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Jagged1 is a novel binding partner of Fe65, and Fe65 may act as a novel effector of Jagged1 signaling.
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 (show APP ELISA Kits)-binding proteins FE65 and FE65L1 (show APBB2 ELISA Kits) are essential for the maintenance of lens transparency.
our data suggest that FE65 serves as a link between VLDLR (show VLDLR ELISA Kits) and APP (show APP ELISA Kits)
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 (show NOTCH1 ELISA Kits) signaling.
a unique role for the 97 kDa isoform in controlling GnRH-1 (show GNRH1 ELISA Kits) neurogenesis that is not redundant with the 60 kDa isoform of FE65.
Results confirm that megalin (show LRP2 ELISA Kits) interacts with APP (show APP ELISA Kits) and FE65, suggesting that these three proteins form a tripartite complex.
Data show that the carboxyl-terminal half of FE65, which contains the PI2 (show SERPINB1 ELISA Kits) domain, failed to stabilize p53 (show TP53 ELISA Kits), suggesting that the amino-terminal half of the protein plays an important role in the stabilization of p53 (show TP53 ELISA Kits) in osmotically stressed cells.
cell cycle progression by down-regulating thymidylate synthase (show TYMS ELISA Kits) expression
Fe65 is an adaptor protein involved in both processing and signaling of the Alzheimer-associated amyloid-beta precursor protein, APP (show APP ELISA Kits). Here, the subcellular localization was further investigated using TAP-tagged Fe65 constructs expressed in human neuroblastoma (show ARHGEF16 ELISA Kits) cells. Our results indicate that PTB2 (show PTBP1 ELISA Kits) rather than the WW domain (show DRP2 ELISA Kits) is important for the nuclear localization of Fe65.
Fe65 Ser289 phosphorylation did not affect the transcriptional activity of the Fe65-APP (show APP ELISA Kits) complex, in contrast to the previously described Ser228 site.
Our findings imply that APBB1 plays an important role in the maintenance of EMT (show ITK ELISA Kits)-associated CSC-like properties and gamma-radiation resistance via activation of IGF1Rbeta/AKT (show AKT1 ELISA Kits)/GSK3beta (show GSK3b ELISA Kits) pathway in lung cancer cells, highlighting APBB1 as a potential target for therapeutic cancer treatment.
Targeted enhancement of the signaling through the Fe65-cortactin (show CTTN ELISA Kits) pathway, by either HDAC6 (show HDAC6 ELISA Kits) inhibition or Tip60 (show KAT5 ELISA Kits) activation, may lead to the development of new therapeutic drugs that are effective for patients with metastatic breast cancers.
FE65 influences APP (show APP ELISA Kits) degradation via the proteasome, and phosphorylation of FE65 Ser (show SIGLEC1 ELISA Kits)(610) by SGK1 (show SGK1 ELISA Kits) regulates binding of FE65 to APP (show APP ELISA Kits), APP (show APP ELISA Kits) turnover and processing.
A novel phosphorylation site was identified within Fe65 which mediates gene transcription.
The SV2A (show SV2A ELISA Kits)/FE65 interaction might play a role in synaptic signal transduction.
Data indicate that Fe65 is a positive estrogen receptor alpha (ERalpha (show ESR1 ELISA Kits)) transcriptional regulator.
FE65 interactions with BLM and MCM proteins may contribute to the neuronal cell cycle re-entry observed in brains affected by Alzheimer's disease.
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.
amyloid beta (A4) precursor protein-binding, family B, member 1 (Fe65)
, amyloid beta A4 precursor protein-binding, family B, member 1
, amyloid beta (A4) precursor protein-binding, family B, member 1 interacting protein
, amyloid beta A4 precursor protein-binding family B member 1-like
, amyloid beta A4 precursor protein-binding family B member 1
, adaptor protein FE65a2
, stat-like protein
, amyloid beta precursor protein-binding B1