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The findings reveal a novel mechanism whereby GSK3beta stimulates amyloidogenic processing of APP by phosphorylation of FE65 at threonine 579.
FE65 is found to activate ELMO1 by diminishing ELMO1 intramolecular autoinhibitory interaction and to promote the targeting of ELMO1 to the plasma membrane, where Rac1 is activated. We also show that FE65, ELMO1, and DOCK180 form a tripartite complex
Fe65 is an adaptor protein involved in both processing and signaling of the Alzheimer-associated amyloid-beta precursor protein, APP. Here, the subcellular localization was further investigated using TAP-tagged Fe65 constructs expressed in human neuroblastoma cells. Our results indicate that PTB2 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 complex, in contrast to the previously described Ser228 site.
Our findings imply that APBB1 plays an important role in the maintenance of EMT-associated CSC-like properties and gamma-radiation resistance via activation of IGF1Rbeta/AKT/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 pathway, by either HDAC6 inhibition or Tip60 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 degradation via the proteasome, and phosphorylation of FE65 Ser(610) by SGK1 regulates binding of FE65 to APP, APP turnover and processing.
A novel phosphorylation site was identified within Fe65 which mediates gene transcription.
The SV2A/FE65 interaction might play a role in synaptic signal transduction.
Data indicate that Fe65 is a positive estrogen receptor alpha (ERalpha) 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.
A ternary complex consisting of AICD, FE65, and TIP60 down-regulates Stathmin1.
Both amyloid-beta precursor protein and Fe65 are co-localized in model Hirano bodies associated with Alzheimer's disease.
Fe65 carries out different functions depending on its location in the regulation of Notch1 signaling.
A novel FE65 isoform and the regulation of the splicing events leading to its production may contribute to elucidating neuronal specific roles of FE65 and its contribution to Alzheimer's disease pathology.
Phosphorylation of LRP1 regulates the interaction with Fe65.
Fe65 binds preferentially to low-density lipoprotein receptor-related protein (LRP) carboxyl terminus when phosphorylated at tyrosine-4507 and in complex with amyloid precursor protein (APP).
Fe65 and Dab1 compete for binding to APP. Dab1 significantly decreased the amount of APP bound to LRP and the level of secreted APP and APP-CTF in LRP expressing cells
reduced levels of Sp1 resulted in downregulation of endogenous FE65 mRNA and protein
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-binding proteins FE65 and FE65L1 are essential for the maintenance of lens transparency.
our data suggest that FE65 serves as a link between VLDLR and APP
FE65 small interfering RNA does not influence Rac1 expression or its activity, although it acts as an adaptor protein with several protein-interaction domains.
a unique role for the 97 kDa isoform in controlling GnRH-1 neurogenesis that is not redundant with the 60 kDa isoform of FE65.
Results confirm that megalin interacts with APP and FE65, suggesting that these three proteins form a tripartite complex.
Data show that the carboxyl-terminal half of FE65, which contains the PI2 domain, failed to stabilize p53, suggesting that the amino-terminal half of the protein plays an important role in the stabilization of p53 in osmotically stressed cells.
cell cycle progression by down-regulating thymidylate synthase expression
The areas of highest Fe65 expression included the hippocampus, in which the earliest abnormalities of Alzheimer's disease are detectable. Fe65 also occurred in the cerebellum, thalamus and some brain stem nuclei. Fe65 occurred in hippocampal astrocytes.
These studies suggest an important and novel function of FE65 in learning and memory.
p65FE65 may be an intracellular mediator in a signaling cascade regulating alpha-secretion of APP
Targeted deletion of two members of the FE65 family of adaptor proteins, FE65 and FE65L1, results in cortical dysplasia and suggests that FE65 proteins are involved in basement membrane assembly.
phosphorylation of APP(amyloid beta-protein precursor) modulates FE65-dependent gene transactivation through the regulation of FE65 intracellular localization.
Fe65 plays an essential role in the response of the cells to DNA damage
The present study shows that 17beta-estradiol inhibits the transcriptional and apoptotic activities of the APPct complex by a process involving the interaction of estrogen receptor alpha (ERalpha) with Fe65.
Notch1 intracellular domain plays the role of a negative regulator in AICD signaling via the disruption of the AICD-Fe65-Tip60 trimeric complex.
a complex including APP, FE65 and an additional protein is involved in neurite outgrowth at early stages of neuronal development
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