Publication for Ccnb2 and Ccnb1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Ccnb2	cyclin B2	12442			[link]
mmu	Ccnb1	cyclin B1	268697

Pubmed ID	Priority	Text
30097513	0.98	Cyclin B2 was significantly up-regulated in the GDF9-Ccnb1-/- oocytes during GVBD (Fig. 4 A).
	0.98	Cyclin B2 compensated for the function of Cyclin B1 to regulate oocyte meiotic resumption.
	0.98	Ccnb1-/- oocytes underwent GVBD normally, this finding suggests that Cyclin B2 may play an unexpected important role that could not be completely compensated in a short period by Cyclin B1 during the resumption of meiosis in mouse oocytes.
	0.98	Cyclin B2 could trigger the GVBD of GDF9-Ccnb1-/-;Ccnb2-/- oocytes and that the GVBD of Ccnb2-null oocytes was delayed, although Ccnb2-null females are fertile, suggesting an important role of Cyclin B2 in regulating meiotic resumption.
	0.98	Cyclin B1 and Cyclin B2, providing new knowledge of the interchangeable functions of Cyclin B members during oocyte meiotic resumption.
	0.97	Cyclin B2 activity can compensate for Cyclin B1 to trigger meiosis resumption.
	0.97	Cyclin B1, CDK1 could be activated by up-regulated Cyclin B2.
	0.97	Ccnb1 and Ccnb2 double knockout permanently arrested the oocytes at the prophase of the first meiotic division.
	0.97	Cyclin B1 and Cyclin B2 in regulating MPF and oocyte meiotic resumption.
	0.97	Cyclin B1 and Cyclin B2 knockout mice have been generated, and it was found that Ccnb2-null mice developed normally and were fertile, whereas Ccnb1-null mice died in utero, which suggests that Cyclin B1 is critical for embryonic development; nevertheless, Cyclin B2 is dispensable for embryonic development and fertility.
	0.97	Ccnb1-null oocytes was due to up-regulation of Cyclin B2 expression, since knockdown of Cyclin B2 in Ccnb1-null oocytes arrested most oocytes at the GV stage.
	0.97	Cyclin B1 and Cyclin B2 may compensate each other in regulating MPF activity as well as the first meiotic resumption and second meiotic arrest in oocytes, which is important for understanding the regulatory mechanism of oocyte meiotic progression.
	0.97	Cyclin B2 is significantly up-regulated in GDF9-Ccnb1-/- oocytes
	0.97	Cyclin B2 was likely imported into the nucleus before GVBD in the GDF9-Ccnb1-/- oocytes to activate CDK1.
	0.97	Cyclin B2 may compensate Cyclin B1 function in CDK1 activation and subsequent GVBD stimulation.
	0.97	Cyclin B2 knockdown in the GDF9-Ccnb1-/- oocytes, the GVBD rate sharply decreased (Fig. 4 E), suggesting that Cyclin B2 promoted the resumption of meiosis in the absence of Cyclin B1.
	0.97	Cyclin B2 can substitute for Cyclin B1 in promoting the resumption of meiosis in mouse oocytes.
	0.97	Cyclin B2 can take on the role of Cyclin B1 to activate MPF for maintaining MII arrest in oocytes.
	0.97	Ccnb2-/- oocytes that underwent GVBD could extrude polar bodies after extended in vitro culture (not depicted), suggesting that Cyclin B1 alone was capable of promoting the meiosis I/meiosis II transition, which accounted for the fertility of the Ccnb2-/- female mice.
	0.97	Ccnb2 knockout mice were viable, compensation of Cyclin B1 function by Cyclin B2 in contributing to CDK1 activity and meiotic resumption was possible in Ccnb1-null oocytes because the translation of Cyclins B1 and B2 is differentially regulated.
	0.97	Cyclin B2 was elevated in GDF9-Ccnb1-/- oocytes, and knockdown of Cyclin B2 arrested most of the Ccnb1-null oocytes at the GV stage.
