Publication for Ccna2 and Ccnb1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Ccna2	cyclin A2	12428			[link]
mmu	Ccnb1	cyclin B1	268697

Pubmed ID	Priority	Text
21952947	0.99	cyclin B1 and cyclin A, and promote accelerated entry in mitosis as part of its oncogenic function during head and neck cancer development.
	0.99	cyclin B1 and cyclin A, and promoting accelerated entry in mitosis.
	0.98	cyclin B1 and cyclin A, and accelerates entry in mitosis.
	0.98	cyclin B1 and cyclin A decreased, and entry in mitosis was delayed, after suppressing K-ras expression in oral tumour cells that express p53R172H.
	0.98	cyclin B1 and cyclin A in cells that express p53R172H.
	0.98	cyclin B1, cyclin A, and other genes found up-regulated in K-p53R172H tumours was confirmed by quantitative real-time-PCR (Figure 3D).
	0.98	cyclin B1 and cyclin A in breast and colon cancer cell lines in response to DNA damage.
	0.98	cyclin B1 and cyclin A in head and neck tumours, and in response to DNA damage.
	0.98	cyclin B1 and cyclin A (Figure 6F and Supporting information, Supplementary Figures 2A and 2B).
	0.98	cyclin B1 and cyclin A only in the presence of mutant p53, and suggest that the increased expression of cyclin B1 and cyclin A and the accelerated entry in mitosis observed in oral tumours that express mutant p53 may respond to oncogenic K-ras activation.
	0.98	cyclin B1 and cyclin A induced by DNA damage in oral tumour cells that express mutant p53, the presence of DNA damage in tumours induced by K-ras activation, the induction of cyclin B1 and cyclin A by K-ras only in oral tumour cells that express mutant p53, and the faster entry in mitosis induced by K-ras in mutant p53 cells suggest that the oncogenic function of mutant p53 in SCCHN may be promoted by oncogene-dependent DNA damage.
	0.98	cyclin B1 and cyclin A, may contribute to the oncogenic function of mutant p53.
	0.98	cyclin B1 and cyclin A and accelerated transition through mitosis contribute to the oncogenic function of mutant p53 during oral tumour development.
	0.98	cyclin B1 and cyclin A in cells that express mutant p53, compared with p53-null cells.
	0.98	cyclin B1 and cyclin A in response to DNA damage promoted by oncogene activation (K-ras) or chemotherapy (doxorubicin).
	0.97	cyclin B1 and cyclin A in oral tumour cells and accelerates entry in mitosis
	0.97	cyclin B1 and cyclin A (Figure 5H), and the protein levels of cyclin B1 and cyclin A were higher in K-p53R172H/- cells than in K-p53-/- cells (Figure 5I).
	0.95	cyclin B1 and cyclin A did not change after K-ras suppression in oral tumour cells that lack p53 (Figure 6G and Supporting information, Supplementary Figures 2C and 2D).
	0.94	cyclin B1 and cyclin A expression was modulated by oncogenic K-ras.
	0.94	cyclin B1 and cyclin A in response to DNA damage and K-ras.
	0.91	cyclin B1 and/or cyclin A can promote progression to carcinoma.
	0.90	cyclin B1 and cyclin A in response DNA damage and K-ras
	0.90	cyclin B1 and cyclin A expression in oral tumour cells that express mutant p53, we treated K-p53R172H/- and K-p53-/- cells with doxorubicin for up to 36 h. We observed that exposure to doxorubicin induced a higher increase in the cyclin B1 and cyclin A levels in K-p53R172H/- cells than in K-p53-/- cells (Figures 6A-6D).
	0.85	cyclin B1 and cyclin A. Therefore, it is unlikely that the observed changes in gene expression are secondary effects resulting from additional mutations that may arise as the tumours progress.
30190546	0.99	cyclin B1 and CDK2/cyclin A2 complexes (Fig. 2g).
	0.98	cyclin B1 complexes are known to be the main regulators of mitosis, whereas CDK2 in complex with cyclin A2 controls S phase progression.
	0.98	cyclin A2, as well as CDK1 and cyclin B1 (Fig. 6e).
	0.97	cyclin B1 and cyclin A2 at different time points after release (Fig. 2f, g).
	0.97	cyclin A2 activation, the nuclear envelope (NE) breaks down and CDK1/cyclin B1 complexes accumulate in the nucleus causing a sequence of events.
