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- W2113070730 endingPage "1280" @default.
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- W2113070730 abstract "The c-Jun NH(2)-terminal kinase (JNK) group of mitogen-activated protein kinases is stimulated in response to a wide array of cellular stresses and proinflammatory cytokines. Mice lacking individual members of the Jnk family (Jnk1, Jnk2, and Jnk3) are viable and survive without overt structural abnormalities. Here we show that mice with a compound deficiency in Jnk expression can survive to birth, but fail to close the optic fissure (retinal coloboma). We demonstrate that JNK initiates a cytokine cascade of bone morphogenetic protein-4 (BMP4) and sonic hedgehog (Shh) that induces the expression of the paired-like homeobox transcription factor Pax2 and closure of the optic fissure. Interestingly, the role of JNK to regulate BMP4 expression during optic fissure closure is conserved in Drosophila during dorsal closure, a related morphogenetic process that requires JNK-regulated expression of the BMP4 ortholog Decapentaplegic (Dpp)." @default.
- W2113070730 created "2016-06-24" @default.
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- W2113070730 date "2003-05-15" @default.
- W2113070730 modified "2023-09-25" @default.
- W2113070730 title "JNK initiates a cytokine cascade that causes Pax2 expression and closure of the optic fissure" @default.
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- W2113070730 doi "https://doi.org/10.1101/gad.1087303" @default.
- W2113070730 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/196061" @default.
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