	0.97	Cyclin B2 compensates Cyclin B1 function in MPF activation and subsequent meiotic resumption as well as vice versa.
	0.96	Cyclin B1, Cyclin B2, and Cyclin B3.
	0.96	Cyclin B2 displayed an apparent increase in the GDF9-Ccnb1-/- oocytes during GVBD, but it showed weak expression after PBE.
	0.96	Cyclin B2 compensation for Cyclin B1 function in the resumption of first meiosis and subsequent M-phase entry but not in chromosome condensation and metaphase arrest of meiosis II remains unclear.
	0.96	Cyclin B2 could substitute for Cyclin B1 to drive the activation of MPF and resumption of the first meiosis and that Cyclin B2 could compensate Cyclin B1's function in metaphase arrest of the second meiosis (Fig. 6 D).
	0.95	Ccnb1 and Ccnb2 permanently arrested oocytes at the GV stage.
	0.95	Cyclin B1 and Cyclin B2 are substrates of anaphase-promoting complex/cyclosome (APC/C), one possibility could be that the accumulation of Cyclin B2 after PBE was too slow to achieve the threshold for reactivating CDK1 in the GDF9-Ccnb1-/- oocytes due to excessive Cyclin B2 degradation by APC/C activity in the absence of Cyclin B1, and introduction of Ccnb2 mRNA into the GDF9-Ccnb1-/- oocytes could restore the MII arrest (Fig. 6 D), implying that Cyclin B2 was destroyed completely by APC/C in the GDF9-Ccnb1-/- oocytes.
	0.94	Cyclin B2 could restore the MII arrest in the Ccnb1-null oocytes.
	0.94	Ccnb1 and Ccnb2 double knockout permanently arrests the oocytes at the GV stage
	0.91	Cyclin B2 can compensate for Cyclin B1 in oocyte meiosis I
	0.91	Ccnb1-/-;Ccnb2-/+ females, most oocytes were arrested at second meiotic interphase, like GDF9-Ccnb1-/- oocytes, and few oocytes remained at the GV stage (Fig. 6 A).
	0.90	Cyclin B2 during GVBD in the GDF9-Ccnb1-/- oocytes.
	0.90	Ccnb2 mRNA into the GDF9-Ccnb1-/-;Ccnb2-/- oocytes overcame the GV arrest, and most oocytes underwent GVBD in the presence of IBMX.
	0.89	Cyclin B2 expression restores the MII arrest in the GDF9-Ccnb1-/- oocytes
	0.85	Cyclin B2 interference in the GDF9-Ccnb1-/- oocytes induced severe GV arrest.
	0.83	Cyclin B2 expression triggers GVBD of GDF9-Ccnb1-/-;Ccnb2-/- oocytes
	0.82	Ccnb1-/- oocytes were arrested at the MII stage after forced expression of Cyclin B2 (Fig. 6 D), while some oocytes seemed to be arrested at the MI stage (Fig. 6 D), which was similar to the phenotype of Cyclin B1 overexpression (Fig. S4 H).
	0.81	Cyclin B2 knockdown suppresses GVBD in GDF9-Ccnb1-/- oocytes
	0.71	Cyclin B2 can take on the role of Cyclin B1 in driving meiotic resumption, we then injected Ccnb2 mRNA into the GDF9-Ccnb1-/-;Ccnb2-/- oocytes to observe whether this could trigger the GVBD.
	0.57	Ccnb1-/-;Ccnb2-/+ oocytes was delayed, and GVBD of GDF9-Ccnb1-/-;Ccnb2-/- oocytes did not occur after extended culture (Fig. 6 B), as is the case in vivo.
	0.53	Ccnb1-/-;Ccnb2-/- mouse oocytes after culture in vitro.
29074977	0.98	Ccnb1, but not Ccnb2, mRNAs is dependent on the RNA binding protein CPEB1.