	0.91	cyclin A2 and cyclin B1 were comparable in control and Cdk1AF MEFs with and without WEE1i treatment (Fig. 6e).
28851945	0.98	cyclin A2 that inhibits efficient ubiquitination of cyclin B1 and securin by the APC/C.
	0.98	cyclin A2 degradation in the first mitosis is atypical, resembling the way in which cyclin B1 is controlled in somatic cells, because its degradation is regulated by both SAC and Plk1 activities.
	0.97	cyclin A2 to be preferentially ubiquitylated by the APC/C over securin and cyclin B1, when APC/C activity is limited.
	0.97	cyclin A2 and cyclin B1 indicates that length of the first M-phase is likely a consequence of delayed APC/C activation.
	0.96	cyclin A2 and cyclin B1.
	0.96	cyclin A2 did not seem to correlate with prolongation of the first embryonic M-phase, we directly addressed whether the high levels of cyclin A2 in zygotes after NEBD might reduce the ability of the APC/C to ubiquitylate cyclin B1 and delay its degradation.
	0.95	cyclin A2 and cyclin B1 corresponded to the prolonged duration of the whole M-phase in zygotes when compared to 2-cell embryos (medians of 111.0 and 57.0 min, respectively, p < 0.001, for cyclin A2-YFP embryos, and 96.0 and 76.5 min, p < 0.001, for cyclin B1-Ruby embryos, Tables 1 and 2).
	0.94	cyclin B1 was degraded at a similar rate during the first and second mitotic divisions (Fig. 1d), but, as with cyclin A2, the onset of cyclin B1 degradation in the first mitotic division was significantly delayed in comparison to the second mitotic division (medians of 48.0 and 18.0 min from NEBD, respectively, p < 0.001, Fig. 1b,d, Table 2).
	0.94	cyclin A2 and cyclin B1 degradation.
	0.94	cyclin B1 and cyclin A2 degradation in a SAC-independent manner
	0.81	cyclin A2 degradation, although it slows it down, but it does prevent cyclin B1 degradation.
	0.76	cyclin A2 and cyclin B1 in mouse zygotes
	0.69	cyclin A2 is responsible for the prolonged M-phase in zygotes, our results do not support this idea because we find that cyclin B1 starts to be degraded when the levels of cyclin A2 are still very high.
	0.59	cyclin A2 is stable in cells for over 30 min after NEBD, and cyclin B1 is stable for more than 45 min.
29217775	0.98	cyclinB1/cdk1, cyclinA2/cdk2 and importin B1 (IMB1), all of which were significantly upregulated (fold change >=2, P<0.05) in Ara-C-treated primary activated B cells (Figure 1A and Online Supplementary Tables S1 and S2).
	0.98	cyclinB1 and cyclinA2 were also upregulated by Ara-C in our newly developed G1XP lymphomas and in CH12 lymphomas (Figure 1A).
	0.98	cyclinB1 and cyclinA2 were indeed upregulated in Ara-C-treated wt or p53 conditional knock-out primary B cells, and in CH12 or G1XP lymphoma cells (Figure 1B).
	0.98	cyclinB1 and cyclinA2 upregulation appears to be an intrinsically programmed DNA damage response, which occurs in both activated primary B cells and various B-cell lymphomas.
	0.97	cyclinA2 and cyclinB1 appears to be an intrinsically programmed DNA damage response; (ii) Ara-C or doxorubicin induces differential cell cycle arrest in different types of B cells; (iii) Wee1 inhibitor sensitizes G2 phase-arrested B lymphoma cells to Ara-C treatment by inducing premature mitotic entry and mitotic catastrophe.
	0.96	cyclinB1, cyclinA2 and pCDK1 in different types of B cells upon Ara-C treatment.
	0.96	cyclinB1, cyclinA2 and pCDK1 in different types of B-cell lymphomas upon doxorubicin (DOX) treatment.
	0.94	cyclinB1 and cyclinA2 in various types of B cells
	0.93	cyclinB1 and cyclinA2 in different types of B cells upon Ara-C treatment.
	0.92	CyclinB1 and cyclinA2 were upregulated after 8 h of Ara-C treatment (data not shown), and significant induction occurred after 20 h or 24 h (Online Supplementary Figure S3C).
