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1. |
The interaction between Ubiquitin carboxyl-Terminal Hydrolase L-1 and the Receptors, Adrenergic, alpha-2A may play an important role in trafficking of the receptor and its response to agonist stimulation. |
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This study found that modest Modest associations (uncorrected P < 0.05) were observed for common variants around UCHL1 in Australia patient with Parkinson's disease. |
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UCH-L1 activity is rapidly upregulated by NMDA receptor activation, which leads to an increase in the levels of free monomeric ubiquitin. |
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Our results support the hypothesis that PARK5 is caused by a gain-of-toxic-function of UCH-L1(Ile93Met) mutant, and suggest that regulation of UCH-L1 in nigral DA cells could be a future target for treatment of PD. |
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Proteasome function is not affected by UCH-L1(membrane associated form), suggesting that it may negatively regulate the lysosomal degradation of alpha-synuclein. |
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Positive staining for PGP9.5 has utility as a marker for parathyroid malignancy, with a slightly superior sensitivity and similar high specificity to that of parafibromin. |
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the association of two polymorphisms of ubiquitin carboxy-terminal hydrolase-L1 gene(UCH-L1), the 54C/A in exon 3 and the 277C/G in exon 4, with sporadic Parkinson's disease(PD) in Hans from North China |
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The C allele in exon 3 of UCH-L1 gene might be one of the risk factors for Parkinson's disease in Shanghai Han Nationality, but the polymorphisms of C/T in exon 4 showed no association with the onset of PD. |
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This study shows for the first time that UCH-L1 plays a key role in the regulation of cell invasion in lung cancer, melanoma and in cancer metastasis, and that UCH-L1 modulates cell morphology by regulating the upstream Akt and influencing cell migration. |
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activity was intense at the top of and labially to the [fetal] alveolar bone |
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Over-expression of ubiquitin carboxy terminal hydrolase-L1 induces apoptosis in breast cancer cells. |
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Findings indicated that PGP9.5 was less frequently methylated in metastatic colorectal cancer, suggesting that PGP9.5 hypomethylation might play an important role in re-expression of the PGP9.5 gene in colorectal cancer. |
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13. |
do not support a role for mutation in UCH-L1 in sporadic Parkinson disease |
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14. |
UCH-L1 directly interacted with the cytosolic region of LAMP-2A. |
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UCH-L1 expression seems to be associated with the metastatic potential of HRCC SN12C cell clones. |
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Epigenetic inactivation of UCHL1 is common in primary hepatocellular carcinomas(HCCs) and other digestive tumors and appears to be functional tumor suppressor involved in tumorigenesis of HCCs and other digestive cancers. |
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methylation of the UCHL1 gene is associated with a poor prognosis in patients with renal cell carcinoma |
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18. |
Mice that lack of UCH-L1 in neurons decrease in their ubiquitin-proteasome system function and enhanced sensitivity to oxidative stress. |
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PGP9.5 is a tumor suppressor gene that is inactivated by promoter methylation or gene deletion in several types of human cancers. |
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20. |
The carbonyl modification of UCH-L1 and subsequent abnormal interactions of carbonyl-modified UCH-L1 with multiple proteins, including tubulin, constitute one of the causes of sporadic Parkinson's disease. |
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21. |
Abberant promoter methylation is the primary mechanism of transcriptional silencing of the UCHL1 gene and methylation of UCHL1 gene promoter increases in the progression of colorectal neoplasms. |
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22. |
2D fingerprinting & mass spectrometry reveal specific targets of protein oxidation in Alzheimer's disease brain, including ubiquitin carboxy-terminal hydrolase L-1, suggesting involvement of oxidatively modified proteins in neurodegeneration. |
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23. |
Observational study and meta-analysis of gene-disease association. (HuGE Navigator) |
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24. |
Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator) |
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25. |
Observational study of gene-disease association and gene-environment interaction. (HuGE Navigator) |
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26. |
Observational study of gene-disease association. (HuGE Navigator) |
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27. |
UCHL1 S18Y is not a major susceptibility factor for PD in white populations although we cannot exclude the possibility that the S18Y variant exerts weak effects on risk, particularly in early-onset disease. |
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28. |
The finding that PGP 9.5 and ChA are expressed by PC-3 and DU145 cells suggests that these cells may have been derived from metastatic adenocarcinomas which had undergone neuroendocrine differentiation or expression occurred as a result of cell culture. |
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29. |
Mutations of the UCH-L1 gene and alterations of its proteins' activity have been found to associate with several neurodegenerative disorders: Parkinson's, Huntington's and Alzheimer's diseases [review] |
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30. |