	0.98	Cyclin B1 and Cyclin B2 are degraded by proteasome after ubiquitination by ubiquitin ligase APCcdh1 in GV oocytes.
	0.98	Ccnb2 translation changes marginally, major increases in Ccnb1 translation take place during prometaphase.
	0.98	Cyclin B2 levels change only marginally, the increasing Cyclin B1 protein between 2 and 4 h during prometaphase likely plays a pivotal role to reinforce the Cdk1 activity and to drive cell cycle progression.
	0.97	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).
	0.97	Ccnb1 and Ccnb2 mRNAs coding for Cyclin B1 and B2 proteins, which are the major components of MPF complex, clearly diverged in their translational pattern (Fig. 1), with Ccnb1 mRNA being recruited to the polysomes at prometaphase whereas the Ccnb2 mRNA association with the polysome increased only marginally or not at all during this transition.
	0.97	Ccnb1 whereas Ccnb2 translation is largely independent of CPEB1.
	0.97	Ccnb2 and Ccnb5 translation is activated first, followed by late translational activation of Ccnb1 and Ccnb4 during metaphase I. Among the three isotypes of Cyclin Bs (B1, B2, and B3) expressed in the female mouse germ cell, two were detected by western blot in GV oocytes.
	0.96	Cyclin B1 and Cyclin B2 is a key determinant for oocyte maturation, mechanisms regulating the translation of their mRNAs in quiescent mouse oocytes have not been explored thoroughly.
	0.96	Ccnb1 and Mos were significantly enriched in the immune complexes while the transcript of Ccnb2 was borderline when compared to transcripts that do not possess CPEs (Fig. 4A).
	0.96	Ccnb1 mRNA and translation of the transcript are modulated by CPEB1, whereas Ccnb2 translation is largely independent of CPEB1.
	0.96	Cyclin B2 degradation is fine-tuned through APC inhibition by Hec1 while the Cyclin B1 rate of degradation is the balance of Cdh1-stimulated and Securin/Bub1b-inhibited APC activity.
	0.95	Ccnb1 and Mos, but not Ccnb2, transcripts is activated after GVBD
	0.93	Ccnb1, Ccnb2, and Mos mRNAs.
	0.92	Ccnb1 (gene for Cyclin B1 protein) and Ccnb2 (gene for Cyclin B2 protein) during maturation of mouse oocytes.
	0.88	Ccnb1 and Ccnb2.
	0.84	Ccnb1, and Ccnb2 mRNA and translation of reporters.
	0.84	Cyclin B1 and Cyclin B2 proteins, unless protein synthesis is blocked.
	0.82	Ccnb2 mRNA is fully loaded with ribosomes in GV whereas Ccnb1 is not (Fig. 1 and Suppl.
	0.62	Ccnb2 or Ccnb1 genes.
23541922	0.98	cyclin B2, which cannot be covered by cyclin B1.
	0.97	cyclin B1 construct (cyclin B1-GFP):which is known to promote GVBD :in cyclin-B2-depleted oocytes induced 3-4 times lower rates of spontaneous GVBD during culture in IBMX than did cyclin B1-GFP overexpression in wild-type oocytes (Figure 3A).
	0.97	cyclin B1, to adequately cover for cyclin B2 loss as occurs in mitosis.
	0.97	Cyclin B2 depletion impairs the ability of cyclin B1-GFP overexpression to induce escape from IBMX-mediated G2-prophase arrest.
	0.97	cyclin B2 depletion, the ability of cyclin B1 overexpression to promote M phase entry is compromised and less efficient than cyclin B2 overexpression.
	0.96	cyclin B2 (encoded by CCNB2) is dispensable in mammals as, during mitosis, its loss can be fully covered by other cyclins, such as cyclin B1 and cyclin A2.
	0.96	cyclin B1, levels of cyclin B2 were roughly halved following Hec1 depletion (Figure 2A; Figures S1A and S1B available online).
	0.95	Cyclin B1-GFP to Promote GVBD Is Significantly Impaired on a Cyclin B2 Knockdown Background
	0.94	cyclin B1 levels between Hec1-depleted and wild-type oocytes (Figure 1B) suggested that cyclin B1 could not readily cover the G2-M defect arising from reductions in cyclin B2.