	0.84	cyclinA2, cyclinB1, or both in knocked down CH12 cells compared with scrambled controls (Online Supplementary Figure S6A).
	0.83	cyclinA2 and cyclinB1 were not required for Ara-C-induced G2 phase arrest
20300579	0.98	cyclin A expression (S G2 and G2 M), MCM7 expression (S phase DNA synthesis), and cyclin B1 expression/CDC2 phosphorylation (G2 M), and these effects were predominantly dose-dependent.
	0.98	cyclin A (2%-3% of serum control), cyclin B1 (12% of control), and MCM7 (30% of control), demonstrating that activated PPARgamma strongly reduced the expression or activity of these regulatory cell cycle proteins.
	0.93	cyclin B1 (2-fold), p-CDC2 and MCM7 (4-fold), pRb (8-fold) and cyclin A (19-fold) versus serum-starved, uninfected cells.
	0.89	cyclin A, cyclin B1 and MCM7, but not p-CDC2.
	0.66	cyclin B1, p-CDC2 and MCM7 3- to 4-fold, pRb 14-fold, and cyclin A 20-fold).
21497086	0.98	cyclin A2-Cdk2 (and Cdk1) prevent illegitimate assembly of prereplication complexes on chromatin when APC/C activity is low in somatic cells during S phase and G2, whereas cyclin B1-Cdk1 initiates mitosis and is required for its progression.
	0.98	cyclin A2, and cyclin B1 (Figure 2A; Figures S2B and S2C), as previously observed in somatic cells.
	0.98	cyclin A2, and cyclin B1 were downregulated in pluripotent cells depleted of Emi1 and dramatically stabilized following treatment with the proteasome inhibitor MG132 (Figure 2A; Figure S2D).
	0.97	cyclin A2, and cyclin B1 are crucial for cell-cycle regulation and maintenance of a diploid DNA content in somatic cells.
	0.53	cyclin A2 or cyclin B1.
24481444	0.98	Cyclin A2, PCNA, pRb) and mitosis (Cyclin B1) post-transcriptionally (Figures 3c and d).
	0.98	Cyclins such as Cyclin A2.
	0.96	Cyclin B1 (driving mitosis) and Cyclin A2 (driving DNA synthesis) are substantially reduced in the Sorafenib-treated cohort.
	0.94	Cyclin A2) and mitosis (Cyclin B1) in liver samples 48 h after PH.
25309961	0.98	Ccna2 (cyclin A2), 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	Ccna2, Ccnb1 and Ccnb2.
	0.97	Ccna2 (cyclin A2), 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.
27708105	0.98	cyclin A2-Cdk activity initiates mitosis by phosphorylating and inactivating the protein kinase Wee1, resulting in activation and nuclear localization of cyclin B1-Cdk1.
	0.98	cyclin A2, which has low sequence conservation among cyclin family members, directly binds to a conserved region in the 3'UTR of Mre11 transcripts to promote their translation, presumably through an interaction with eIF4A2.
	0.88	cyclin A2 interactor, supershifted GST-cyclin A2302-432-bound Mre11 RNA complexes but did not bind the probe in the absence of cyclin A2 (Fig. 4E).
	0.86	cyclin A2302-432(4M), which carries mutations in four putative ribonucleic acid contact sites required for restoration of Mre11 and Rad50 expression in Ccna2-/H MEFs by ectopic expression of cyclin A2 (fig. S17, B to E), was able to bind the Mre11 RNA probe (Fig. 4D).
29594255	0.98	Ccna2 and Ccnb1 levels were increased in the islets of pregnant mice, and treatment with HI-TOPK-032 attenuated Ccnb1 expression.
	0.97	Ccna2, Ccnb1, Ccnb2, Ccnd2, Ccnd3, Cdk1, and Cdk4.
	0.95	Ccnb1 and Ccna2 may induce beta-cell proliferation.
	0.91	Ccnb1 and possibly Ccna2.
21961992	0.98	Ccna2, Ccnb1 and Ccne1, whose products are involved in later G1/S-phase and G2/M-phase cell cycle events, were up-regulated greater than 3-fold subsequently at 8 hours (Table 1 and Figure 2C).
