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Fe65 is an adaptor protein involved in both processing and signaling of the Alzheimer-associated amyloid-beta precursor protein, APP (zeige APP Proteine). Here, the subcellular localization was further investigated using TAP-tagged Fe65 constructs expressed in human neuroblastoma (zeige ARHGEF16 Proteine) cells. Our results indicate that PTB2 (zeige PTBP1 Proteine) rather than the WW domain is important for the nuclear localization of Fe65.
Fe65 Ser289 phosphorylation did not affect the transcriptional activity of the Fe65-APP (zeige APP Proteine) complex, in contrast to the previously described Ser228 site.
Our findings imply that APBB1 plays an important role in the maintenance of EMT (zeige ITK Proteine)-associated CSC-like properties and gamma-radiation resistance via activation of IGF1Rbeta/AKT (zeige AKT1 Proteine)/GSK3beta pathway in lung cancer cells, highlighting APBB1 as a potential target for therapeutic cancer treatment.
Targeted enhancement of the signaling through the Fe65-cortactin (zeige CTTN Proteine) pathway, by either HDAC6 (zeige HDAC6 Proteine) inhibition or Tip60 (zeige KAT5 Proteine) activation, may lead to the development of new therapeutic drugs that are effective for patients with metastatic breast cancers.
Jagged1 is a novel binding partner of Fe65, and Fe65 may act as a novel effector of Jagged1 signaling.
FE65 influences APP (zeige APP Proteine) degradation via the proteasome, and phosphorylation of FE65 Ser (zeige SIGLEC1 Proteine)(610) by SGK1 (zeige SGK1 Proteine) regulates binding of FE65 to APP (zeige APP Proteine), APP (zeige APP Proteine) turnover and processing.
A novel phosphorylation site was identified within Fe65 which mediates gene transcription.
The SV2A (zeige SV2A Proteine)/FE65 interaction might play a role in synaptic signal transduction.
Data indicate that Fe65 is a positive estrogen receptor alpha (ERalpha (zeige ESR1 Proteine)) transcriptional regulator.
FE65 interactions with BLM (zeige BLM Proteine) and MCM proteins may contribute to the neuronal cell cycle re-entry observed in brains affected by Alzheimer's disease.
These data demonstrate a role for FE65 proteins at central and peripheral synapses.
results provide strong evidence that Fe65 plays a role in DNA damage response and cell viability by epigenomic regulation of specific transcriptional programs activated upon genotoxic stress.
Findings show that amyloid precursor protein (zeige APP Proteine)-binding proteins FE65 and FE65L1 (zeige APBB2 Proteine) are essential for the maintenance of lens transparency.
our data suggest that FE65 serves as a link between VLDLR (zeige VLDLR Proteine) and APP (zeige APP Proteine)
FE65 small interfering RNA does not influence Rac1 expression or its activity, although it acts as an adaptor protein with several protein-interaction domains.
Fe65 carries out different functions depending on its location in the regulation of Notch1 (zeige NOTCH1 Proteine) signaling.
a unique role for the 97 kDa isoform in controlling GnRH-1 (zeige GNRH1 Proteine) neurogenesis that is not redundant with the 60 kDa isoform of FE65.
Results confirm that megalin (zeige LRP2 Proteine) interacts with APP (zeige APP Proteine) and FE65, suggesting that these three proteins form a tripartite complex.
Data show that the carboxyl-terminal half of FE65, which contains the PI2 (zeige SERPINB1 Proteine) domain, failed to stabilize p53 (zeige TP53 Proteine), suggesting that the amino-terminal half of the protein plays an important role in the stabilization of p53 (zeige TP53 Proteine) in osmotically stressed cells.
The protein encoded by this gene is a member of the Fe65 protein family. It is an adaptor protein localized in the nucleus. It interacts with the Alzheimer's disease amyloid precursor protein (APP), transcription factor CP2/LSF/LBP1 and the low-density lipoprotein receptor-related protein. APP functions as a cytosolic anchoring site that can prevent the gene product's nuclear translocation. This encoded protein could play an important role in the pathogenesis of Alzheimer's disease. It is thought to regulate transcription. Also it is observed to block cell cycle progression by downregulating thymidylate synthase expression. Multiple alternatively spliced transcript variants encoding different isoforms have been described for this gene.
adaptor protein FE65a2
, amyloid beta A4 precursor protein-binding family B member 1
, stat-like protein
, amyloid beta (A4) precursor protein-binding, family B, member 1 (Fe65)
, amyloid beta A4 precursor protein-binding, family B, member 1
, amyloid beta precursor protein-binding B1
, amyloid beta A4 precursor protein-binding family B member 1-like