Neurexins induce differentiation of GABA and glutamate postsynaptic specializations via neuroligins.

By E. Graf, Xuezhao Zhang, Shan-xue Jin, M. Linhoff, Ann Marie Craig. Cell, 2004

1,009 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/cb0278101e241da456f22b0b0829f013ebfe3f86

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In Cellular and Molecular Neuroscience

In Molecular Biology

In Sensory Systems

T. Sūdhof

Citations in the corpus

Extracellular Domains of α-Neurexins Participate in Regulating Synaptic Transmission by Selectively Affecting N- and P/Q-Type Ca2+ Channels (2005, background): “…and Craig laboratories suggests, as originally proposed when neurexins were first identified (Ushkaryov et al., 1992), that neurexins can promote the formation of de novo synapses and differentiation of postsynaptic receptors (Scheiffele et al., 2000; Dean et al., 2003; Graf et al., 2004).”
Neuroligins determine synapse maturation and function. (2006, methodology): “Analogous effects were observed upon expression of b-NXs in nonneuronal cells (Graf et al., 2004; Nam and Chen, 2005).”
A synaptic trek to autism. (2009, background): “Secondly, NLGNs and NRXNs are emerging as central organizing molecules for excitatory glutamatergic and inhibitory GABAergic synapses in the mammalian brain [30,31].”
Neurexin-neuroligin signaling in synapse development. (2007, background): “Neuroligins induce formation of glutamatergic and GABAergic presynaptic specializations, with neuroligin 2 being relatively more active on GABAergic axons [3 ,5 ,35].”
Modelling learning and memory in Drosophila to understand Intellectual Disabilities. (2020, neutral): “Neurexin and their binding partners, the neuroligins, are central organizing molecules at synapses that work as adhesion proteins and regulate pre- and post- synapse maturation and activity (Scheiffele et al., 2000; Graf et al., 2004; Varoqueaux et al., 2006; Südhof, 2017).”
Structural Components of Synaptic Plasticity and Memory Consolidation. (2015, background): “This extracellular binding modulates presynaptic vesicle release and promotes synapse initiation and stabilization together with N-cadherin (Ichtchenko et al. 1995; Song et al. 1999; Scheiffele et al. 2000; Dean et al. 2003; Graf et al. 2004; Futai et al. 2007; Heine et al. 2008; Sudhof 2008; deWit ”
Mapping autism risk loci using genetic linkage and chromosomal rearrangements (2007, background): “Called CNVs were also examined for overlap with genomic features including mapped chromosome rearrangement breakpoints annotated in the Autism Chromo-some Rearrangement Database and polymorphic CNVs in the Database of Genomic Variants.”
Activity-dependent validation of excitatory versus inhibitory synapses by neuroligin-1 versus neuroligin-2. (2007, positive): “In support of a central role of neurexins in the synapse-inducing activity of NLs, expression of neurexins in nonneuronal cells elicits formation of postsynaptic specializations by cocultured neurons onto these cells (Graf et al., 2004; Nam and Chen, 2005).”
Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “Although evidence about the functional roles of NLGNs and NRXNs initially came from coculturing experiments showing that expression of these proteins in nonneuronal cells can induce presynaptic and postsynaptic specialization, respectively (Scheiffele et al. 2000; Graf et al. 2004; Nam and Chen 2005”