	0.98	Ccna2 and Ccnd1 have been previously designated as putative MYC targets through high-throughput screening, and Ccnb1 and Ccnd2 have been previously confirmed as direct transcriptional targets of MYC through the use of chromatin Immunoprecipitation (ChIP) analysis.
	0.94	Ccna2 and Ccnb1 showed increased expression at later time points (32 hours).
22057438	0.98	Cyclin A (CycA)- and Cyclin B1 (CycB1)-related nuclear fluorescence (Fig. 1a).
	0.98	CycA and CycB1.
	0.96	CycA and CycB1 (Fig. 3a, d).
25701202	0.98	cyclin A2, and cyclin B1 and decreased the levels of cyclin-dependent kinase inhibitor 1A prior to growth inhibition.
	0.98	Cyclins (Ccnd2, Ccne1, Ccna2, and Ccnb1) and cyclin dependent kinases (Cdk4) promote progression through the cell cycle, whereas cyclin dependent kinase inhibitors (Cdkn1a, also known as p21) promote cell cycle arrest.
	0.97	Ccna2, and Ccnb1.
28670514	0.98	Cyclin A2, and Cyclin B1.
	0.98	Cyclin A2 and Cyclin B1 in aged Nos2 KO mice probably retard the progression of hepatocytes into the cell cycle.
	0.97	Cyclin A2 and Cyclin B1 and protein expression level of proliferation marker Ki67 and proliferation-associated transcription factors JNK1, NF-kB and STAT3 were decreased or delayed.
29264547	0.98	cyclin A2, cyclin B1, cyclin D2, and cyclin E2 significantly increased (Fig. 7).
	0.98	cyclin A2, cyclin B1, cyclin D2, and cyclin E2.
	0.97	cyclin A2, cyclin B1, and cyclin E2 also significantly increased in the isolated islets.
31347666	0.98	cyclin A can induce GVBD in the absence of cyclin B1 and cyclin B2 (unpublished data), indicating that cyclin A is able to activate MPF directly independent of cyclin B in meiosis.
	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.
	0.80	Ccnb1 or Ccna2 results in embryonic lethality, making it impossible to study their functions in meiosis.
18056452	0.98	cyclin A2 (B), cyclin B1 (C) and cyclin E1 (D) and sustains downstream cyclin dependent kinase activity.
	0.97	cyclin A2 and cyclin B1 mRNA were sustained in Runx2-/- MEFs and persisted even as the cells reached confluence.
19001847	0.98	cyclin A2 and cyclin B1, while yet other cyclins, although expressed at specific stages of germ cell development, may have less essential function in the male germline.
	0.97	cyclin A2 or cyclin B1 function has precluded understanding their function in the germ line, where they are both abundantly expressed.
19562686	0.98	cyclin A2, cyclin B1 and B-Myb also appear to be highly abundant in ES cells, but are down-regulated upon differentiation.
	0.98	cyclin A and c-Myc are highest in S and G2, and cyclin B1 in the G2 phase.. NANOG also regulates S-phase entry in hESCs via transcriptional regulation of cell cycle regulatory components.
20169079	0.98	cyclin A, cyclin B1, cyclin D, CDK2, cdc2, p27, p21 and the RB family members p107, p130.
	0.96	cyclin A, cyclin B1, cdc2, cdk2, p27 and the Rb family members p107 and p130 but surprisingly not survivin.
22167461	0.98	Cyclin A and cyclin B1 expression was significantly increased at 6 h after TBI (Fig. 2a, b [cyclin A]; 2a, 2c [cyclin B1]; p<0.001 vs sham).
	0.97	cyclin A (Fig. 1a, b; p<0.01 vs sham) and cyclin B1 (Fig. 1a, c; p< 0.05 vs sham) expression levels at 6 h after TBI.
24615360	0.98	cyclin A, cyclin B1 and cyclin D1 during myoblast proliferation.
	0.92	cyclins stimulating cell cycle progression (cyclin A, B1, D1), proteins essential for cell cycle arrest and the onset of myogenesis (cyclin D3, p21, pRb and MyoD), as well as the distribution of cyclin D1 and p21 in the cdk4 complexes in mouse C2C12 myoblasts exposed to HGHI.
25158956	0.98	Cyclin B1, and Cyclin A, and an increase in the G1 marker, cyclin E, in response to treatment with a chemotherapeutic agent.
