Psychiatry related information on Apbb1

• Fe65 modulates trafficking and processing of APP, including production of the beta-amyloid peptide that is believed to be central to the pathogenesis of Alzheimer's disease [1].

High impact information on Apbb1

• 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 [2].
• These results demonstrate that Fe65 plays an essential role in the response of the cells to DNA damage [3].
• These mice do not show any obvious phenotype; however, when fibroblasts (mouse embryonic fibroblasts), isolated from Fe65 KO embryos, were exposed to low doses of DNA damaging agents, such as etoposide or H(2)O(2), an increased sensitivity to genotoxic stress, compared with wild type animals, clearly emerged [3].
• Nuclear Fe65 is necessary to rescue the observed phenotype, and few minutes after the exposure of MEFs to DNA damaging agents, Fe65 undergoes phosphorylation in the nucleus [3].
• Furthermore, APP-C59 binds to the DNA binding protein Fe65, although this does not increase the half-life of APP-C59 [4].

Biological context of Apbb1

• In addition, Fe65 functions in regulation of the actin cytoskeleton and cell movement [1].

Anatomical context of Apbb1

• Fe65 was also highly expressed in the cerebellum, thalamus and selected brain stem nuclei [1].
• Fe65 was evident in a sub-set of astrocytes within the stratum oriens and radiatum in the hippocampus [1].

References