Publication for Mcm2 and Mcm4

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Mcm2	minichromosome maintenance complex component 2	17216			[link]
mmu	Mcm4	minichromosome maintenance complex component 4	17217

Pubmed ID	Priority	Text
20838603	0.98	Mcm4Chaos3/Chaos3 mice, we hypothesize that in the context of Mcm2, 6 or 7 heterozygosity, which further reduces overall and chromatin-bound MCM levels below that already caused by Mcm4Chaos3 (measured to be <20% of WT mRNA levels for Mcm2), MCMs are reduced to a degree that compromises cell proliferation.
	0.98	MCM2 elimination during S phase is regulated, since in situations of decreased MCMs (as in the Mcm4Chaos3/Chaos3 mutant), there is decreased loss of nuclear MCM2 during S phase.
	0.97	MCM2 levels decrease as S-phase progresses, and moreso in WT than in Mcm4Chaos3/Chaos3 MEFs, is consistent with the dormant origin hypothesis.
	0.95	MCM2 and MCM4 were unaffected by hemizygosity of Mcm3 in Mcm4Chaos3/Chaos3 cells (Figure 7B).
	0.95	Mcm4Chaos3/Chaos3 Mcm2Gt/+ MEFs were reversed by Mcm3 heterozygosity, but levels of total MCM2 and MCM4 were not restored.
	0.95	MCM2 in S phase compared to Mcm4Chaos3/Chaos3 cells hemizygous for Mcm2 alone, despite overall reduced MCM2 levels in the cell (Figure 7B, left panel).
	0.94	Mcm4Chaos3/Chaos3, cells lacking 1 dose of Mcm2 had relatively lower levels of S phase MCM2 (DeltaS) compared to early G1.
	0.93	MCM2 from Mcm4Chaos3/Chaos3 cells is sufficient to produce greatly elevated cancer predisposition to the already-underrepresented survivors at wean.
	0.93	Mcm2 levels were genetically reduced by half, a condition causing the severe phenotypic effects described earlier, this caused a marked decrease in the level of chromatin-bound MCM3 and MCM4 (in addition to MCM2 itself), although total and nuclear MCM3/4 levels were affected to a lower degree or not at all.
	0.92	Mcm2, Mcm6 or Mcm7 in an Mcm4Chaos3/Chaos3 background causes partial synthetic lethality, severe growth defects and (for Mcm2) dramatically accelerated cancer onset
	0.92	Mcm2 hemizygosity decreases efficiency of reprogramming Mcm4Chaos3/Chaos3 MEFs into iPS cells, and Mcm3 hemizygosity significantly increases reprogramming efficiency.
	0.89	Mcm2 and Mcm3 led to corresponding decreases in the cognate mRNA levels (Figure 7C), with only minor additional decreases of other MCM mRNAs (beyond that already caused by homozygosity for Mcm4Chaos3) occuring in the context of Mcm2 hemizygosity (similar to Mcm2Gt/+ MEFs in Figure 2B).
	0.87	MCM2 levels in WT and Mcm4Chaos3/Chaos3 G1 nuclei were essentially the same (P = .65; t-test), mutant cells transitioned from G1 to S with 40% less nuclear MCM2 content than in WT (P<.02; t-test).
	0.84	Mcm4Chaos3/Chaos3 Mcm2Gt/+ MEFs had 45% the amount of Mcm2 mRNA as Mcm4Chaos3/Chaos3 cells (Figure 7C), which already had a 38% reduction compared to WT (Figure 1).
	0.84	MCM2-depleted mice were reported to have stem cell defects, and Mcm4Chaos3/Chaos3 Mcm#Gt/+ mice had clear developmental abnormalities, we examined the efficiency of reprogramming mutant MEFs into induced pluripotent stem cells (iPS).
	0.81	Mcm2, there was a striking and highly significant shortfall of Mcm4Chaos3/Chaos3 Mcm2Gt/+ offspring at birth (Figure 3A; Figure S2).
	0.78	Mcm4Chaos3 and Mcm2Gt that is related to MCM2 levels.
	0.75	Mcm4Chaos3/Chaos3 MEFs with or without the Mcm3Gt and/or Mcm2Gt alleles, and examined the effects of Mcm3 dosage on the levels of nuclear and chromatin-bound MCM2 and MCM4.
	0.75	Mcm4Chaos3/Chaos3 Mcm2Gt/+ mice, it is unclear whether the type of tumor is dictated primarily by the particular Mcm depletion (in this case MCM2, thus resembling Mcm2IRES-CreERT2/IRES-CreERT2 animals), the genetic background, or the age of particular cancer onset (if animals die of thymic lymphoma at an early age, they will be unable to manifest later-arising mammary tumors).
	0.57	Mcm4Chaos3/Chaos3 ; Mcm4Chaos3/Chaos3 Mcm2/6Gt/+ ; Mcm4Chaos3/Gt) by additional MCM3 reduction (Mcm3Gt/+).
21315719	0.98	Mcm2 and Mcm4 proteins in the adult mouse intestine (Figure 5A, B).
	0.97	Mcm2 and Mcm4 proteins in P7 mutants (Figure 4C), with a 20% reduction of chromatin bound Mcm2 in P15 mutants, as revealed by quantification of Western blot band intensity (Figure 5C).
	0.97	Mcm2 and Mcm4 and Elys in the adult mouse intestine.
	0.82	Mcm2 and Mcm4 were unchanged in P60 mutants (Figure 5D).
23133403	0.98	Mcm2 and Mcm4 hypomorphic mice.
