTR Exon III (p75NTR ExonIII-/- ) maintain expression of an alternatively spliced form of p75NTR (s-p75NTR). Here, we report that p75NTR ExonIV-/- mice express a p75NTR gene product that encodes a truncated protein containing the extracellular stalk region together with the entire transmembrane and intracellular domains. The gene product is initiated from a cryptic Kozak consensus/initiator ATG sequence within a region of Exon IV located 3′ to the pGK-Neo insertion site. Overexpression of this fragment in heterologous cells results in activation of Jun kinase and induces Pro-caspase-3 cleavage, indicating that it activates p75NTR signaling cascades. These results indicate that aspects of the p75NTR ExonIV-/- phenotype may reflect a gain-of-function mutation rather than loss of p75NTR function." @default.
• W2096290989 created "2016-06-24" @default.
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• W2096290989 date "2004-02-25" @default.
• W2096290989 modified "2023-10-18" @default.
• W2096290989 title "A Pro-Apoptotic Fragment of the p75 Neurotrophin Receptor Is Expressed in p75NTR^ExonIVNull Mice" @default.
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• W2096290989 doi "https://doi.org/10.1523/jneurosci.5397-03.2004" @default.
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