	0.94	cyclin B1 restraint, increased dependency is placed on cyclin B2 to prevent basal Cdk1 tone from dropping too low and to reinforce cyclin B1 pathways during Cdk1 activation.
	0.93	cyclin B1-GFP overexpression that were sufficient to accelerate GVBD in wild-type oocytes only partially rescued GVBD following either Hec1 or cyclin B2 depletion, the full restoration of which required ~2-fold higher cyclin B1-GFP expression (Figures 3B, S2A, S2C, and S2D).
	0.89	cyclin B1 against APCCdh1 in GV-stage oocytes :as the mechanism by which Hec1 stabilizes cyclin B2.
	0.87	cyclin B1 could not readily compensate for cyclin B2 loss in oocytes.
	0.84	cyclin B2-GFP that were capable of fully restoring GVBD were lower than those at which cyclin B1-GFP could only partially restore GVBD (Figure 3B; Figures S2B-S2D).
	0.84	cyclin B2 in oocytes, it neither readily explains the lack of similar effect on cyclin B1 nor does such a model conform with our finding that cyclin B2 levels are not increased by Hec1 overexpression.
	0.53	cyclin B2, but not cyclin B1 (Figures S5E and S5F).
31347666	0.98	Ccnb1-/- oocytes readily underwent GVBD (equivalent to G2/M) because of the presence of cyclin B2 (Figure 1), indicating that MPF was activated by cyclin B2 in the absence of cyclin B1.
	0.98	cyclin B2 induced GVBD more efficiently than cyclin B1 in the presence of dbcAMP, also illustrating the significance of cyclin B2 in meiotic resumption.
	0.98	cyclin B1 and cyclin B2 (unpublished data), indicating that cyclin A is able to activate MPF directly independent of cyclin B in meiosis.
	0.98	cyclin B2 perfectly regulates MPF activity for meiosis I progression in the cyclin B1-null oocytes.
	0.97	Cyclin B1 has long been believed to be the major partner of CDK1; in addition, cyclin B2 (CCNB2) and cyclins A1 (CCNA1) and A2 (CCNA2) can also combine with CDK1.
	0.97	cyclin B1 and cyclin B2 cooperate in the control of MPF activity in oocytes.
	0.97	cyclin B1-null oocytes can be rescued by exogenous cyclin B2 supplement, implying that cyclin B2 may be too low to reactivate MPF and the APC/C activity is relatively higher in the absence of cyclin B1.
	0.97	cyclin B1's functional compensation by cyclin B2 in MPF activation for meiotic resumption.
	0.94	cyclin B1 cannot compensate for the loss of cyclin B2 during meiotic resumption.
	0.88	cyclin B2 combines with different substrates from cyclin B1, facilitating MPF activation.
	0.79	cyclin B1 covered all functions of cyclin B2 in reproduction given the knockout phenotype; however, cyclin B2 may play a special role in meiosis.
	0.75	cyclin B2 and cyclin B1 in MPF activation, updating our understanding of MPF.
29072697	0.98	B-type cyclins, cyclin B1 (encoded by ccnb1) and cyclin B2 (encoded by ccnb2), have been reported to associate with Cdk1 and promote MPF activation.
	0.97	ccnb1 or ccnb2 mRNA into immature oocytes could induce germinal vesicle breakdown (GVBD); co-inhibition of ccnb1 and ccnb2 endogenous mRNA translation, but not one of them, with antisense RNAs can inhibit progesterone-induced GVBD.
	0.97	Ccnb1-null mice die in utero, whereas Ccnb2-null mice is viable and fertile, suggesting that CCNB1 is critically required for mouse embryogenesis, whereas CCNB2 is largely redundant in mouse embryogenesis and productivity.
	0.97	CCNB1 in premeiotic male germ cells did not have effect on meiosis of spermatocytes and male fertility, suggesting that CCNB1 may be redundant in meiosis of spermatocytes, and other cyclins such as CCNB2 may compensate the role of CCNB1 in meiosis of spermatocytes in mutant mice.
