Association of synapse‐associated protein 90/ postsynaptic density‐95‐associated protein (SAPAP) with neurofilaments

Abstract

Background: Synapse-associated protein (SAP) 90/Postsynaptic density (PSD)-95-associated protein (SAPAP) (also called Guanylate kinase-associated protein/hDLG-associated protein) interacts with the guanylate kinase domains of PSD-95 and synaptic scaffolding molecule (S-SCAM) via the middle region containing 5 repeats of 14 amino acids. SAPAP also binds the recently identi®ed proteins, nArgBP2 and synamon (also called Shank 1a), via the proline-rich region and the C-terminus, respectively. SAPAP is highly enriched in the Triton X-100-insoluble PSD fraction, and recruits PSD-95 into the Triton X-100-insoluble fraction in transfected cells. We have further characterized here the Triton X-100-insolubility of SAPAP and tried to identify the Triton X-100-insoluble structures which SAPAP interacts with.

Neuronal damage in hydrocephalus and its restoration by shunt insertion in experimental hydrocephalus: a study involving the neurofilament-immunostaining method

“…15,34 As the major component of the neuronal cytoskeleton, neurofilament is known to participate in the maintenance of cytoplasmic morphology. Because it is also thought to take part in neurosecretion with mitochondria, 47 synaptic conduction, 20 and axonal transport, 26,32 the reduction of neurofilament immunoreactivity in cortical neurons demonstrated in this study is assumed to indicate that cortical neurons are affected by structural as well as functional changes to the cytoskeleton as a result of the progression of hydrocephalus.…”

Specialized roles of neurofilament proteins in synapses: Relevance to neuropsychiatric disorders

“…The synapse-specific PSD95-associated protein SAPAP interacts via its N-terminal region with all 4 NF subunits, co-immunoprecipitates with NF proteins from rat brain, and co-localizes with NFs in transfected COS cells [80]. Spinophilin, a synaptic protein highly enriched in dendritic spines [3], regulates the formation and function of the spines [59].…”

Maintenance Treatment with Fluoxetine is Necessary to Sustain Normal Levels of Synaptic Markers in an Experimental Model of Depression: Correlation with Behavioral Response

“…Since NFL diminution is a common trait between persistent despaired behavior and its recurrence after FLX withdrawal, it may be speculated based on our findings that this cytoskeletal alteration might contribute to the labile effect of FLX on synapses. In fact, it has been proposed a role for NFL in scaffolding synaptic components as this NF subunit is linked to postsynaptic density proteins (Hirao et al, 2000;Terry-Lorenzo et al, 2000).…”