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These results reveal a novel RTK-AKT (zeige AKT1 Proteine)-p300 (zeige EP300 Proteine)-ADA3 signaling pathway involved in growth factor-induced cell cycle progression.
PCAF (zeige KAT2B Proteine) and ADA3 transcriptionally regulate PACS1 and PACS1 is a key regulator of BAX (zeige BAX Proteine)/BAK (zeige BAK1 Proteine) oligomerization and the intrinsic (mitochondrial) pathway to apoptosis.
ADA3 overexpression enhances cell proliferation that is associated with increased expression of c-MYC (zeige MYC Proteine). Expression patterns with respect to ADA3/c-MYC (zeige MYC Proteine) can divide patients into four significantly different subgroups, with c-MYC (zeige MYC Proteine) High and ADA3 Low status independently predicting poor survival in patients.
review on hADA3 with a comprehensive outlook on the molecular and functional roles of hADA3
Findings demonstrate that acetylation of ADA3 by its associated histone acetyltransferases is essential for its key role in histone acetylation and cell cycle progression.
results thus demonstrate that the catalytic activity of GCN5 (zeige KAT2A Proteine) is stimulated by subunits of the ADA2a (zeige TADA2A Proteine)- or ADA2b (zeige TADA2B Proteine)-containing HAT (zeige MGEA5 Proteine) modules and is further increased by incorporation of the distinct HAT (zeige MGEA5 Proteine) modules in the ATAC (zeige XCL1 Proteine) or SAGA holo-complexes
PCAF (zeige KAT2B Proteine) and ADA3 regulate Bid (zeige BID Proteine) processing via PACS2 (zeige PACS2 Proteine), to modulate the mitochondrial cell death pathway in response to hGrzB.
Cytoplasmic localization of alteration/deficiency in activation 3 (ADA3) predicts poor clinical outcome in breast cancer patients.
Expression of the interacting proteins altered expression of an hADA3-regulated reporter gene, suggesting functional consequences for the interactions.
a critical role of Ada3 in embryogenesis and cell cycle progression as an essential component of HAT complex.
demonstrate a novel ADA3 interaction with CENP-B (zeige CENPB Proteine)-centromere that may account for its previously known function in mitosis
The loss of Ada3 led to enhanced chromosomal aberrations, such as chromosome breaks, fragments, deletions and translocations, which further increased upon DNA damage.
Many DNA-binding transcriptional activator proteins enhance the initiation rate of RNA polymerase II-mediated gene transcription by interacting functionally with the general transcription machinery bound at the basal promoter. Adaptor proteins are usually required for this activation, possibly to acetylate and destabilize nucleosomes, thereby relieving chromatin constraints at the promoter. The protein encoded by this gene is a transcriptional activator adaptor and has been found to be part of the PCAF histone acetylase complex. In addition, it associates with the tumor suppressor protein p53 and is required for full activity of p53 and p53-mediated apoptosis. At least four alternatively spliced variants have been found for this gene, but the full-length nature of some variants has not been determined.
, ADA3-like protein
, transcriptional adapter 3
, transcriptional adaptor 3
, transcriptional adapter 3-like
, ADA3 homolog B
, ADA3-like protein B
, Transcriptional adapter 3-like B
, transcriptional adapter 3-B