	0.96	Ccnb2 mRNAs were found primarily in mitotically dividing spermatocytes, whereas Ccnb1 transcripts were most abundant in the postmeiotic germ cells.
	0.96	CCNB2 might compensate the role of CCNB1 in meiosis of spermatocytes in mutant mice.
	0.95	ccnb1 and ccnb2 have redundant roles in the mitosis and meiosis of frog.
	0.95	CCNB2, which is also highly expressed in testis, may compensate the loss of CCNB1 in mutant mice.
29074707	0.98	Cyclin B1 is that whereas Cyclin B1 shuttles between the nucleus and the cytoplasm in interphase and binds to the mitotic apparatus in mitosis, Cyclin B2 is localized primarily to the Golgi apparatus and thus cannot phosphorylate the majority of substrates recognized by Cyclin B1.
	0.98	Cyclin B2 can only affect the structure of the Golgi apparatus, whereas Cyclin B1 can reorganize the cytoskeleton and disassemble the nuclear lamina.
	0.97	Cyclin B2 was not essential for development, but later siRNA studies in cell culture concluded that Cyclin B2 could compensate for Cyclin B1 in mitosis.
	0.92	Cyclin B2 does not compensate for Cyclin B1 in promoting mitosis.
	0.89	Cyclin B2 can compensate for the absence of Cyclin B1.
	0.70	Cyclin B2 made any contribution to driving the second division in Cyclin B1-/- embryos.
22242187	0.98	Ccnb1 and Ccnb2 regulate the G2/M phase transition and are ubiquitously expressed in the lung during development.
	0.94	Ccnb1, Ccnb2, Cdc2, Cdkn2c, and Mcm2.
	0.94	Ccnb1 and Ccnb2, and c-Met.
	0.92	Ccnb1, Ccnb2, and Pik3ca by reduction of Nkx2-1 (Figure 3E).
24776885	0.98	cyclin B1 inhibiting separase activation and cyclin B2 accelerating aurora-A-mediated Plk1 activation and centrosome separation.
	0.97	cyclin B1 and ~20-fold cyclin B2 overexpression, respectively (Fig. 1d,e).
	0.95	CCNB1 and CCNB2 expression were not simply a consequence of increased numbers of cycling cells (Supplementary Fig. 7c,d).
	0.54	Ccnb1; APC+/Min and Ccnb2; APC+/Min tumours show areas where intramucosal invasion has occurred to illustrate that these tumours have a more aggressive tumour phenotype.
25309961	0.98	Ccnb1 (cyclin B1), Ccnb2 (cyclin B2) and Top2a (topoisomerase IIalpha).
	0.98	Ccnb1 as well as other mitotic regulators (e.g., Ccna2, Ccnb2) implicated in CIN in other systems.
	0.98	Ccnb1 and Ccnb2.
	0.97	Ccnb1 (cyclin B1) and Ccnb2 (cyclin B2) in TLX1-expressing DN2mt versus TLX1-negative progenitor cells, similar to the results obtained by Hough et al. for primary TLX1-expressing B cells that exhibited a heightened susceptibility to aneuploidy following treatment with microtubule targeting agents.
26615533	0.98	cyclin B2, but not cyclin B1, was found to be the unique activating binding partner of Cdk1 in the Cdk1-Aurora A-Plk1-Mst2-Nek2A signaling cascade that induces centrosome disjunction.
	0.81	cyclin B1 or cyclin B2).
	0.77	cyclin B1 may fully compensate for the loss of cyclin B2 in mice, as cyclin B2 knockout mice are viable and apparently normal.
28702326	0.98	Ccnb1, Ccnb2), cell division cyclin 25c (Cdc25c), cyclin a2 (Ccna2), and topoisomerase DNAIIalpha (Top2a).
	0.98	Ccnb1, Ccnb2, Cdc25c, Ccna2, and Top2a) in proliferating and not differentiating myoblasts (Figure 2F), suggesting that Rev-Erb repression of NF-Y target genes is dependent on NF-YA interaction with cognate CCAAT-boxes.
