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Validated All-in-One™ qPCR Primer for ITCH(NM_001324197.2) Search again
Product ID:
HQP184402
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ADMFD, AIF4, AIP4, NAPP1
Gene Description:
itchy E3 ubiquitin protein ligase
Target Gene Accession:
NM_001324197.2(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.
Summary
Atrophin-1 contains a polyglutamine repeat, expansion of which is responsible for dentatorubral and pallidoluysian atrophy.
Gene References into function
- gene expression regulation; coregulates hematopoietic transcription factor NF-E2
- The tight junction-specific protein occludin is a functional target of the E3 ubiquitin-protein ligase itch
- novel E3 ubiquitin-protein ligase; role in regulation of immune response - review
- Data demonstrate that two E3 ligases of different classes, CBLC and AIP4, can interact and cooperate to down-regulate EGFR signaling.
- First demonstration of ubiquitin-protein ligase AIP4 from human lung cDNA library recruited by penton base proteins of adenovirus serotypes Ad2 and Ad3 in vitro and in vivo.
- Data show that the Nedd4-like E3 ubiquitin ligase AIP4 mediates ubiquitination of CXCR4 at the plasma membrane, and of the ubiquitin binding protein Hrs on endosomes.
- Reults demonstrate the function of atrophin-1-interacting protein 4 as an ubiquitin E3 ligase for human enhancer of filamentation 1.
- The visualization of ubiquitinated Jun in living cells has uncovered a lysosomal pathway for Jun degradation that involves ubiquitination by Itch/AIP4.
- Upon DNA damage Itch itself is downregulated, allowing p73 protein levels to rise and thus interfere with p73 function
- Both neural precursor cell expressed, developmentally down-regulated 4 and Itch participate in the degradation of Melan-A
- AIP4 restricts transforming growth factor-beta signaling through a ubiquitination-independent mechanism
- CISK strongly interacts and colocalizes with the E3 ubiquitin ligase AIP4, which is important for the ubiquitin-dependent lysosomal degradation of CXCR4
- AIP4-generated polyubiquitin chains are mainly conjugated through lysine 29 of ubiquitin in vivo, indicating a link between this type of chain and lysosomal degradation.
- transient overexpression of FAM/USP9X resulted in the deubiquitylation of Itch. Moreover, we show that Itch auto-ubiquitylation leads to its degradation in the proteasome
- AIP4 promotes the endocytosis of TRPV4 and decreases its amount at the plasma membrane. TRPC4, another member of the TRP channel family, is also strongly ubiquitinated in the presence of AIP4
- Hedgehog transcription factor Gli1 is targeted by Numb for Itch-dependent ubiquitination, which suppresses Hedgehog signals, thus arresting growth and promoting cell differentiation.
- the AIP4.arrestin-2 complex functions on endosomes to regulate sorting of CXCR4 into the degradative pathway
- AIP4/Itch regulates Notch receptor degradation in the absence of ligand
- The modified Yap1 does not co-activate Runx in supporting Itch transcription. The subsequent reduction in the Itch level gives rise to p73 accumulation.
- This is the first in vivo evidence for the interaction between p45/NF-E2 and the E3 ubiquitin ligase Itch, and the subsequent ubiquitination of p45/NF-E2 by Itch.
- demonstrate that the decay rate of a catalytic inactive Itch mutant, which is devoided of self-ubiquitylating activity, is barely indistinguishable from the one of the wild-type protein
- hypothesize a correlated slow-frequency motion that involves two different hinge regions of the HECT domain of itch
- Itch gene sequence is highly conserved in healthy subjects; no relevant SNPs located in putative functional regions of Itch were found in atopic dermatitis and rheumatoid arthritis patients
- ITCH is a putative target for a novel 20q11.22 amplification detected in anaplastic thyroid carcinoma cells by array-based comparative genomic hybridization.
- These data suggests that caspase-dependent Itch cleavage might be an important regulator of Itch at the endogenous level under both physiological and stressed conditions.
- Ubiquitination of cFLIP(L) inhibits the interaction between cFLIP(L) and Itch in T. cruzi-infected cells.