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1  we identified adenomatous polyposis coli 1 (APC1) as an interaction partner of KHC in controlling di
2    In addition they accumulate with APC2 and APC1 in nerves formed by axons of the progeny of each ne
3                                     APC2 and APC1 localize to very different places when expressed in
4  dependent on APC1, suggesting that APC2 and APC1 may act cooperatively in the destruction complex.
5 d ovaries and embryos null for both APC2 and APC1, and assessed the consequences of total loss of APC
6 s between the N-terminal domain of CDC20 and APC1 and APC8.
7                          Only the CDC27- and APC1-depleted cells were enriched in the G2/M phase with
8 brain: APC2 localizes to the cell cortex and APC1 to centrosomes and microtubules.
9 linker protein Short stop works with EB1 and APC1 to help carry out this function.
10 erestingly, both Apoptin multimerization and APC1 interaction are mediated by domains that overlap wi
11 APC in a model epithelium, we generated APC2 APC1 double null clones in the Drosophila wing imaginal
12 ulate Wnt signaling in APC2 null and in APC2 APC1 double-null embryos.
13 d of eight protein subunits, including BimE (APC1), CDC27 (APC3), CDC16 (APC6), and CDC23 (APC8).
14 evelopment, simultaneously inactivating both APC1 and APC2 in clones of cells in the Drosophila larva
15     Further studies indicated that T. brucei APC1 and CDC27 failed to complement the corresponding de
16        Seven core subunit homologs of APC/C (APC1, APC2, APC11, CDC16, CDC23, CDC27, and DOC1) were i
17                                   Drosophila APC1 and Dia directly interacted and collaborated to pro
18 and Drosophila APC Basic domains, Drosophila APC1 collaborates with Dia to stimulate actin assembly i
19 ddress this question, we purified Drosophila APC1 and Dia and determined their individual and combine
20 shuttling activity is critical for efficient APC1 association and induction of apoptosis in transform
21 if is conserved in human APC2, but not human APC1.
22 mally prevented by an autoinhibitory loop in APC1 and that its mitotic phosphorylation relieves this
23 sphorylation of an N-terminal loop region in APC1 is sufficient for binding and activation of APC/C b
24  and sufficient to induce the degradation of APC1, in addition to the previously reported APC4 and AP
25 ate that Apoptin expression, or depletion of APC1 by RNA interference, inhibits APC/C function in p53
26 ess in uninfected cells whereby depletion of APC1, APC4, APC5, or APC8 recapitulates the pattern of H
27      Surprisingly, although complete loss of APC1 and APC2 resulted in strong activation of Wingless
28 estruction complex function was dependent on APC1, suggesting that APC2 and APC1 may act cooperativel
29  studies show that both Cdh1 and the subunit APC1 become dissociated from the complex.
30 n the levels of all three platform subunits, APC1, APC4, and APC5, upon the depletion of any one of t
31                                Surprisingly, APC1 function in embryos occurs at levels of expression
32                   Deletion of the N-terminal APC1 loop enables APC/C(CDC20) activation in the absence
33     The predicted location of the N-terminal APC1 loop implies that this loop controls interactions b
34                                 We find that APC1 and APC2 play overlapping roles in regulating Wingl
35                           Our data show that APC1, similar to its vertebrate homologue, bound to acti
36 phase-like mitotic spindles, suggesting that APC1 and CDC27 may play essential roles in promoting ana
37                       We discovered that the APC1 subunit, which along with APC4 and APC5 form the pl
38 iously shown that Apoptin interacts with the APC1 subunit of the anaphase-promoting complex/cyclosome
39 ubunits redistribute to the cytoplasm, while APC1 remains nuclear.
40  of subunits APC4 and APC5, which along with APC1 form the APC/C platform subcomplex.
41 ransformed cells, Apoptin is associated with APC1, a subunit of the anaphase-promoting complex/cyclos

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