	0.97	CCNB1, CCNB2, TOP2A, and TK1) were similarly induced by the Rev-Erb antagonist SR8278 and repressed by the Rev-Erb agonist SR9011 (Supplemental Figure 4).
30770433	0.98	cyclin B2 could compensate for Ccnb1 in oocyte meiosis I, which implies that there are specific modulations in the meiotic cell cycle regulation.
	0.97	Ccnb1 may lead to compensatory increasing of Ccnb2 with normally GVBD occurrence.
	0.97	Ccnb2 or cyclin A2 may complement Ccnb1 for maintaining high CDK1 activity to initiate GVBD and block the AnaI onset in oocytes lacking Ccnb3.
31970406	0.98	CCNB2 results in defective meiosis re-entry, while CCNB1-depleted oocytes are able to resume meiosis, but are unable to enter meiosis II.
	0.97	CcnB1 and CcnB2 mRNA levels are present at comparable levels in fully-grown oocytes, their translation diverges substantially in GV oocytes.
	0.95	CcnB2 mRNA is translated at sustained rates while CcnB1 is one of the most repressed mRNAs in prophase I. During maturation, the translation of CcnB1 mRNA increases four-fold, while little change in the translation of CcnB2 mRNA is detected.
18431504	0.98	Cyclin B1, Cyclin B2, Cdk1, Cdc25C, Dhfr, Topoisimerase II alpha, Tk) (Figure 2A, lane 2).
	0.97	cyclin B1, cyclin B2, cdk1, cdc25A, cdc25C, chk2, dhfr, topoisomerase IIalpha, and mdr-1, during different phases of the cell cycle and in response to DNA damage.
19001847	0.98	cyclin B1 (Ccnb1) and B2 (Ccnb2) genes in both the male and female germ cells.
	0.93	Ccnb1 nor Ccnb2 transcripts was detected in the mitotically dividing spermatogonia.
28508871	0.98	Ccnb1, Ccnb2), cell proliferation (Mki67, Pcna) and HCC (alpha-fetoprotein or Afp), were profoundly induced by FGF19 expression in livers from Stat3f/f mice, but not Stat3DeltaHep mice (Supplementary Fig. 1e and f).
	0.98	Ccnb1, Ccnb2; Supplementary Fig. 6d), and markers of proliferation (Mki67; Supplementary Fig. 6e) and HCC (Afp; Supplementary Fig. 6e) in livers from FGF19-expressing mice, further demonstrating the role of IL-6 in mediating FGF19-driven tumour growth.
19555225	0.98	cyclin B1 (Ccnb1), Cyclin B2 (Ccnb2), Chek1, Tnfrsf12a, Gadd45g, and Top2a, were also upregulated in O3-exposed ATTP-/- mice.
23678289	0.98	Ccnb1, Ccnb2) and E2f 1,2,3,4 Transcription Factors.
27217483	0.98	Ccnb1, Ccnb2, and Ccnd1 (which, respectively, encode cyclins A2, B1, B2, and D1), and Foxm1, all previously implicated as regulators of gestational beta-cell proliferation (Fig. 4D).
27767095	0.98	cyclin B1 and cyclin B2 or through Wee1B/Myt1-mediated phosphorylation of Cdk1.
27801298	0.98	Ccnb1, Ccnb2 and Ccna2, as well as with cyclin inactivator Cdc20 and the spindle assembler Cdca8.
29666442	0.98	CCNB1, CCNB2, CCNA2) and the established YAP/TAZ targets (CTGF, ANKRD1).
30285700	0.98	Ccnb1 and Ccnb2 is ubiquitously expressed in proliferating cells in many tissues, while Ccnb3 is specifically expressed in germ cells.
30723090	0.98	cyclin B1 and cyclin B2 mRNA association with polysomes is regulated in a distinct manner in mouse oocytes, resulting in translation of cyclin B1 transcripts but not cyclin B2.
30787318	0.98	Ccnb1, Ccnb2, Cdk1 and Cdc20 (Table S2).