	0.97	Cyclin B1, Cdc2, and Cyclin A, the levels of which are up-regulated in G2 and mitosis.
27217483	0.98	Ccna2, 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).
	0.96	cyclin A2 and cyclin B1, and MafB. However, the requirement for PRLR signaling to induce expression of these factors and the physiologic significance of the gestational MafB+ beta-cell subpopulation are unknown.
19555225	0.98	cyclin A2 (Ccna2), cyclin B1 (Ccnb1), Cyclin B2 (Ccnb2), Chek1, Tnfrsf12a, Gadd45g, and Top2a, were also upregulated in O3-exposed ATTP-/- mice.
21352476	0.98	Ccna2, 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.
22735340	0.98	Cyclin A2 regulates the initiation and progression of DNA synthesis, and at the G2/M transition, it plays a critical role in triggering Cyclin B1-CDK1 activation.
23997793	0.98	cyclin a, cyclin b1, and cyclin e. Kdr and its coreceptor nrp-1, which are the main angiogenic receptors in the vegf pathway, are downregulated.
24269842	0.98	cyclin A2, cyclin B1, cyclin E1, Cdk1, and p53 (Fig. 5B).
23064266	0.97	cyclin A2) and M phase-specific proteins (cyclin B1 and phosphorylated-H3, P-H3) (Fig. 2f, g) and the appearance of numerous TGCs in metaphase and anaphase (Fig. 2h).
	0.96	cyclin A2-, cyclin B1- and P-H3-positive hepatocytes were significantly elevated in 2-month-old Alb-8ko mice and even more so in similarly aged Alb-78dko mice (Fig. 3g).
	0.71	cyclin A2, cyclin B1 and P-H3 expression levels, and ectopic karyokinesis (Fig. 2d, 2g and 2j; red bars).
23784826	0.97	cyclin A2, cyclin B1 and Cdk1, other cyclins and Cdks, originally thought to be essential for mitotic cell cycle regulation, are in fact largely dispensable.
	0.97	cyclin A2 could help initiate mitosis through its effects on cyclin B1.
	0.93	cyclin A2 and cyclin B1 resulted in early embryonic lethality, which argues that they are non-redundant.
23626729	0.97	Ccna2 and Ccnb1, indicating that the treatment induced hepatocyte proliferation as expected (Fig. 4B-D).
	0.93	Ccna2, Ccnb1, Mcm2 or Mki67, which were increased with TCPOBOP treatment (Table S2).
19771240	0.97	cyclin-A2 (CCNA-2), G2/M specific cyclin- B1(Cyclin-B1), G1 specific Cyclin-C (Cyclin-C), Cyclin dependent kinase-4 (Cdk4), Cyclin dependent kinase-7 (Cdk7), Mitogen activated protein kinase (MAP-K), c-Myb transcription factor and Ubiquitin-B (UB) were downregulated after blocking of c-kit expression in SGCs (Figure 3c).
23541922	0.97	cyclin B1 and cyclin A2.
23787781	0.97	CcnA2 and CcnB1 and marginal Rb phosphorylation, whereas PCNA was normally regulated in these animals (Fig. 4D).
26765561	0.97	Ccna2 and Ccnb1 transcription and expression of the equivalent proteins CDK1, CyclinA and CyclinB. Analysis of mRNA levels revealed that, in Rock1 / /Rock2 / cells, Cdk1 and Ccna2 mRNA levels were significantly reduced, whereas Cks1b mRNA remained unchanged (Figure 4D).
29074977	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).
30560875	0.97	cyclinA2, cyclinB1 and cyclinE1 were significantly higher in ASPP2+/- mice than in ASPP2+/+ mice at 12 hours after PHX (Fig. 2C).
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.
30770433	0.97	cyclin A2 may complement Ccnb1 for maintaining high CDK1 activity to initiate GVBD and block the AnaI onset in oocytes lacking Ccnb3.
24802190	0.96	cyclin B1 complexes are detected in cyclin A2null MEFs but not in the other genotypes.
	0.94	cyclin B1 (see Fig. S8A); however, elevated levels of Cdk1 were bound to cyclin B1 in cyclin A2null MEFs, but such an increase could not be detected in DKO MEFs (Fig. 5C).
	0.93	cyclin B1 complexes at low levels in cyclin A2null MEFs (Fig. S8C).
