Publication for Cdc20 and Ccnb1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Cdc20	cell division cycle 20	107995			[link]
mmu	Ccnb1	cyclin B1	268697

Pubmed ID	Priority	Text
20956380	0.98	Cdc20 is an activator of the anaphase-promoting complex/cyclosome that initiates anaphase onset by ordering the destruction of cyclin B1 and securin in metaphase.
	0.98	cyclin B1 is newly synthesized during mitosis via cytoplasmic polyadenylation element-binding protein-dependent translation, causing its rapid accumulation between prometaphase and metaphase of Cdc20 hypomorphic cells.
	0.98	Cdc20 is particularly rate limiting for cyclin B1 destruction because of regulated de novo synthesis of this cyclin after prometaphase onset.
	0.98	Cdc20, we have obtained important new insights into the in vivo functions of Cdc20 and the regulation of cyclin B1 expression in mitosis.
	0.98	Cdc20-/H metaphases and anaphases showed elevated levels of phosphorylated Cdk substrates (Fig. 4, E and F), suggesting that the rise in cyclin B1 expression resulted in increased cyclin B1-Cdk1 activity.
	0.98	Cdc20-/H MEFs produce cyclin B1 in mitosis via a mechanism that involves translation of preexisting cyclin B1 transcripts.
	0.98	cyclin B1-Venus degradation was consistently delayed in Cdc20-/H MEFs suggested that the timing of mitosis was altered in these cells.
	0.98	cyclin B1 is de novo synthesized in mitosis via CPEB-dependent translation, causing accumulation of cyclin B1 in prometaphase and, most likely, delayed anaphase onset in Cdc20 hypomorphic cells.
	0.98	Cdc20 hypomorphic cells retain high levels of cyclin B1 in metaphase, allowing cyclin B1-Cdk1 activity to persist at a time that it should be rapidly declining.
	0.98	Cdc20 show a remarkable increase in cyclin B1 levels that starts after NEBD and peaks in metaphase.
	0.98	cyclin B1 in mitotic Cdc20 hypomorphic MEFs is dependent on CPEB-binding sequences in the 3'UTR of cyclin B1 mRNA.
	0.98	cyclin B1, as demonstrated by a recent study showing that Cdc20 continues to be synthesized after mitosis onset as a means to counteract APC/C-mediated Cdc20 degradation in the presence of active mitotic checkpoint signaling.
	0.97	cyclin B1 by APC/C. It is assumed that the inhibitory signal consists of Mad2 that has been primed by kinetochore-associated Mad1-Mad2 to stably interact with the APC/C-activating subunit Cdc20.
	0.97	Cyclin B1 levels spike during metaphase of Cdc20 hypomorphic cells.
	0.97	cyclin B1 levels markedly increased in Cdc20-/H MEFs (Fig. 4, C and D).
	0.97	Cdc20+/+ mitotic MEFs increase cyclin B1 levels in response to MT depolymerization but not when protein synthesis is blocked with CHX.
	0.97	cyclin B1 3'UTR sequences in our expression plasmid might explain why Cdc20-/H MEFs failed to show a marked increase in cyclin B1-Venus in mitosis.
	0.96	Cdc20, triggering the destruction of cyclin B1 and securin.
	0.96	cyclin B1 levels gradually declined from prometaphase to anaphase in Cdc20+/+ MEFs (Fig. 4 B).
	0.96	cyclin B1 levels from prometaphase to metaphase in Cdc20-/H MEFs was intriguing, which prompted us to further explore the underlying mechanism.
	0.96	cyclin B1 levels prolong metaphase, CHX restored normal metaphase timing in Cdc20-/H MEFs (Fig. 7 A).
	0.95	cyclin B1 protein synthesis during normal mitosis, Cdc20+/+ metaphases that had been exposed to CHX for 15 min exhibited significantly lower cyclin B1 immunofluorescence than untreated counterparts (Fig. 5, D and E).
	0.95	cyclin B1-Venus started to accumulate profoundly in Cdc20-/H MEFs, reaching peak levels ~12 min later.
	0.95	cyclin B1-Venus proteolysis in both Cdc20-/H and Cdc20+/+ MEFs.
	0.93	Cdc20 hypomorphic mice fail to counteract de novo synthesis of cyclin B1 in mitosis
	0.93	cyclin B1 3'UTR was placed in the antisense orientation, Cdc20-/H MEFs failed to accumulate cyclin B1-Venus in mitosis (unpublished data).
	0.92	cyclin B1 protein levels in Cdc20+/+ metaphases, it prevented the increase in cyclin B1 that is characteristic for Cdc20-/H metaphases (Fig. 4, G and H).
