![]() ![]() In addition, we highlight the findings that aberrant synaptic adhesion signaling leads to alterations in the structures, transmission, and plasticity of specific synapses across diverse brain areas. Here, we review the literature on the roles of a diverse group of central synaptic organizers, including neurexins (Nrxns), leukocyte common antigen-related receptor protein tyrosine phosphatases (LAR-RPTPs), and their associated binding proteins, in regulating properties of specific type of synapses and neural circuits. ![]() Recent studies have pinpointed the putative roles of trans-synaptic cell-adhesion molecules in mediating various cognitive functions. Trans-synaptic cell-adhesion molecules are critical for governing various stages of synapse development and specifying neural circuit properties via the formation of multifarious signaling pathways. Altogether, these data support the introduction of NUC inhibitors into cancer treatment research. Gene set enrichment analysis–based search for vulnerabilities reveals prospective weak points in RAC1- and kalirin–GEF1–suppressed ADRN-type NB cells, including activities of H3K27- and DNA methyltransferases. The computational analysis shows that, in a context of overall gene set poverty, the upregulomes in RAC1- and kalirin–GEF1–suppressed ADRN-type cells are a batch of AU-rich element–containing mRNAs, which suggests a link between NUC migration and mRNA stability. ![]() Using three clinically relevant expression dichotomies, we reveal that most of up-regulated mRNAs in RAC1- and kalirin–GEF1–suppressed ADRN-type NB cells are associated with low-risk characteristics. Inhibition of NUC migration by RAC1 and kalirin-GEF1 inhibitors occurs without hampering cell proliferation and ADRN identity. Using RNAi and time-lapse imaging, we show that ADRN-type NB cells exhibit RAC1- and kalirin-dependent nucleokinetic (NUC) migration that relies on several integral components of neuronal migration. The migrational propensity of neuroblastoma is affected by cell identity, but the mechanisms behind the divergence remain unknown. ![]()
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