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Adaptor Protein Complex 3Adaptor Protein Complex 1Adaptor Protein Complex 2Adaptor Protein Complex 4Adaptor Protein Complex SubunitsAdaptor Protein Complex delta SubunitsAdaptor Protein Complex mu SubunitsAdaptor Proteins, Vesicular TransportAdaptor Protein Complex gamma SubunitsAdaptor Protein Complex beta SubunitsAdaptor Protein Complex alpha SubunitsAdaptor Proteins, Signal TransducingClathrinHuman CharacteristicsMonomeric Clathrin Assembly ProteinsGRB2 Adaptor ProteinShc Signaling Adaptor ProteinsAdaptor Protein Complex sigma SubunitsEndocytosisCoated VesiclesProtein Bindingtrans-Golgi NetworkClathrin-Coated VesiclesEndosomesMembrane ProteinsProtein TransportCarrier ProteinsMolecular Sequence DataAmino Acid SequenceTransport VesiclesPhosphoproteinsCoated Pits, Cell-MembraneGRB10 Adaptor ProteinGene Products, nefRecombinant Fusion Proteinssrc Homology DomainsMultiprotein ComplexesCell LineBrefeldin ASignal Transductionnef Gene Products, Human Immunodeficiency VirusMutationHeLa CellsProteinsCell MembraneLysosomesProto-Oncogene Proteins c-crkProtein Structure, TertiaryTransfectionPhosphorylationProtein Interaction MappingCRADD Signaling Adaptor ProteinMyeloid Differentiation Factor 88Two-Hybrid System TechniquesBinding SitesImmunoprecipitationTyrosineAmino Acid MotifsIntracellular Signaling Peptides and ProteinsNuclear ProteinsCOS CellsModels, BiologicalGRB7 Adaptor ProteinPrecipitin TestsDNA-Binding ProteinsSequence Homology, Amino AcidMice, KnockoutNerve Tissue ProteinsCytoskeletal ProteinsProtein Interaction Domains and MotifsSaccharomyces cerevisiae ProteinsJurkat CellsCrk-Associated Substrate ProteinHEK293 CellsOncogene ProteinsVesicular Transport ProteinsProto-Oncogene Proteins c-cblModels, MolecularCells, CulturedProtein-Tyrosine KinasesSaccharomyces cerevisiaeBase SequenceReceptors, Interleukin-1PhosphotyrosineMacromolecular SubstancesTranscription FactorsImmunoblottingEnzyme ActivationSon of Sevenless ProteinsRNA, Small InterferingCARD Signaling Adaptor ProteinsRecombinant ProteinsProto-Oncogene ProteinsDrosophila Proteinssrc-Family KinasesProtein SubunitsCytoplasmPhospholipase C gammaBlotting, WesternMembrane Glycoproteins

The adaptor protein AP-4 as a component of the clathrin coat machinery: a morphological study. (1/10)

The four members of the AP (adaptor protein) family are heterotetrameric cytosolic complexes that are involved in the intracellular trafficking of cargo proteins between different organelles. They interact with motifs present in the cytoplasmic tails of their specific cargo proteins at different intracellular locations. While AP-1, AP-2 and AP-3 have been investigated extensively, very few studies have focused on the fourth member, AP-4. In the present study, we report on the intracellular localization of AP-4 in the MDCK (Madin-Darby canine kidney) and MelJuSo cell lines after immunogold labelling of ultrathin cryosections. We find that AP-4 is localized mainly in the Golgi complex, as well as on endosomes and transport vesicles. Interestingly, we show for the first time that AP-4 is localized with the clathrin coat machinery in the Golgi complex and in the endocytic pathway. Furthermore, we find that AP-4 is localized with the CI-MPR (cation-independent mannose 6-phosphate receptor), but not with the transferrin receptor, LAMP-2 (lysosomal-associated membrane protein-2) or invariant chain. The difference in morphology between CI-MPR/AP-4-positive vesicles and CI-MPR/AP-1-positive vesicles raises the possibility that AP-4 acts at a location different from that of AP-1 in the intracellular trafficking pathway of CI-MPR.  (+info)

Accumulation of AMPA receptors in autophagosomes in neuronal axons lacking adaptor protein AP-4. (2/10)

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AP-4: autophagy-four mislocalized proteins in axons. (3/10)

Neurons are highly polarized cells composed of two distinct domains, the axon and the somatodendritic domain. Although AMPA-type glutamate receptors, which mediate fast excitatory neurotransmission in the vertebrate CNS, are preferentially expressed in the somatodendritic domain, the molecular mechanisms underlying such polarized distribution have remained elusive. We recently demonstrated that adaptor protein complex-4 (AP-4) binds to transmembrane AMPA receptor regulatory proteins (TARPs), thereby mediating the selective trafficking of AMPA receptors to the somatodendritic domain; genetic disruption of AP-4 (AP-4beta(-/-)), results in the mislocalization of TARPs and AMPA receptors in the axons. Similarly, low-density lipoprotein receptors and delta2 glutamate receptors are mislocalized in axons, while other cargos, such as NMDA receptors and metabotropic glutamate receptors, are properly excluded from AP-4beta(-/-) axons. These findings indicate that there exist AP-4-dependent and -independent sorting mechanisms. Unexpectedly, mislocalized AMPA receptors do not reach the cell surface and accumulate in autophagosomes in the bulging portions of AP-4beta(-/-) axons. Several lines of evidence indicate that mislocalized AMPA receptors activate the autophagic pathway. Since increased autophagy and axonal swelling are suggested to occur in various neuronal disorders, further studies using AP-4beta(-/-) mice are warranted to understand the mechanisms regulating autophagy in axons.  (+info)

Mutation in the AP4M1 gene provides a model for neuroaxonal injury in cerebral palsy. (4/10)

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Sorting of the Alzheimer's disease amyloid precursor protein mediated by the AP-4 complex. (5/10)

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Adaptor protein complex-4 (AP-4) deficiency causes a novel autosomal recessive cerebral palsy syndrome with microcephaly and intellectual disability. (6/10)

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Adaptor protein complex 4 deficiency causes severe autosomal-recessive intellectual disability, progressive spastic paraplegia, shy character, and short stature. (7/10)

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Breast cancer cells proliferation is regulated by tyrosine phosphatase SHP1 through c-jun N-terminal kinase and cooperative induction of RFX-1 and AP-4 transcription factors. (8/10)

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