|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for USP7(NM_003470.2) Search again
Product ID:
HQP018818
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
C16DELp13.2, DEL16P13.2, HAFOUS, HAUSP, TEF1
Gene Description:
ubiquitin specific peptidase 7
Target Gene Accession:
NM_003470.2(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:
|
|
| A | B |
|
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. |
|
Gene References into function
- Deubiquitination of p53 by HAUSP is an important pathway for p53 stabilization
- analysis of protein interaction domains of the ubiquitin-specific protease, USP7/HAUSP
- HAUSP regulates MDM2 and has a dynamic role in the p53-MDM2 pathway.
- the net deubiquitination of the various targets of HAUSP determines the steady-state level of p53
- USP7 is an Epstein-Barr virus target [review]
- crystal structure of the p53 binding domain of USP7 alone and bound to an EBNA1 peptide
- Results suggest that impaired deubiquitination of Hdmx/Hdm2 by HAUSP contributes to the DNA damage-induced degradation of Hdmx and transient instability of Hdm2.
- HAUSP regulates apoptosis of cervical adenocarcinoma cells
- ICP0 targets USP7 for ubiquitination and proteasome-dependent degradation; concluded that USP7-mediated stabilization of ICP0 is dominant over ICP0-induced degradation of USP7 during productive HSV-1 infection
- N-terminal domain of USP7 binds two closely spaced 4-residue sites in both p53 and MDM2, falling between p53 residues 359-367 and MDM2 residues 147-159.
- Finding suggests that USP7-mediated deubiquitination of Chfr leads to its accumulation, which might be a key regulatory step for Chfr activation.
- Data suggest that interaction partners might be required for USP7 nuclear import.
- USP7 may have a role not only in transcriptional regulation but also in DNA replication, apoptosis, and possibly endosomal organization
- MARCH7 can be stabilized by both USP9X and USP7, which deubiquitylate MARCH7 in the cytosol and nucleus, respectively
- Our data suggest that changes in HAUSP modulate tumor growth and apoptotic sensitivity in vivo.
- RASSF1A associates with MDM2 and death-domain-associated protein (DAXX) in the nucleus, thereby disrupting the interactions between MDM2, DAXX, and the deubiquitinase, HAUSP, and enhancing the self-ubiquitin ligase activity of MDM2.
- Herpes simplex virus type-1 immediate early protein ICP0 can interact with a previously unidentified isoform of USP7 that is not a predominantly ubiquitinated, SUMO-modified, or phosphorylated but is expressed in a number of different cell types
- results delineate a previously unknown PML-DAXX-HAUSP molecular network controlling PTEN deubiquitinylation and trafficking, which is perturbed by oncogenic cues in human cancer
- PML disruption by EBNA1 requires binding to the cellular ubiquitin specific protease, USP7 or HAUSP, but is independent of p53.
- USP7 specifically opposes the SCF(betaTrCP)- but not APC(Cdh1)-mediated degradation of Claspin.