	0.89	Cdc20 seems to be rate limiting for timely destruction of cyclin B1.
	0.88	Cdc20-/H MEFs had elevated cyclin B1 levels at this stage of mitosis.
	0.85	cyclin B1-Venus destruction was considerably delayed in Cdc20 hypomorphic cells.
	0.82	Cdc20-/H MEFs entered anaphase, they did so with elevated levels of cyclin B1 compared with Cdc20+/+ MEFs.
	0.79	Cyclin B1 levels of Cdc20 hypomorphic cells rise in metaphase
	0.79	Cdc20+/+ MEFs also showed increased cyclin B1-Venus levels after NEBD, but this increase was very small compared with that of Cdc20-/H MEFs.
	0.77	Cdc20+/+ MEFs, cyclin B1-Venus levels were quite stable until ~6 min after NEBD, after which they rapidly declined (Fig. 6, A and B).
	0.75	Cdc20-/H MEFs in the presence of MG132, a proteasome inhibitor that extends metaphase by preventing cyclin B1 and securin degradation.
	0.73	Cdc20+/+ metaphases in which de novo protein synthesis is blocked by CHX show decreased cyclin B1 immunofluorescence.
20941357	0.98	Cdc20, the activating subunit of the anaphase-promoting complex/cyclosome (APC/C), initiates sister-chromatid separation by ordering the destruction of two key anaphase inhibitors, cyclin B1 and securin, at the transition from metaphase to anaphase.
	0.98	Cdc20, a critical activator of the APC/C E3 ubiquitin ligase that initiates sister chromosome separation by ordering the destruction of cyclin B1 and securin, as a female infertility gene.
	0.98	Cdc20 inhibition, triggering the ubiquitination and destruction of cyclin B1 and securin.
	0.98	Cdc20 knockdown experiments in primary oocytes indicate that APC/CCdc20 is active in late meiosis I, where it is responsible for driving oocytes into anaphase via the destruction of cyclin B1and securin, much like mitosis in somatic cells.
	0.98	cyclin B1 and p-(Ser) Cdk substrates are increased in the Cdc20 -/H oocyte.
	0.97	Cdc20 +/+ oocytes degraded most of their cyclin B1-EGFP during late prometaphase and early metaphase.
	0.94	Cyclin B1-EGFP degradation was monitored by time lapse microscopy as oocytes progressed through meiosis I. (A) Still images illustrating that cyclin B1 degradation is delayed in Cdc20 -/H primary oocytes.
	0.93	Cdc20 -/H primary oocytes, we measured the rate of degradation of two key APC/CCdc20 substrates, cyclin B1 and securin.
	0.92	Cdc20 -/- embryos, which typically arrest in metaphase at the two-cell stage due to inability to degrade cyclin B1 and securin in the absence of Cdc20.
	0.92	Cdc20 Impairs Degradation of Mitotic Cyclins and Securin in Metaphase I
	0.71	cyclin B1 degradation was delayed, we used indirect immunofluorescence to measure endogenously expressed cyclin B1 levels of Cdc20 +/+ and Cdc20 -/H oocytes in metaphase I. As shown in Figure 7C and 7D, cyclin B1 levels were indeed higher in Cdc20 -/H oocytes than in Cdc20 +/+ oocytes.
	0.65	Cyclin B1 degradation is delayed during metaphase I if Cdc20 are low.
22649246	0.98	cyclinb1 degradation through activation of the anaphase promoting complex (APC) system, involving cdh1 and cdc20.
	0.98	Cdc20 and cdh1 promote cyclinb1 degradation through the APC system.
	0.97	cyclinb1, cdc20 and cdh1.
	0.97	cyclinb1, cdh1 and cdc20 gradually declined as cells progressed through M-phase.
	0.95	cdc20, which promoted cyclinb1 degradation through the APC system, however, also underwent significantly slower rates of clearance in the FlnAy/- progenitors compared to FlnAy/+ cells.
	0.94	cdc20 and cdh1 (APC regulators that promote progression through metaphase to anaphase and anaphase to G1 as well as cyclinb1 degradation) in null FlnA progenitors were not decreased but increased, and their degradation rates were also slower, similar to that of cyclinb1.
	0.90	Cyclinb1 and cdc20 in FlnAy/+ progenitors underwent gradual degradation over a period of 240 min, but their degradation rates were significantly delayed in FlnAy/- progenitors.
	0.60	cyclinb1 and cdc20 after addition of the protein synthesis inhibitor, cyclohexamide (Fig. 7b).
24551245	0.98	Cdc20 was decreased in the FlnB knockdown cells, and would therefore inhibit Cyclin B1 degradation (and therefore hinder G2/M phase progression).