	0.93	cyclin B1-associated kinase activities were increased in cyclin A2null MEFs (Fig. 5A: lanes 8-14) but remained unchanged in Cdk2null (Fig. 5A: lanes 15-21) and DKO MEFs (Fig. 5A: lanes 22-28).
25822823	0.96	cyclin A, cyclin B1, cyclin D1, cyclin E, cyclin-dependent kinase 2 (Cdk2), and Cdk4.
	0.72	cyclin A, cyclin B1, cyclin D1, cyclin E, Cdk2, and Cdk4 were not changed after expression of 1N3R-tau when compared with expression of vector or 2N4R (Fig. 4).
20798132	0.96	cyclin B1 at the mRNA and protein levels without affecting the cyclin A or cdk2 protein levels.
20941357	0.96	cyclin B1, cyclin A2, and securin are inefficiently degraded in metaphase I; and anaphase I onset is markedly delayed.
21289097	0.96	Cyclin A, Cdc6, Cyclin B1) and inhibitors (e.g., Geminin, Mad2) of replication and mitotic progression.
27940445	0.96	Ccnb1 or other regulators of cell cycle such as, Ccna2 and Ccnd1 and a tendency of higher Cdkn1A levels in non-regenerating aged animals (Fig 3B).
24367005	0.95	Ccna2, 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).
	0.85	Cyclin A, Cyclin B1, and FoxM1 protein were similarly abundant at day 5 after immunization in both groups but expression of these proteins was maintained only in OT-I CD8 T cells from DC+CpG-immunized hosts at day 7 after immunization (Fig. 2 H).
21816347	0.95	cyclin A in the cytoplasm with cyclin B1, yet mouse cells genetically null for cyclin B1 arrest in G2 phase (B. Strauss, M. Zernicka-Goetz, and JP, unpublished results).
22253905	0.93	CyclinA was increased in a time-dependent manner, while gene expression levels of Cyclin B1 and CyclinD1 were increased up to day30 and then returned to the control level after day60.
	0.91	CyclinB1 and CyclinD1 gene expression increased up to day30 and then returned to control level after day60; Gadd45beta, CyclinA and PCNA increased all over the period; ERK1/2 was permanently activated.
21346194	0.92	Ccna, Ccnb1, and Ccnd1) (Wang et al.,; Lal et al.,), as well as the basic helix-loop-helix transcription factors MyoD and myogenin (Myod1 and Myog) (Figueroa et al.,), which are closely related to the proneural genes.
25975747	0.92	cyclin B1 (Ccnb1); mutS homolog 6 (Msh6); cyclin A2 (Ccna2); and cyclin B2 (Ccnb2), were expressed in the two types of mouse.
29074707	0.91	Cyclin B1 is essential in the earliest cell divisions and that from the four-cell stage onward, its function cannot be replaced by Cyclin A2 or B2.
	0.90	Cyclin B1 RNA or possibly by rising levels of Cyclin A2-Cdk activity.
	0.88	Cyclin A2 and Cyclin B2 can compensate for the absence of Cyclin B1.
21630154	0.91	Ccna2 gene resulted in early embryonic lethality, apparently around the peri-implantation stage, as did loss of function of the cyclin B1 gene.
30056207	0.90	Ccna2, Ccne1, Ccnb1, Cdk4, Cdkn1a, Ccnd2), members of the cytochrome P450 superfamily of genes (Cyp11a1, Cyp17a1, Cyp19a1, Cyp1a1, Cyp1b1), key genes involved in steroidogenesis (Hsd3b2, Hsd17b1, Star), or estrogen receptor genes (Esr1, Esr2) in the ovary.
	0.80	Ccna2, Ccne1, Ccnb1, Cdk4, Cdkn1a, or Ccnd2 in the ovary.
19381288	0.88	cyclin B1 in three out of seven independent cultures tested for each wild-type and NFAT5-/- T cells, whereas cyclin A2 was not affected in the majority of experiments (Fig. 4A and S5).
27371320	0.88	cyclins and observed that immunoprecipitates of Cdk1, Cdk2, cyclin A2, and cyclin E1 formed with comparable efficiency in the mutant and WT cells (Figure 1B).
21358637	0.55	cyclin B1, Cdk2/cyclin A, Cdk4/cyclin D1, and Cdk6/cyclin D1 (Fig. 4a and Supplementary Fig. 5).