VPS35 Antibody

1. these results suggest that VPS35 D620N mutation-induced excessive mitochondrial fission leads to the defects in the assembled complex I and supercomplex and causes bioenergetics deficits. PMID: 28765075
2. These experimental data establish the retromer complex as a key spatiotemporal regulator of IFNAR endosomal sorting and a new factor in type-I IFN-induced JAK/STAT signalling and gene transcription. PMID: 27917878
3. Present data support a role for perturbed VPS35 and retromer function in the pathogenesis of Parkinson's disease. PMID: 28222538
4. These findings provide new mechanistic insights into the role of VPS35 in the regulation of AIMP2 levels and cell death. PMID: 28383562
5. The retromer complex is a highly conserved membrane trafficking assembly composed of three proteins - Vps26, Vps29 and Vps35, which are impaired in neurodegenerative diseases. (Review) PMID: 26965691
6. It could interact with DRD1 and regulate DRD1 cell surface recycling, as well as DRD1- mediated dopamine signaling. PMID: 27460146
7. The absence of mutations in VPS35 genes reveals that they are uncommon causes of Parkinson disease in Brazil PMID: 27777137
8. VPS35 has been associated with autosomal dominant forms of Parkinson's disease with a high but incomplete penetrance . PMID: 26947123
9. results lend further support to the notion that VPS35-DLP1 interaction is key to the retromer-dependent recycling of mitochondrial DLP1 complex during mitochondrial fission and provide a novel therapeutic target to control excessive fission and associated mitochondrial deficits. PMID: 28040727
10. Silencing VPS35 increased N-Ras's association with cytoplasmic vesicles, diminished GTP loading of Ras, and inhibited mitogen-activated protein kinase signaling and growth of N-Ras-dependent melanoma cells. PMID: 27502489
11. deletion of VPS35 in yeast (vps35Delta) leads to a dose-dependent growth defect towards copper. This increased sensitivity could be rescued by transformation with yeast wild-type VPS35 but not by the expression of a construct harboring the yeast equivalent (i.e. D686N) of the most commonly identified VPS35-associated Parkinson disease mutation, p.D620N PMID: 27262440
12. the Vps35 R524W-containing retromer has a decreased endosomal association, which can be partially rescued by R55, a small molecule previously shown to stabilize the retromer complex, supporting the potential for future targeting of the retromer complex in the treatment of Parkinson disease. PMID: 27385586
13. X-ray crystallographic analysis of a 4-component complex comprising the VPS26 & VPS35 subunits of retromer, sorting nexin SNX3, & recycling signal from the divalent cation transporter DMT1-II; analysis identifies a binding site for canonical recycling signals at the interface between VPS26 & SNX3; shows cooperative interactions among the VPS subunits, SNX3 & cargo that couple signal-recognition to membrane recruitment. PMID: 27889239
14. findings provide evidence that the VPS35 D620N mutation likely confers pathogenicity through a partial loss of function mechanism and that this may be linked to other known pathogenic mechanisms such as mitochondrial dysfunction PMID: 26251041
15. VPS35 mutations cause mitochondrial fragmentation and cell death in cultured neurons in vitro, in mouse substantia nigra neurons in vivo and in human fibroblasts from an individual with PD who has the VPS35(D620N) mutation. PMID: 26618722
16. neither the R120W nor the N370S variant of the GBA gene nor D620N mutation of the VPS35 gene were detected among the Parkinson disease cases or the controls. PMID: 26547032
17. Mutagenesis studies coupled with coimmunoprecipitations revealed that retromer-mediated trafficking requires the Env cytoplasmic tail that we show binds directly to retromer components Vps35 and Vps26. PMID: 25393110
18. VPS35 D620N and EIF4G1 R1205H mutations are not a common cause of Parkinson disease in the Greek population. PMID: 26300542
19. provides molecular insights into the essential role of Vps26 and Vps35 in Rab7-mediated recruitment of the core retromer complex PMID: 25367362
20. This study demonstrated that Genetic variability of VPS35 in parkinsonism. PMID: 25475142
21. VPS35 p.D620N is loss-of-function mutation with respect to VPS35 regulating synaptic transmission and AMPA-type glutamate receptors recycling in mouse cortical neurons and dopamine neuron-like cells produced from stem cells of human p.D620N carriers. PMID: 25416282