29115400	0.97	CCNB1 and CCNB2, and CDK1 may regulate myocardial cell cycle at birth.
	0.96	CCNB1 and CCNB2 through ubiquitination.
	0.96	CCNB1, CCNB2 and CDK1.
	0.91	CCNB1, CCNB2, CDK1 and PTTG1 through ubiquitination, was activated through CDC20.
	0.90	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.
	0.90	CCNB1 and CCNB2 via ubiquitination.
	0.52	CCNB1, CCNB2 and CCNE1), genes encoding CDKs (CDK1, CDK2, CDK4 and CDK6), CDKN2D, genes encoding the cyclin-dependent kinase regulatory subunit [CDC28 protein kinase regulatory subunit (CKS)1b and CKS2], and cell cycle-associated genes (CDC20, CDC25A and CDC25B).
20067618	0.97	Ccnb1, Ccnb2, Ccna2, Aurka, Cdca3, Cdc2a, Bub1b, Cdca8).
	0.96	Ccnb1, Ccnb2, Ccna2, Ube2c, Aurka, Cdc2a) genes, in a similar manner as seen for BLM and N-ac-AAF.
	0.91	Ccnb1, Ccnb2, Ccna2, Aurka).
23784826	0.97	Ccnb1 and Ccnb2) share homology with the classic B type cyclin genes found in flies, worms, frogs, and mammals.
24874427	0.97	CyclinB1 (CCNB1), CyclinB2 (CCNB1), as well as decreased expression of proliferating cell nuclear antigen (PCNA) (Fig. 4G and Supplemental Figs. V-VI).
28380054	0.97	Cyclin B1 and B2 (CCNB1, CCNB2) are expressed in both mitotically and meiotically dividing cells.
29594255	0.97	Ccnb1, Ccnb2, Ccnd2, Ccnd3, Cdk1, and Cdk4.
30761733	0.97	cyclin B1 and inhibits hepatocellular carcinoma cell proliferation in vitro and in vivo.25 Zhang et al demonstrated that IL-18 can augment cell proliferation via the p38/ATF2 pathway by targeting cyclin B1, cyclin B2, cyclin A2 and Bcl-2 in BRL-3A rat liver cells.24 These experiments implied that changes in cyclin B1 expression induced by different factors coincide with the alteration of cyclin B1 mRNA.
30235877	0.96	CCNB1, we did intriguingly identify Ccnb2-derived transcripts enriched over 11-fold in polysomal fractions from AF compared to YF oocytes (Figure 5a).
24367005	0.95	Ccnb1, Ccnb2, Foxm1, and Ccne2) between OT-I CD8 T cells from DC+CpG and DC alone-immunized hosts at day 5 after immunization (Fig. 2 E).
27025256	0.94	cyclin B1 die early in embryogenesis, while cyclin B2 has no role in meiosis and cyclin B3 appears to inhibit prophase I. It therefore seems that meiotic Cdk2 might be regulated by a cyclin-independent mechanism, which prompted us to investigate the role of RingoA in meiosis.
25975747	0.91	cyclin B1 (Ccnb1); mutS homolog 6 (Msh6); cyclin A2 (Ccna2); and cyclin B2 (Ccnb2), were expressed in the two types of mouse.
25785582	0.87	cyclin B2 (Ccnb2, 5.4 fold), cyclin B1 (Ccnb1, 4.6 fold), and cyclin E1 (Ccne1, 2.6 fold), whilst expression of one member, cyclin A1 (Ccna1, -2.0 fold) was found to be decreased (Table 3).
20660152	0.63	Cyclin B1, cyclin B2, and cyclin B1/B2 double knockdown cells also generally completed mitosis in the absence of nocodazole, with cyclin B1 and cyclin B1/B2 knockdown cells taking slightly longer to complete mitosis (data not shown).
	0.59	cyclin B1 knockdown cells and 61% of the cyclin B1/B2 double knockdown cells exited mitosis before the end of the video, whereas mitotic exit was rarely seen in GL3 cells (0.5%) and cyclin B2 knockdown cells (6%) (Figure 8B).