	0.98	Mcm2IRES-CreERT2/IRES-CreERT2 and Mcm4chaos3/chaos3 mice harbor reductions in MCM levels detectable by Western analysis, which leads to a loss of backup origins that normally maintain genomic instability by firing during times of replicative stress.
	0.96	Mcm2 (Mcm2IRES-CreERT2) or Mcm4 (Mcm4chaos3) show reductions in MCM protein levels and develop tumors only in the homozygous state.
	0.84	Mcm2 (Mcm2IRES-CreERT2) or Mcm4 (Mcm4chaos3) hypomorphic alleles in which tumors were only observed in the homozygous state.
26658157	0.98	Mcm4, Mcm2), consistent with the increase in cycling HSCs observed in Fancb-/y mice.
	0.98	Mcm4 and Mcm2, (Fig. 5D, Upper) and Wnt/pluripotency genes, such as Wnt5a, Fzd8, Prkcb, Wnt3a, Wnt6 and Fzd5, are deregulated in Fancb-/y LSK cells (Fig. 5D, Lower).
	0.98	Mcm4, Mcm2) and HSC function (Wnt10a, Wnt16, Wnt3a, Fzd1, Fzd5, Fzd8, Prkcb) (Fig. 5).
22362746	0.98	Mcm2 or Mcm4 (Figure 5B), suggesting that this protein improves MCM2-7 function or formation, but that the disrupted interaction with MCM5 and/or XPO1 specifically obliterates the negative regulatory role of MCM3.
	0.93	Mcm2 or Mcm4 expression rescued the G2/M delay (Figure 5B and C), while expression of WT Mcm3 (or MCM3S5A) aggravated the G2/M arrest.
28641940	0.98	MCM4 is conserved in vertebrates, and several serine and threonine residues in this domain are phosphorylated by CDK, influencing biochemical properties of MCM2-7 helicase.
	0.97	MCM2, MCM3, MCM4, MCM5, MCM6 and MCM7 (thereafter called MCM2-7) are loaded onto DNA to license replication origins.
28827707	0.98	Mcm2 and Mcm4) are also involved in E2-induced uterine proliferation.
	0.54	Mcm2 and Mcm4 transcripts tended to be induced by E2 but not at significant levels.
31728285	0.98	MCM2, MCM4, MCM6, MCM8, MCM10, RFC4, RRM2, GINS1, FAAP100, RAN1, FANCA, FANCD2, FANCF, FANCI, FANCL) expression in SK-Hep1 (Figure S11a, Supporting Information).
	0.96	MCM2 (FC = 0.24 +- 0.006, p = 0.0014), MCM4 (FC = 0.25 +- 0.022, p = 0.0021), MCM6 (FC = 0.45 +- 0.014, p < 0.0001), MCM8 (FC = 0.37 +- 0.06, p = 0.0004), MCM10 (FC = 0.44 +- 0.06, p = 0.0014), RFC4 (FC = 0.35 +- 0.026, p = 0.0002), GINS1 (FC = 0.37 +- 0.06, p = 0.0001), and RRM2 (FC = 0.33 +- 0.072, p = 0.0018), were downregulated in SK-Hep1 treated with [4]helicenium (Figure 4c).
21957244	0.98	MCM2, together with MCM4, 6 and 7, forms the pre-replication complex, which is essential for the initiation of eukaryotic genome replication.
22046353	0.98	Mcm2, Mcm3, Mcm4, Mcm5, and Mcm7) are up-regulated in polyploid decidual cells (Table S3).
22904560	0.98	MCM2 or MCM4 have reduced levels of chromatin bound Mcm2-7, resulting in a reduction in the number of dormant origins.
30246716	0.98	mcm2, mcm3, mcm4, mcm5, mcm6, and mcm7), and proliferation cell nuclear antigen (PCNA) were significantly upregulated in ATF3-overexpressing CFs [Figure 3a].
21641805	0.97	MCM2 or MCM4 suggest that dormant origins play an important role in maintaining genetic stability.
	0.94	MCM2IRES-CreERT2 or MCM4Chaos3 mutations are cancer-prone.
	0.91	MCM2IRES-CreERT2 and MCM4Chaos3 mutant mice showed a dramatic increase in cancer (see below).
21611832	0.97	MCM2 and MCM4 compared to F1 and C3H wildtype cells (Fig. S3A).
31443434	0.96	Mcm2, Mcm3, Mcm4, Mcm5, Mcm6, Mcm7) and Origin Recognition Complex (ORC) family genes (Orc1, Orc2, Orc3, Orc4, Orc6) (Figure 5C) had the same expression trend as Cdk or Cdc family genes.
30787433	0.95	MCM2 and MCM4 (especially MCM4) in Chaos3 mutant genotypes, regardless of maternal genotype or whether the dams were NSAID-treated (Extended Data Fig. 2a-c).
	0.91	Mcm4C3/+ Mcm2Gt/+; Mcm4C3/+ Mcm2+/+; Mcm4C3/C3 Mcm2+/+) and the sex-biased lethal genotype (Mcm4C3/C3 Mcm2Gt/+; Extended Data Fig. 1), indicating that X-inactivation occurs normally.
19633410	0.93	MCM4 hypomorphic mutation and transgenic mice with lowered level of MCM2 develop mammary adenocarcinomas or lymphoma.
26876972	0.84	MCM4chaos mutation that impairs the stability of the MCM4 subunit, or an MCM2IRES-CreERT2 mutation that reduces the levels of MCM2, suffer from impaired proliferation, slow replication rates and genomic instability, comparable to trisomic and tetrasomic cell lines in this study.