22. D620N mutation in VPS35 restricts WASH complex recruitment to endosomes, inhibiting autophagy. The autophagy defects can be explained, at least in part, by abnormal trafficking of the autophagy protein ATG9A. PMID: 24819384
23. the major defect of the D620N mutation in the retromer component VPS35 lies in the association to the actin-nucleating Wiskott-Aldrich syndrome and SCAR homolog (WASH) complex. PMID: 24980502
24. Data indicate that vesicular transport proteins VPS35 and VPS29 influence the levels of the other subunit of retromer. PMID: 25937119
25. dominant VPS35 mutations lead to neurodegeneration in Parkinson's disease. PMID: 24740878
26. Its mutation is not a common cause of familial Parkinson's disease. PMID: 24854799
27. Dominant expression of Vps35 D620N mutation results in endosomal trafficking alterations that may underpin its role in PD. PMID: 24152121
28. In 2011 two groups reported the identification of the same missense mutation (p.Asp620Asn) in the vacuolar protein sorting 35 (VPS35) gene, as a novel cause of autosomal dominant parkinson disease. PMID: 24262182
29. Its mutation causes Parkinson's disease in Indian population. PMID: 23726718
30. Pathogenic VPS35 mutations provide important insights into novel molecular targets for parkinson disease. PMID: 23536430
31. Mutations in VPS35 were found to not play a role in Parkinson disease patients from Southwest China. PMID: 23261770
32. Pathogenic mutation in VPS35 impairs its protection against MPP(+) cytotoxicity in dopaminergic neurons in Parkinson's disease. PMID: 23411763
33. result suggests that mutation in the VPS35 coding region probably does not represent a major cause of late-onset Parkinson Disease in the Chinese Han population. PMID: 22891780
34. VPS35 variants are not associated with Parkinson's disease in the mainland Chinese population. PMID: 22673036
35. There is no evidence for an overall contribution of genetic variability in VPS35 (or EIF4G1) to Parkinson disease development in this large family. PMID: 23408866
36. Our study apart from identifying the p.Asp620Asn variant in familial cases also identified it in idiopathic Parkinson disease cases, and thus provides genetic evidence for a role of p.Asp620Asn in Parkinson disease in different populations worldwide. PMID: 23125461
37. VPS35 mutations are a rare cause of PD in different populations. PMID: 22801713
38. This study reported that VPS35 mutation in Japanese patients with typical Parkinson's disease. PMID: 22991136
39. Hence, our data do not support a major role for VPS35 variations in the genetic etiology of Lewy body disorders in the Flanders-Belgian population. PMID: 22336192
40. Failed to find any case of VPS35 pAsp620Asn mutation in a cohort of Italian patients with familial Parkinson disease. PMID: 22278960
41. Data show that a component of the WASH regulatory complex (SHRC), FAM21, directly interacts with the retromer CSC protein VPS35. PMID: 22513087
42. This study suggested that VPS35 Asp620Asn may be not associated with PD in Chinese population. PMID: 22410496
43. We have extended the number of autosomal dominant PD families with VPS35 mutations to 13 families, worldwide; D620N is the most frequent. PMID: 22517097
44. The results of this study concluded that VPS35 c.1858G>A mutation is an uncommon cause of familial Parkinson's disease. PMID: 22154191
45. Knockdown of retromer protein VPS35 activity produces no change in the quantity or cellular distribution of total cellular amyloid precursor protein (APP) and has no affect on internalization of cell-surface APP. PMID: 21515373
46. Frameshift mutations of VPS genes and losses of expression of Vps13A and Vps35 proteins are common in gastric cancers and colorectal cancers with high microsatellite instability. PMID: 21733561
47. The amino-terminal conserved, glutamate-rich sequence of herpesvirus saimiri Tip specifically interacts with the human retromer subunit Vps35 and inhibits retromer activity. PMID: 21849449
48. Disruption of VPS35 and retromer-mediated trans-membrane protein sorting, rescue, and recycling in the neurodegenerative process led to Parkinson disease. PMID: 21763482
49. Only a single heterozygous variant in the VPS35 gene caused late-onset Parkinson disease in this family. PMID: 21763483
50. Vps35 mediates vesicle transport between the mitochondria and peroxisomes. PMID: 20619655

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HGNC: 13487

OMIM: 601501

KEGG: hsa:55737

STRING: 9606.ENSP00000299138

UniGene: Hs.454528