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Validated All-in-One™ qPCR Primer for SQSTM1(NM_003900.4) Search again
Product ID:
HQP115182
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
A170, DMRV, FTDALS3, NADGP, OSIL, PDB3, ZIP3, p60, p62, p62B
Gene Description:
sequestosome 1
Target Gene Accession:
NM_003900.4(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
This gene encodes a multifunctional protein that binds ubiquitin and regulates activation of the nuclear factor kappa-B (NF-kB) signaling pathway. The protein functions as a scaffolding/adaptor protein in concert with TNF receptor-associated factor 6 to mediate activation of NF-kB in response to upstream signals. Alternatively spliced transcript variants encoding either the same or different isoforms have been identified for this gene.
Gene References into function
- the constant presence of p62 in Mallory bodies suggests that binding of p62 to abnormal keratins may allow hepatocytes to dispose potentially harmful proteins in a biologically inert manner.
- Recurrent mutation of the gene encoding sequestosome 1 (SQSTM1/p62) in Paget disease of bone.
- mutations affecting the ubiquitin-binding domain of SQSTM1 are a common cause of familial and sporadic Paget's disease of bone
- p62 protein is overexpressed in breast cancer. Its mRNA & protein increase in response to PSI. PDEF upregulates p62 promoter activity at 2 sites. PSI downregulates PDEF-induced p62 promoter activation through one of these sites.
- In frontotemporal dementia, the degenerative process involves p62, and the process takes place not only in neurons but also in glial cells.
- structure of the ubiquitin-associated domain of p62 (SQSTM1) and implications for mutations that cause Paget's disease of bone
- functional ubiquitin-binding motifs in Atx-3 and p62 proteins are required for the localization of both proteins into aggregates
- SQSTM1 mutations may play a role in the majority of familial Paget's disease of bone
- During formation of Lewy bodies associated with Parkinson disease the most robust immunoreactivity for p62 is seen in small intranuclear inclusions distinctly outlined, with spherical, uniformly staining bodies.
- minor involvement of the SQSTM1 gene in the pathogenesis of sporadic Italian Paget's cases
- causal role of SQSTM1 gene mutations in the pathogenesis of Paget's disease
- The SQSTM1 P392L mutation is a recurrent mutation causing Paget's Disease of bone in different populations. We were not able to show an association between SQSTM1 polymorphisms and PDB in our population.
- p62 may act as a critical ubiquitin chain-targeting factor that shuttles substrates for proteasomal degradation
- mutations in the UBA domain of SQSTM1 (p62) have effects on binding sites and secondary structure and have a role in Paget's disease of bone [review]
- a founder effect may be responsible for teh SQSTM1 P392L mutation in Paget's disease of bone patients of British descent, irrespective of family history
- Sequestosome 1/p62 is co-localized with ubiquitinated proteins and UCH-L1 in cytoplasmic aggregates induced by PGJ2. Preventing sequestosome 1/p62 up-regulation by RNAi abolishes aggregation but not increase of ubiquitinated proteins or PGJ2 toxicity.
- p62 interacts with lysine63-polyubiquitinated tau through its ubiquitin-associated (UBA) domain and serves a novel role in regulating tau proteasomal degradation.
- Taken together, the data suggest p62 is a regulator of neuronal cell survival and differentiation.
- p62 regulates nerve growth factor-induced NF-kappaB activation by influencing TRAF6 polyubiquitination
- Results suggest that p62 fibrils may influence cell viability and indicates an important role for p62 in aggresome formation.
- p62 may, via LC3, be involved in linking polyubiquitinated protein aggregates to the autophagy machinery and has a protective effect on huntingtin-induced cell death
- Cytosolic overexpression of p62 is a novel immunohistochemical characteristic in prostatic adenocarcinoma and high-grade PIN, suggesting that p62 might be a novel marker for prostatic malignancy.
- There is sound evidence incriminating Sequestosome 1 (SQSTM1) on the long arm of chromosome 5 (5q35-qter), of which nine mutations have been described in Paget's disease of bone.
- The disease mechanism in PDB with SQSTM1 mutations involves a loss of ubiquitin binding function of SQSTM1, implicating a sequence extrinsic to the compact globular region of the UBA domain as a critical determinant of ubiquitin recognition by SQSTM1.
- Our results suggested that p62 plays important roles in forming the inclusions and may be associated with the protection of the neurons from degenerative processes involving ubiquitin.
- Understanding how loss of ubiquitin-binding function of p62 impacts on signal transduction events in osteoclasts will further understanding Paget's disease of bone at the molecular level.
- G1205C splice site mutation probably disrupts the ubiquitin-binding properties of the protein.
- Expression on osteoclasts is not sufficient to induce the full paget disease but p62 mutations cause a predisposition to the development of Paget disease by increasing the sensitivity of osteoclast precursors to osteoclastogenic cytokines.
- frequency estimates for SQSTM1/p62 mutations and haplotype distribution in familial Paget's disease of bone
- p62, a ubiquitin proteasome system related protein, was found in the majority of Neurofibrillary Tangles , but in only a small proportion of neuronal alpha-synuclein inclusions in cases of combined multiple system atrophy and Alzheimer's disease.
- The specific interaction between p62 and LC3, mediated by a 22-residue sequence of p62 containing an evolutionarily conserved motif, is instrumental in mediating autophagic degradation of the p62-positive bodies.
- Development of Mallory bodies requires overexpression of keratin 8, ubiquitin, and p62 containing the ubiquitin binding domain, whereas intracellular hyaline bodies result from overexpression of p62 together with ubiquitin without keratin involvement.
- analyse the expression of p62 in muscle biopsies from patients suffering from myotilinopathy and desminopathy
- The solution structure of a 52 residue construct containing the ubiquitin associated domain of p62 has been characterized using heteronuclear nuclear magnetic resonance (NMR) methods.
- Ubiquitin recognition by the ubiquitin-associated domain of p62 involves a novel conformational switch.
- Frontotemporal lobar degeneration with ubiquitin-positive inclusions visualized with ubiquitin-binding protein p62.
- analysis of sequestosome 1 (SQSTM1) mutations in Paget's disease of bone from the United States
- This study revealed genetic associations of SLC1A4, SQSTM1, and EIF4EBP1 with MSA. These results may lend genetic support to the hypothesis that oxidative stress is associated with the pathogenesis of MSA.
- In this study, the lysine selection process for TRAF6/p62 ubiquitination was examined.
- strong evidence for a founder effect of the P392L SQSTM1 mutation in Belgian, Dutch, and Spanish patients with Paget's Disease of Bone
- LC3 is responsible for recruiting p62 into autophagosomes, a process mediated by phenylalanine 52, located within the ubiquitin core, and the N-terminal region of the protein.
- The autophagy-unrelated association of GFP-LC3 with protein aggregates is dependent on its interaction with p62.
- P62 immunoreactive inclusions were found in the frontal cortex, hippocampus and cerebellum only in subjects with a history of psychiatric morbidity.
- We confirm the data on the existence of both a mutational hotspot at the UBA domain of SQSTM1/p62 and a founder effect in the PDB population.
- Mammalian cells thus use a common pathway involving ubiquitin and p62 for targeting diverse types of substrates for autophagy