UCH-L1 is not expressed specifically in dopamine neurons. The abundant expression of UCH-L1 in peripheral neurons may be of relevance for the spectrum of symptoms in different forms of Parkinson's. |
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31. |
The tyrosine variant was significantly inversely associated with PD (P=0.049) and with a low age of onset (50 years) (P=0.017) in the case-control material, supporting the hypothesis of a protective function. |
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32. |
UCHL1 may partially attenuate vascular remodeling through inhibition of NF-kappaB activity. |
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33. |
Alterations in alpha-helical content and hydrolase activity of parkinsonism-associated ubiquitin carboxyl-terminal hydrolase L1 variants. |
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34. |
Analyses confirmed a significant inverse association of the UCHL1 S18Y polymorphism with PD overall (OR=0.18, 95% CI=0.05-0.64, p=0.002, recessive model) and in several strata. |
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35. |
UCHL1 expression seems to be associated with the metastatic phenotype of renal cell carcinoma |
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36. |
Down-regulation of UCH-L1 is associated with Uterine Cervical Neoplasms |
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37. |
Silencing of the UCHL1 gene is associated with colorectal and ovarian cancers |
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38. |
ubiquitin carboxyl-terminal hydrolase L1 is oxidatively modified and downregulated in idiopathic Parkinson's and Alzheimer's diseases |
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39. |
PGP9.5 colocalizes with JAB1 and p27(Kip1)in the nucleus |
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40. |
The relative amount of nerve fibers in rat prostate, detected by PGP 9.5, does not change during postnatal development |
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41. |
Excess UCH-L1 influenced the distribution of proliferating cell nuclear antigen and suggests a specific role for UCH-L1 in the processes of mitotic proliferation and differentiation of spermatogonial stem cells during spermatogenesis. |
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42. |
A statistically significant inverse genetic association of the UCHL1 S18Y variant has been found confirming UCHL1 as a susceptibility gene for Parkinson's disease. |
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43. |
multiple functional balance is closely linked to the intermolecular interactions between the UCH-L1 monomer and the final dimeric configuration |
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44. |
UCHL1 is involved in the degradation of unwanted, misfolded, or damaged proteins and is overexpressed in >50% of lung cancers, its overexpression in chronic smokers may represent an early event in the transformation from normal epithelium to malignancy. |
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45. |
Important issues regarding UCHL-1 and its role in Parkinson disease remain inconclusive, especially regarding the pathogenicity of the mendelian I93M mutation |
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These results suggest that UCH-L1 spatially mediates and enhances neurogenesis in the embryonic brain by regulating progenitor cell morphology. |
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47. |
The identification of pathogenic mutations in the ubiquitin carboxy-terminal hydrolase L1 (UCHL1) has elucidated the ubiquitin proteasome system (UPS) and its potential role as a causal pathway in Parkinson's disease (PD). |
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48. |
UCH-L1 accumulation is likely to play a pathological role in inclusion formation in Parkinson's disease |
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49. |
exhibits a second, dimerization-dependent, ubiquityl ligase activity; a polymorphic variant of UCH-L1 that is associated with decreased Parkinson's disease risk has reduced ligase activity but comparable hydrolase activity as the wild-type enzyme |
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50. |
the three-dimensional structure of human UCH-L1 at 2.4-A resolution by x-ray crystallography was determined. |
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51. |
Ubiquitin side chains critical for establishing the Michaelis complex and enabling catalysis were identified, and features of this complex that differ between UCH-L1 and a homologue, UCH-L3 are revealed. |
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52. |
Data show that impairment of UCH-L1 ubiquitin hydrolase activity may be an important contributor to neurodegeneration associated with accumulation of ubiquitinated proteins and inflammation. |
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53. |
study expands the immunophenotype of granular cell tumor (S100, CD68, protein gene product 9.5, and inhibin-alpha) regardless of location and supports a neural origin |
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54. |
Together, these observations show reduced UCHL-1 expression as a contributory factor in the abnormal protein aggregation in DLB, and points UCHL-1 as a putative therapeutic target in the treatment of DLB. |
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55. |
functional relevance of S18Y polymorphism of UCHL1 in 946 Caucasian Huntington's disease patients; allelic variation on locus S18Y is responsible for 1.1% of the variance in the HD age-at-onset, & the rare Y allele is associated with younger-aged cases |
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56. |
allele and YY genotype of S18Y in the UCH-L1 gene may have a protective effect against sporadic AD in female subjects, probably due to altering the function of UCH-L1 and the interactions among different risk factors. |
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57. |
UCH-L1 deficiency and impairment of the ubiquitin-dependent protein degradation pathway can contribute to the increased cell death observed in many lysosomal storage disorders. |
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58. |
Exposure to chronic hyperglycemia following 90% partial pancreatectomy leads to reduced Uch-L1 expression |