	0.98	Cyclin B1, Cdc20 and Cdc25c, are downregulated following Cdk1 inhibitor treatment, with the exception of total Cdk1 protein levels.
	0.98	Cyclin B1 and Cdc20.
	0.97	Cyclin B1-associated markers, including Cyclin B1, Cdc20, Cdc25c, Pkmyt1, 14-3-3, and Wee1, within the FlnB knockdown ATDC5 cells.
	0.96	Cyclin B1, Cdc20 and Cdc25c, were downregulated, except that total Cdk1 protein levels were comparable (Fig. 6C).
	0.88	Cyclin B1, Cdc20, and Cdc25c (rhodamine).
28458300	0.98	Cyclin B1 and Cdc20, and thus regulated the oocyte meiotic maturation process by controlling mRNA expression and degradation.
	0.98	Cyclin B1 and Cdc20, to regulate meiotic cell cycle progression.
	0.97	Cyclin B1 and Cdc20 mRNAs, whose contents changed with LSM14b expression, were likely direct targets of LSM14b.
	0.97	Cdc20 depletion caused APC/C inactivity, preventing Cyclin B1 from being degraded and thus the oocytes from completing the metaphase-anaphase transition.
	0.93	Cyclin B1 and Cdc20 mRNA contents were also reduced to the same level.
25938585	0.98	Cdc20 (APC-Cdc20) occurred on-time in NAM-treated oocytes, Cdc20 levels were higher in very late meiosis I, pointing to exaggerated APC-Cdc20-mediated proteolysis as a reason for lower cyclin B1 levels.
	0.98	Cdc20 levels with concomitant reductions in securin and cyclin B1 levels during meiosis I exit, together suggestive of increased APC-Cdc20-mediated proteolysis.
	0.96	Cdc20 substrates, securin and cyclin B1, are required for exit from meiosis I. The pattern of securin destruction has therefore been used as a surrogate marker of APC-Cdc20 activity in mouse oocytes with the onset of securin destruction correlating with initial APC-Cdc20 activation.
	0.91	cyclin B1 levels were 40-50% lower in NAM-treated oocytes than in control oocytes at all three time-points (Fig 7A), consistent with the trend towards reduced securin and increased Cdc20 levels we observed previously (Fig 5A and 5B).
22918942	0.98	CDC20, the most downstream target of the SAC and coactivator of the APC, needed to induce cyclin B1 degradation; and second, reduced amounts of the SAC component BUBR1, which, although not a substrate of the APC, requires FZR1 for its stability.
	0.97	CDC20, cyclin B1, and BUBR1.
	0.96	CDC20 and cyclin B1 suggest that both proteins are regulated in oocytes by APCFZR1 activity, but it is interesting that this is not the case for all potential substrates.
28737671	0.98	cyclin B1, which is caused by a ubiquitin protein ligase called the anaphase-promoting complex or cyclosome (APC/C) in association with Cdc20 (APC/CCdc20).
	0.98	APC/CCdc20 to degrade cyclin B1 and securin, which causes the loss of sister chromatid cohesion (Figure 2A).
	0.97	APC/CCdc20 inactivation, which cannot degrade securin and cyclin B1 to cause the cleavage of cohesion structure and anaphase onset.
19528295	0.98	Cdc20 by Mad2 and BubR1, and thus, the stabilization of securin and cyclin B1.
	0.98	Cdc20AAA/AAA MEFs contained reduced levels of securin and cyclin B1 (Fig. S2).
22592113	0.98	Ccnb1 and Cdc20 in MCL-like lymphomas of c-myc-3'RR/p53+/- mice appear directly linked to the p53+/- mutation that increases the rate and occurrence of c-myc-induced lymphomas.
	0.98	Ccnb1 overexpression in lymphomas is caused by non-functional p53, while Cdc20 is negatively regulated by p53.
28851945	0.98	cyclin B1 and securin degradation is controlled by the SAC, which prevents the APC/C from recognising cyclin B1 and securin by inactivating Cdc20.
	0.98	Cdc20 is released to activate the APC/C against cyclin B1 and securin, leading to the activation of separase and subsequently M-phase exit.
32188885	0.98	Cdc20, Ccnb1, and Ccnb2, were significantly decreased in the islets at P1, compared with islets not only at G18 but also from nonpregnant mice (Fig. 4E,F,I,J).
	0.98	Cdc20, Ccnb1, and Ccnb2 in the islets at P1 were significantly decreased compared with the non-pregnant islets (Fig. 4), implying that parturition negatively regulates cellular proliferation below normal homeostatic levels.
18706976	0.98	CDC20-dependent activation of Cyclosome-APC is necessary for degrading proteins such as Securin and Cyclin B1.
