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• W2123575778 endingPage "1336" @default.
• W2123575778 startingPage "1323" @default.
• W2123575778 abstract "Cell adhesion is critical to the establishment of proper connections in the nervous system. Some receptor-type protein tyrosine phosphatases (RPTPs) have adhesion molecule–like extracellular segments with intracellular tyrosine phosphatase domains that may transduce signals in response to adhesion. PTPμ is a RPTP that mediates cell aggregation and is expressed at high levels in the nervous system. In this study, we demonstrate that PTPμ promotes neurite outgrowth of retinal ganglion cells when used as a culture substrate. In addition, PTPμ was found in a complex with N-cadherin in retinal cells. To determine the physiological significance of the association between PTPμ and N-cadherin, the expression level and enzymatic activity of PTPμ were perturbed in retinal explant cultures. Downregulation of PTPμ expression through antisense techniques resulted in a significant decrease in neurite outgrowth on an N-cadherin substrate, whereas there was no effect on laminin or L1-dependent neurite outgrowth. The overexpression of a catalytically inactive form of PTPμ significantly decreased neurite outgrowth on N-cadherin. These data indicate that PTPμ specifically regulates signals required for neurites to extend on an N-cadherin substrate, implicating reversible tyrosine phosphorylation in the control of N-cadherin function. Together, these results suggest that PTPμ plays a dual role in the regulation of neurite outgrowth." @default.
• W2123575778 created "2016-06-24" @default.
• W2123575778 creator A5043407578 @default.
• W2123575778 creator A5065482075 @default.
• W2123575778 date "1999-03-22" @default.
• W2123575778 modified "2023-10-11" @default.
• W2123575778 title "PTPμ Regulates N-Cadherin–dependent Neurite Outgrowth" @default.
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• W2123575778 doi "https://doi.org/10.1083/jcb.144.6.1323" @default.
• W2123575778 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2150569" @default.
• W2123575778 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10087273" @default.
• W2123575778 hasPublicationYear "1999" @default.
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