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Validated All-in-One™ qPCR Primer for APBB1(NM_001257320.2) Search again
Product ID:
HQP069065
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
FE65, MGC:9072, RIR
Gene Description:
amyloid beta precursor protein binding family B member 1
Target Gene Accession:
NM_001257320.2(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
The protein encoded by this gene is a member of the Fe65 protein family. It is an adaptor protein localized in the nucleus.
Gene References into function
- The transcriptional activity of the APP intracellular domain-Fe65 complex is inhibited by activation of the NF-kappaB pathway.
- Adjusting for age and sex, we found a slight risk associated with the deletion in intron 13 of the APBB1 gene for subjects less than 65 years.
- gamma-Secretase cleavage and binding to FE65 regulate the nuclear translocation of the intracellular C-terminal domain (ICD) of the APP family of proteins.
- APP and Fe65 mediate transactivation with low density lipoprotein receptor-related protein
- Abnormal accumulations of the amyloid-beta precursor protein associated with the aging cellular muscle fibers and appear to be the key pathogenic event in iclusion-body myositis.
- Alcadein and amyloid beta-protein precursor regulates FE65-dependent gene transactivation
- Fe65 is activated by the APP intracellular domain during transcriptional transactivation
- p65FE65 may be an intracellular mediator in a signaling cascade regulating alpha-secretion of APP
- The present work provides evidence that FE65 plays a role in the regulation of amyloid precursor protein processing in an in vivo transgenic mouse model.
- multiple interactions of AICD with FE65 and 14-3-3gamma modulate FE65-dependent gene transactivation
- FE65 is the key agent of Gal4DB-mediated transcriptional transactivation, whereas Tip60 is an FE65-associated repressor.
- Notch1 intracellular domain plays the role of a negative regulator in AICD signaling via the disruption of the AICD-Fe65-Tip60 trimeric complex.
- Nek6 binds to Fe65 through its (267)PPLP(270) motif; the protein-protein interaction between Nek6 and Fe65 regulates their subcellular localization and cell apoptosis
- We demonstrated that treatment with EGCG reduced the A beta levels by enhancing endogenous APP nonamyloidogenic proteolytic processing.
- Results describe the crystal structures of the human FE65 WW domain (residues 253-289) in the apo form and bound to the peptides PPPPPPLPP and PPPPPPPPPL, which correspond to human Mena residues 313-321 and 347-356, respectively.
- Fe65 regulation of APP proteolysis may be integrally associated with its nuclear signaling function, as all antecedent proteolytic steps prior to release of Fe65 from the membrane are fostered by the APP-Fe65 interaction
- APP-regulated FE65 plays an important role in the early stress response of cells and that FE65 deregulated from APP induces apoptosis.
- crystallographic analysis of the human Fe65-phosphotyrosine domain
- Single nucleotide polymorphisms in APBB1 gene is associated with nicotine dependence.
- the beta-sheet edge in some natively folded amyloid oligomers is designed positively to prevent beta aggregation
- Study determined the crystal structure of the carboxy-terminal APP intracellular domain in complex with the C-terminal phosphotyrosine-binding (PTB) domain of Fe65; The unique interface involves the NPxY PTB-binding motif and two alpha helices.
- Dexras1 functions as a suppressor of FE65-APP-mediated transcription, and FE65 tyrosine 547 phosphorylation enhances FE65-APP-mediated transcription, at least in part, by modulating the interaction between FE65 and Dexras1