19160489	0.98	Cdc20 and APC-Cdh1 are implicated in the control of mitosis through mediating ubiquitination of mitotic regulators such as cyclin B1 and securin.
19838054	0.98	Cdc20 is inhibited by Mad2 and BubR1, preventing the degradation of securin and cyclin B1.
21352476	0.98	Ccnb1, Ccng1 and Ccnl1) cell division cycle homologues (Cdc20, Cdc27 and Cdc2l5) and cyclin-dependent kinase (Cdk7) were mostly highly up-regulated at 15 hrs time-point.
21497201	0.98	cyclins and cdc20, driving cellular exit from mitosis.
23300461	0.98	Cdc20 leading to the polyubiquitination of securin and cyclin B1, two inhibitors of separase, a protease that initiates anaphase by cleaving cohesin rings that physically join duplicated sister chromosomes together.
25309961	0.98	cyclin B1 and Cdc20 mitotic regulatory proteins as correlating with the ability of TLX1 to facilitate bypass of spindle checkpoint arrest.
27801298	0.98	Ccnb1, Ccnb2 and Ccna2, as well as with cyclin inactivator Cdc20 and the spindle assembler Cdca8.
30613277	0.98	CDC20-APC was found to ubiquitinate multiple substrates, including Nek2A, cyclin A, securin, cyclin B1, Bim, and Mcl-1, and target them for degradation by the proteasome.
30787318	0.98	Ccnb1, Ccnb2, Cdk1 and Cdc20 (Table S2).
31185583	0.98	CDC20 complex degrades cyclin B1 and CDK1 to end cell division.
29074977	0.97	Cdc20, Ncd80 (Hec1), Ccnb1, Mos, Bub1b, and Ccna2 increased progressively during maturation, while the translation of another set of transcripts (Cdh1, Cdc25b, Ccnb3 and Ccnb2) declines or remains unchanged as the oocytes progress through meiosis (Fig. 1).
15611331	0.96	Cdc20-4AVGR-injected oocytes could still be released from their anaphase-like arrest by strontium, suggested that the activated Cdc20 mutant could either not effectively turn on the APC/C in the presence of CSF, or that cyclin B1 was selectively protected from proteolysis by CSF.
	0.94	Cdc20-4AVGR caused the formation of interphase nuclei, it appears that APC/C control was only relaxed for some, but not all targets, i.e., caused the activation of separase (via Pds1/securin degradation), but to a lesser extent the degradation of cyclin B1.
29115400	0.95	CCNB1, CCNB2, CDK1 and PTTG1 through ubiquitination, was activated through CDC20.
	0.94	CDC20 also inhibited CCNB1 and CCNB2 through ubiquitination.
	0.91	CDC20, CDK1, MYC, CDC25C and GADD45alpha, which exhibited the CDK1 and PTTG1 through ubiquitination, and was activated by CDC20, which also inhibited the expression CCNB1 and CCNB2 via ubiquitination.
	0.87	CCNB1, CCNB2 and CCNE1), CDK genes (CDK1, CDK2, CDK4 and CDK6) and cell cycle-related genes (CDC20, CDC25A and CDC25B) were involved in profile 2.
27528194	0.95	Cdc20 to activate the APC/C. Co-activation of APC/C by Cdc20 in metaphase results in the polyubiquitination and subsequent proteasomal degradation of cyclin B1 and securin, thereby triggering sister chromatid separation and anaphase onset.
22936984	0.93	ccnb1, wee1, cdc20 and plk1.
28502659	0.90	cyclin B1 is presumably responsible for this phenomenon, as it can be reproduced merely by injecting oocytes lacking Cdc20 with mRNA encoding a non-degradable form of cyclin B1 (Delta90-cyclin B1; Figure 1H).
	0.76	cyclin B1 and securin proteolysis shortly before the first meiotic division and because Cdc20 and Cdh1 appear to be the sole accessory APC/C factors in mammals, Apc2 depletion should phenocopy that of Cdh1.
18270576	0.90	Cyclin B1 and Cyclin B2 showed a similar expression pattern to that of Cdc20, with the exception of being more biased toward the scleral edge of the retina, especially at earlier stages such as E12.5 and E16.5 (Figure 12E-G and data not shown).
25808367	0.90	Cdc20, Plk1, Birc5, Cenpe, Ccnb1, Mki67 and Aurka represent the top eight cell cycle expression network members.
25217616	0.88	Cdc20 for Cdh1, but we found there was no difference in the ability of mouse embryonic fibroblasts (MEFs) lacking Cdh1 to degrade cyclin B1 in metaphase or anaphase (Fig. 3E,F).