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Depleting Huntingtin-associated protein 1 (Hap1) promoted the dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A)-DDB1 and CUL4 associated factor 7 (Dcaf7) interaction and increased the DYRK1A protein level.
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This study also validated the interaction between HAP1 and Sec23A using co-immunoprecipitation experiments with endogenous proteins. This manuscript also reports on the high confidence interacting partners of HAP1 identified by the non-biased approach used in this study, which interestingly, consists of predominantly trafficking-related proteins
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HAP1 co-localizes with synapsin I in cortical neurons as discrete puncta
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findings suggest that Hap1 is important for insulin secretion of pancreatic beta-cells via regulating the intracellular trafficking and plasma membrane localization of Cav1.2, providing new insight into the mechanisms that regulate insulin release from pancreatic beta-cells.
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Early loss of Hap1 significantly reduces postnatal hippocampal neurogenesis, and leads to adult depressive-like behavior.
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Hap1 interacts with Bcr on microtubules to regulate neuronal differentiation.
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HAP1 regulates exocytosis by influencing the morphological docking of vesicles at the plasma membrane, the ability of vesicles to be released rapidly upon stimulation, and the early stages of fusion pore formation.
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these studies identify htt and HAP1 as regulators of autophagosome transport in neurons
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In the absence of HAP1, postnatal hypothalamic neurons exhibited reduced receptor tropomyosin-related kinase B (TRKB) levels.
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Hap1-Tsc1 interaction regulates neuronal mTORC1 signaling and neuronal morphogenesis.
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Mutant mice with Hap1 deficiency in pancreatic beta-cells had impaired glucose tolerance and decreased insulin release in response to intraperitoneally injected glucose.
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Loss of Htt impaired the retrograde trafficking of PCM1 and thereby reduced primary cilia formation.
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sortilin stabilizes the proBDNF.HAP1 complex
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Results indicate that the Hap1-Ahi1 complex in the brainstem works as a sensor for insulin signals in feeding control.
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Hap1 is critical for the transport of multiple proteins to the nerve terminals to maintain the integrity of neuronal processes
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HAP1 may participate in axonal transport and activity-dependent release of pro-BDNF by interacting with the BDNF prodomain.
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results demonstrate that HAP-1 plays an essential role in regulating postnatal feeding
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HAP-1 is highly expressed in hypothalamus. Mice lacking HAP1 die after birth because of depressed feeding. The effect of mutant huntingtin on HAP1 and EGFR signaling may contribute to hypothalamic neurodegeneration and weight loss in Huntington disease
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HAP1 facilitates potentiation of InsP3 receptor-1 mediated Ca2+ release.
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may be involved in protective pathways that contribute to the resistance of interneurons to neurodegeneration in HD.
