APAF1


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APAF1

A gene on chromosome 12q23.1 that encodes a cytoplasmic protein, which initiates apoptosis. Apoptotic peptidase-activating factor 1 contains several copies of the WD-40 domain, a caspase recruitment domain (CARD) and an ATPase domain (NB-ARC). Upon binding cytochrome c and dATP, APAF-1 forms an oligomeric apoptosome, which binds and cleaves caspase-9 preproprotein, releasing the activated form, which stimulates the caspase cascade that commits the cell to apoptosis.
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In the present study, we found that LPS significantly elevated apoptosis-related gene expression, including PI3K and AKT, as well as Cyto-C, Apaf1, caspase-9, and caspase-3 (Figures 4(a)-4(f)).
(a-f) Sophocarpine decreased the mRNA expression of PI3K, AKT, Cyto-C, Apaf1, caspase-9, and caspase-3 analyzed by real-time PCR; the data are expressed as mean [+ or -] SEM, #P < 0.001.
[4] Human genes: APAF1, apoptotic peptidase activating factor 1; MAP2K4, mitogen-activated protein kinase kinase 4; TP53, tumor protein p53; DLC1, deleted in liver cancer 1; NMT1, N-myristoyltransferase 1; EF2S1, eukaryotic translation initiation factor 2, subunit 1 alpha, 35kDa; DYNLL1, dynein, light chain, LC8-type 1.
De Zio et al., "Apaf1 plays a pro-survival role by regulating centrosome morphology and function," Journal of Cell Science, vol.
Based on NCBI database, the screened differentially expressed genes Apaf1, Bace2, and Plcb4 were enriched in the "Alzheimer's disease-reference pathway" (P < 0.01) (Figure 4) and meanwhile significantly downregulated in A[[beta].sub.25-35]-injured PC12 cells after ME intervention as compared with A[[beta].sub.25-35] group (P < 0.05) (Table 3).
It has been demonstrated that interdigital cells and thymocytes obtained from mice lacking the caspase activator Apaf1 undergo necroptosis instead of apoptosis [43].
Changes of mitochondrial transition pore opening, decreased mitochondrial membrane potential, CL oxidation, and the release of proapoptotic cytochrome c and Apaf1 molecules are necessary for the execution of the intrinsic mitochondrial apoptotic pathway [140, 141].
This study demonstrated that high doses of AraC, DNR, and MIT did not induce apoptosis-related mRNAs (GADD, SUMO, Apaf1, Bfl1, BclII, Bim, Bik, Bid, Bad, Bcl-xs, Bak, and Bax) (data not shown).
It maybe possible to reverse epigenetic modifications that confer resistance to chemotherapy, such as the silencing of APAF1 in metastatic melanoma.
This in turn releases proapoptotic proteins: cytochrome c (Cyt C) [124] binds to apoptotic protease activating factor-1 (Apaf1) and then forms apoptosome that activates the caspase-9 and caspase-3 protease system and induces apoptosis, Smac/DIABLO [125] activates caspases by sequestering caspase-inhibitory proteins, and endonuclease-G (endoG) [126] mediates DNA fragmentation.
p53 modulates the expression of Bcl-2 family proteins (e.g., Bax, Bid) and other apoptosis-related gene targets (e.g., Apaf1).
In cells with severe DNA damage, p53 drives Fas-R, Bax, Puma, Noxa, Apaf1, and Pidd expression, activating intrinsic and extrinsic apoptotic pathways.