Association of the Kinesin Motor KIF1A with the Multimodular Protein Liprin-α

Shin, Hye‐Won; Wyszynski, Michael; Huh, Kyung Hye; Valtschanoff, Juli G.; Lee, Jae Ran; Ko, Jaewon; Streuli, Michel; Weinberg, Richard J.; Sheng, Morgan; Kim, Eunjoon

doi:10.1074/jbc.m211874200

Cited by 194 publications

(175 citation statements)

References 54 publications

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“…Some studies suggest that GRIP1 anchors AMPARs at synapses or delivers AMPARs to dendrites through binding to kinesin heavy chain or liprin-α (7,25,32,33). Other studies rather suggest that GRIP1 retains AMPARs within intracellular compartments (22,34).…”

Section: Discussionmentioning

confidence: 99%

GRIP1 is required for homeostatic regulation of AMPAR trafficking

Tan

Queenan

Huganir

2015

Proc. Natl. Acad. Sci. U.S.A.

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Homeostatic plasticity is a negative feedback mechanism that stabilizes neurons during periods of perturbed activity. The best-studied form of homeostatic plasticity in the central nervous system is the scaling of excitatory synapses. Postsynaptic AMPA-type glutamate receptors (AMPARs) can be inserted into synapses to compensate for neuronal inactivity or removed to compensate for hyperactivity. However, the molecular mechanisms underlying the homeostatic regulation of AMPARs remain elusive. Here, we show that the expression of GRIP1, a multi-PDZ (postsynaptic density 95/discs large/zona occludens) domain AMPAR-binding protein, is bidirectionally altered by neuronal activity. Furthermore, we observe a subcellular redistribution of GRIP1 and a change in the binding of GRIP1 to GluA2 during synaptic scaling. Using a combination of biochemical, genetic, and electrophysiological methods, we find that loss of GRIP1 blocks the accumulation of surface AMPARs and the scaling up of synaptic strength that occur in response to chronic activity blockade. Collectively, our data point to an essential role of GRIP1-mediated AMPAR trafficking during inactivity-induced synaptic scaling.synaptic scaling | postsynaptic density | glutamate receptor | PDZ domain

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Section: Discussionmentioning

confidence: 99%

GRIP1 is required for homeostatic regulation of AMPAR trafficking

Tan

Queenan

Huganir

2015

Proc. Natl. Acad. Sci. U.S.A.

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“…Although it has been proven that SYD-2 regulates the Liprin-α/SYD-2 is proposed to act as an intracellular anchor for RPTP signaling at synaptic junctions [9,31] , and it has been shown that Liprin-α/SYD-2 binds Rim, CAST/ERC and kinesin [10,[32][33] . In addition, for the possible functional link between SYD-2, LAR and Nidogen, reports indicated that SYD-2 might recruit other density components to facilitate its assemble, and the presynaptic activity of SYD-2 might be modulated by LAR-Nidofen interaction to secure the synaptic assembly [21,22] .…”

Section: Discussionmentioning

confidence: 99%

HLB-1 functions as a new regulator for the organization and function of neuromuscular junctions in nematode Caenorhabditis elegans

Wang

2009

Neurosci. Bull.

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Rescue and mosaic analysis experiments suggested that HLB-1 regulated synaptic functions in a cell nonautonomously way.Moreover, HLB-1 expression was not required for the presynaptic active zone morphology. Genetic evidence further demonstrated that hlb-1 acted in a parallel pathway with syd-2 to regulate the synaptic functions. Conclusion HLB-1 appeared as a new regulator for the organization and function of neuromuscular junctions in C. elegans.

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“…80 KIF1A kinesin motor is associated with liprina and liprin-a-interacting Rab3A-interacting molecules, assisting in kinesin-mediated neuronal transport. 81 The functional significance of liprin-a at the mammalian synapses is largely unknown. Liprin-a binds to receptor protein tyrosine phosphatase (Dlar), which suggests that liprin-a3 and Dlar are involved in the formation of presynaptic active zones.…”

Section: Discussionmentioning

confidence: 99%

Cytosolic proteomic alterations in the nucleus accumbens of cocaine overdose victims

2006

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Chronic cocaine use in humans and animal models is known to lead to pronounced alterations in neuronal function in the nucleus accumbens (NAc), a brain region associated with drug reinforcement. Two-dimensional gel electrophoresis was used to compare protein alterations in the NAc between cocaine overdose (COD) victims (n = 10) and controls (n = 10). Following image normalization, spots with significantly differential image intensities (P < 0.05) were identified, excised, trypsin digested and analyzed by matrix-assisted laser desorption ionization-time of flight-time of flight. A total of 1407 spots were found to be present in a minimum of five subjects per group and the intensity of 18 spots was found to be differentially abundant between the groups, leading to positive identification of 15 proteins by peptide mass fingerprinting (PMF). Of an additional 37 protein spots that were constitutively expressed, 32 proteins were positively identified by PMF. Increased proteins in COD included b-tubulin, liprin-a3 and neuronal enolase, whereas decreased proteins included parvalbumin, ATP synthase b-chain and peroxiredoxin 2. The present data provide a preliminary protein profile of COD, suggesting the involvement of novel proteins and pathways in the expression of this complex disease. Additional studies are warranted to further characterize alterations in the differentially regulated proteins. Understanding the coordinated involvement of multiple proteins in cocaine abuse provides insight into the molecular basis of the disease and offers new targets for pharmacotherapeutic intervention for drug abuse-related disorders.

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Association of the Kinesin Motor KIF1A with the Multimodular Protein Liprin-α

Cited by 194 publications

References 54 publications

GRIP1 is required for homeostatic regulation of AMPAR trafficking

GRIP1 is required for homeostatic regulation of AMPAR trafficking

HLB-1 functions as a new regulator for the organization and function of neuromuscular junctions in nematode Caenorhabditis elegans

Cytosolic proteomic alterations in the nucleus accumbens of cocaine overdose victims

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