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Human Huntingtin Associated Protein 1 (HAP1) interaction partners

1. HAP1 is expressed in endocrine cells of the human gut.

2. data fully support that HAP1 is a GKAP, anchoring specifically to the cGMP-dependent protein kinase isoform Ibeta, and provide further evidence that also PKG spatiotemporal signaling is largely controlled by anchoring proteins

3. The -141 T > G polymorphism, but not the 1349 T > G polymorphism, may have protective effects for lung cancer.

4. HAP1 gene expression is related to the radiosensitivity of breast cancer cells and may play an important role in the regulation of cellular radiosensitivity

5. Overexpression of HAP1 reduced in vitro cell growth in breast cancer cell lines.

6. The results of this study found no association was found between the HAP1 T441M polymorphism and the age at onset of Huntington's disease .

7. The results of this study suggested that HAP1 co-localizes and associates with APP in physiological conditions of mouse and human brain.

8. WT HTT regulates ciliogenesis by interacting through huntingtin-associated protein 1 (HAP1) with pericentriolar material 1 protein (PCM1).

9. HAP1/stigmoid body interacts with the normal ataxin-3 through Josephin domain

10. sortilin stabilizes the proBDNF.HAP1 complex

11. ADORA2A, but not HAP1 or OGG1, may have a role in age at onset in Huntington's disease

12. REVIEW: function of HAP1

13. HAP1 may participate in axonal transport and activity-dependent release of pro-BDNF by interacting with the BDNF prodomain.

14. The combination of siRNA, the SB transposon, and an accurate transgenic mouse model may permit evaluation of this approach in preventing the pathogenesis associated with expression of mutant Htt.

15. Study provides genetic and functional evidence that the M441-HAP1 polymorphism modifies the age-at-onset of Huntington's disease .

16. REST/NRSF, dynactin p150(Glued), huntingtin, HAP1, and RILP form a complex involved in the translocation of REST/NRSF into the nucleus and HAP1 controls REST/NRSF cellular localization in neurons

Mouse (Murine) Huntingtin Associated Protein 1 (HAP1) interaction partners

1. 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.

2. 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

3. HAP1 co-localizes with synapsin I in cortical neurons as discrete puncta

4. 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.

5. Early loss of Hap1 significantly reduces postnatal hippocampal neurogenesis, and leads to adult depressive-like behavior.

6. Hap1 interacts with Bcr on microtubules to regulate neuronal differentiation.

7. 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.

8. these studies identify htt and HAP1 as regulators of autophagosome transport in neurons

9. In the absence of HAP1, postnatal hypothalamic neurons exhibited reduced receptor tropomyosin-related kinase B (TRKB) levels.

10. Hap1-Tsc1 interaction regulates neuronal mTORC1 signaling and neuronal morphogenesis.

11. Mutant mice with Hap1 deficiency in pancreatic beta-cells had impaired glucose tolerance and decreased insulin release in response to intraperitoneally injected glucose.

12. Loss of Htt impaired the retrograde trafficking of PCM1 and thereby reduced primary cilia formation.

13. sortilin stabilizes the proBDNF.HAP1 complex

14. Results indicate that the Hap1-Ahi1 complex in the brainstem works as a sensor for insulin signals in feeding control.

15. Hap1 is critical for the transport of multiple proteins to the nerve terminals to maintain the integrity of neuronal processes

16. HAP1 may participate in axonal transport and activity-dependent release of pro-BDNF by interacting with the BDNF prodomain.

17. results demonstrate that HAP-1 plays an essential role in regulating postnatal feeding

18. 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

19. HAP1 facilitates potentiation of InsP3 receptor-1 mediated Ca2+ release.

20. may be involved in protective pathways that contribute to the resistance of interneurons to neurodegeneration in HD.