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we identify an additional variant (N407S) with a dominant-negative effect on axon growth although it is well-localized at the membrane and properly binds to Contactin2
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During development, CNTN2 absence can transiently affect the expression levels of myelin and myelin-regulating genes, and results in impaired oligodendrocyte branching and hypomyelination of fiber tracts. During de- and remyelination, Cntn2 absence did not affect oligodendrocyte survival or the extent of remyelination.
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We further demonstrate that Cre expression initiates after birth with preservation of native Cntn2 protein. Finally, we show that Cntn23'UTR-IRES-Cre-EGFP/+ mice maintain normal cardiac mechanical and electrical function.
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Tag1 is crucial for the olfactory circuit formation in mice.
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Interaction proteomics revealed the interactors of Caspr2, including CNTN2, KCNAs, members of the ADAM family (ADAM22, ADAM23 and ADAM11), members of LGI family and MAGUKs (DLGs and MPPs).
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Our results clearly demonstrate that mouse and human contactin-2 are physiological substrates for BACE1
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the TAG-1-mediated cell-to-cell interaction between the unpolarized multipolar cells and the pioneering axons regulates the polarization of multipolar cells partly through Lyn kinase and Rac1
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This study demonistrated that knockdown of the cell-surface molecule TAG-1 resulted in retraction of neocortical progenitors' basal processes.
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These results suggest that the Tax-induced decline in p53 function, which is independent of NF-kappaB activation in the early stage, might be the first stage in the onset of ATLL.
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two novel genes, Cntnap2 and Tag1, are implicated in the regulation of diet-induced obesity.
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These observations identify a novel role for TAG1 in modulating the intracellular sorting of signaling receptor complexes.
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These findings are consistent with a regulatory role for Tag-1 in axon emergence as well as migratory behavior by developing mouse cerebellar granule neurons.
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Data show that TAG1 and F3 act antagonistically to control SHH-induced proliferation: F3 suppresses SHH-induced GNP proliferation and induces differentiation, whereas TAG1 antagonises F3.
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Ultrastructural and behavioral analysis of Tag-1 knockout mice shows that the expression of glial TAG-1 is sufficient to restore the axonal and myelin deficits
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These findings suggest that an age-related reduction of TAG-1 expression may predispose neurons to cell death, induced by the binding of TGFbeta2 to APP.
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Although several aspects of the role of TAG-1 in developing sensory axons are consistent with the defects seen in Brn3a knockout mice, it is unlikely that changes in TAG-1 expression directly mediate these defects.
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In the absence of TAG-1, axonal Caspr2 did not accumulate at juxtaparanodes, and shaker-type K+ channels in these regions were severely disrupted, in the central and peripheral nervous systems.
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The TAX-1 upstream sequence includes elements not only sufficient to restrict expression to the nervous system, but also to recapitulate to a great extent the endogenous pattern of the TAG-1 expression in the developing CNS.
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TAG-1 function is required for survival of the neurons of some precerebellar nuclei, while it is not required for cortical interneuron migration in vivo.
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a TAG1-APP signalling pathway negatively modulates neurogenesis through Fe65
