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Validated All-in-One™ qPCR Primer for UCHL1(NM_004181.4) Search again
Product ID:
HQP111081
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HEL-117, HEL-S-53, NDGOA, PARK5, PGP 9.5, PGP9.5, PGP95, SPG79, SPG79A, UCHL-1, Uch-L1
Gene Description:
ubiquitin C-terminal hydrolase L1
Target Gene Accession:
NM_004181.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
UCHL1 is a member of a gene family whose products hydrolyze small C-terminal adducts of ubiquitin to generate the ubiquitin monomer. Expression of UCHL1 is highly specific to neurons and to cells of the diffuse neuroendocrine system and their tumors. It is present in all neurons (Doran et al., 1983 [PubMed 6343558]).[supplied by OMIM].
Gene References into function
- PGP9.5 colocalizes with JAB1 and p27(Kip1)in the nucleus
- 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.
- 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
- Alterations in alpha-helical content and hydrolase activity of parkinsonism-associated ubiquitin carboxyl-terminal hydrolase L1 variants.
- 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).
- ubiquitin carboxyl-terminal hydrolase L1 is oxidatively modified and downregulated in idiopathic Parkinson's and Alzheimer's diseases
- A statistically significant inverse genetic association of the UCHL1 S18Y variant has been found confirming UCHL1 as a susceptibility gene for Parkinson's disease.
- 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.
- 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
- Important issues regarding UCHL-1 and its role in Parkinson disease remain inconclusive, especially regarding the pathogenicity of the mendelian I93M mutation
- UCH-L1 accumulation is likely to play a pathological role in inclusion formation in Parkinson's disease
- The relative amount of nerve fibers in rat prostate, detected by PGP 9.5, does not change during postnatal development
- 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.
- 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.
- multiple functional balance is closely linked to the intermolecular interactions between the UCH-L1 monomer and the final dimeric configuration
- 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
- These results suggest that UCH-L1 spatially mediates and enhances neurogenesis in the embryonic brain by regulating progenitor cell morphology.
- 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.
- Down-regulation of UCH-L1 is associated with Uterine Cervical Neoplasms
- the three-dimensional structure of human UCH-L1 at 2.4-A resolution by x-ray crystallography was determined.
- 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.
- Silencing of the UCHL1 gene is associated with colorectal and ovarian cancers
- Exposure to chronic hyperglycemia following 90% partial pancreatectomy leads to reduced Uch-L1 expression
- 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.
- 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.
- 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.
- UCHL1 expression seems to be associated with the metastatic phenotype of renal cell carcinoma
- 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.
- 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.
- UCHL1 may partially attenuate vascular remodeling through inhibition of NF-kappaB activity.
- 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]
- 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.
- 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.
- 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.
- 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.
- Mice that lack of UCH-L1 in neurons decrease in their ubiquitin-proteasome system function and enhanced sensitivity to oxidative stress.
- UCH-L1 expression seems to be associated with the metastatic potential of HRCC SN12C cell clones.
- methylation of the UCHL1 gene is associated with a poor prognosis in patients with renal cell carcinoma
- PGP9.5 is a tumor suppressor gene that is inactivated by promoter methylation or gene deletion in several types of human cancers.
- 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.
- UCH-L1 directly interacted with the cytosolic region of LAMP-2A.
- do not support a role for mutation in UCH-L1 in sporadic Parkinson disease
- 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.
- 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
- 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
- Over-expression of ubiquitin carboxy terminal hydrolase-L1 induces apoptosis in breast cancer cells.
- activity was intense at the top of and labially to the [fetal] alveolar bone
- 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.