Publication for Mcm3 and Mcm4

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Mcm3	minichromosome maintenance complex component 3	17215			[link]
mmu	Mcm4	minichromosome maintenance complex component 4	17217

Pubmed ID	Priority	Text
31601942	0.98	MCM3 and MCM4 could be detected in WT and KO somites, respectively, suggesting that loss of CK2alpha affects MCM protein levels in vivo during early mouse development.
	0.93	MCM3 and MCM4 specific signal was strongly detected in the cell nucleus.
	0.80	MCM3 and MCM4, was investigated in tissues of WT and CK2alpha-knockout embryos i.e.: the hearts (Fig. 7b,c) and somites at E10.5 (Fig. 7d,e).
	0.79	MCM3 and MCM4 specific signal was strongly detected in the cell nucleus (Fig. 7d,e) while negative controls showed little background signal (Fig. S1b).
15598610	0.98	MCM3, MCM4, MCM5, ORC1, ORC6, RRM1, RRM2) and genes required for postreplicative phases of the cell division cycle (e.g., CCNB1, PLK1) are coordinately induced and reach maximal expression levels between 8 and 24 hr (Figure 6B), consistent with the timing of the histologic changes observed in Figure 6A.
21185283	0.98	Mcm3, Mcm4, Mcm5, Mcm7, Mcm8).
22046353	0.98	Mcm3, Mcm4, Mcm5, and Mcm7) are up-regulated in polyploid decidual cells (Table S3).
27828963	0.98	Mcm3 and Mcm4), Cdc6 and Brca2 (Fig 2A and S1 Table).
30246716	0.98	mcm3, mcm4, mcm5, mcm6, and mcm7), and proliferation cell nuclear antigen (PCNA) were significantly upregulated in ATF3-overexpressing CFs [Figure 3a].
30792348	0.98	MCM3, MCM4, MCM6, BIRC5, and other proteins previously associated with melanoma invasiveness and progression signatures in human patients (Fig. 5A).
20838603	0.97	MCM3 are proportionally reduced in Mcm4Chaos3/Chaos3 cells (Figure 1).
	0.96	MCM4 were unaffected by hemizygosity of Mcm3 in Mcm4Chaos3/Chaos3 cells (Figure 7B).
	0.95	Mcm3 delayed (or eliminated) the onset of mammary tumorigenesis in Mcm4Chaos3/Chaos3 females by ~4 or more months (Figure 6B).
	0.95	Mcm3 dose partially rescued the DeltaS value, indicating that these cells had ~16% more nuclear 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 Mcm2Gt/+ MEFs were reversed by Mcm3 heterozygosity, but levels of total MCM2 and MCM4 were not restored.
	0.93	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).
	0.92	Mcm4Chaos3 and Mcm2Gt alleles causes elevated GIN (micronuclei in RBCs), we considered the possibility that the Mcm3 rescue effect might be related to an attentuation of GIN.
	0.90	Mcm3 hemizygosity rescued viability of Mcm4Chaos3/Gt mice (Figure 5A), these animals were cancer prone with a shorter latency (by ~6 months) and different spectrum (primarily lymphomas) than Mcm4Chaos3 homozygotes.
	0.90	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.
	0.89	MCM3 relative to MCM4 and MCM2/6/7 have a dominant negative effect.
	0.87	Mcm4Chaos3/Chaos3 Mcm2Gt/+ MEF proliferation defects are partially rescued by Mcm3 hemizygosity.
	0.87	Mcm4Chaos3/Chaos3 MEFs into iPS cells, and Mcm3 hemizygosity significantly increases reprogramming efficiency.
	0.81	Mcm4Chaos3/Chaos3 and Mcm4Chaos3/Chaos3 Mcm2Gt/+ mice by reducing Mcm3 genetic dosage
	0.74	Mcm3 by 50% increased iPS formation from both Mcm4Chaos3/Chaos3and Mcm4Chaos3/Chaos3 Mcm2Gt/+ MEFs by ~2.5 and 10 fold, respectively.
	0.71	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.
	0.64	Mcm4Chaos3/Chaos3 Mcm2Gt/+ mice, Mcm3Gt heterozygosity significantly rescued their viability to 72.5% from 29.7% (Figure 5A and Fig S3).
	0.63	Mcm3, which alone had no effect on CD71 ratios of Chaos3 mice, corrected completely this abnormal phenotype in Mcm4Chaos3/Chaos3 Mcm2Gt/+animals (Figure 5E).
	0.61	Mcm3 hemizygosity also significantly rescued the near 100% lethality of Mcm4Chaos3/Gt animals (nearly 6 fold increased viability), and doubled the viability of Mcm4Chaos3/Chaos3 Mcm6Gt/+ mice (Figure 5A; Figure S3).
	0.61	Mcm4Chaos3/Chaos3 ; Mcm4Chaos3/Chaos3 Mcm2/6Gt/+ ; Mcm4Chaos3/Gt) by additional MCM3 reduction (Mcm3Gt/+).
22362746	0.97	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.
	0.92	MCM3 reduction applies to the circumstance of overall MCM2-7 depletion, rather than any specific structural defects in the MCM2-7 helicase caused by the Mcm4Chaos3 allele, such as that resulting in the intra-hexamer instability.
	0.92	Mcm4 expression rescued the G2/M delay (Figure 5B and C), while expression of WT Mcm3 (or MCM3S5A) aggravated the G2/M arrest.
22158038	0.97	Mcm3 levels have been shown to partially rescue the cancer phenotype of mice carrying the Mcm4 mutant allele Chaos3.
28641940	0.97	MCM3, MCM4, MCM5, MCM6 and MCM7 (thereafter called MCM2-7) are loaded onto DNA to license replication origins.
31443434	0.96	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	0.87	Mcm3 heterozygosity also increased viability of Mcm4C3/C3 Mcm2Gt/+ newborns from 30% to 72%, but both sexes were rescued approximately proportionately (Fig. 1a; Table S3); preferential female rescue may be related to overall degree of lethality in compound mutants (93%, 82% and 70% lethality for Mcm4C3/Gt , Mcm4C3/C3 Mcm6Gt/+ and Mcm4C3/C3 Mcm2Gt/+, respectively) .