Publication for Foxm1 and Mki67

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Foxm1	forkhead box M1	14235			[link]
mmu	Mki67	antigen identified by monoclonal antibody Ki 67	17345

Pubmed ID	Priority	Text
29208957	0.98	Foxm1 and its target genes as well as that of the Mki67 gene in islets, thereby enhancing beta-cell proliferation during obesity development.
	0.98	FoxM1 target gene and Mki67 gene expression levels in murine islets, with increases similar to those produced by CPVG treatment (Supplementary Fig. 4c).
	0.97	Foxm1 and its target genes as well as that of the Mki67 gene in islets and induces beta-cell proliferation via vagal nerves.
	0.97	Foxm1 and its target genes as well as Mki67 in islets were upregulated (Supplementary Fig. 1c) in ob/ob mice.
	0.97	Foxm1 and its target genes, as well as that of Mki67, in islets of ob/ob mice (Fig. 2a).
	0.97	Foxm1, Cdk1, Ccna2, and Plk1 as well as that of Mki67 were observed in islets of wild-type control mice after the HFD loading (Supplementary Fig. 3a).
	0.97	FoxM1 target genes and that of the Mki67 gene in a fashion similar to that observed with CPVG (Supplementary Fig. 4a).
	0.97	FoxM1 target genes and the Mki67 gene were markedly blunted in CP-treated islets isolated from these mice (Fig. 4f).
	0.97	FoxM1 and its target genes as well as that of the Mki67 gene were observed as early as only 1 week after HFD loading (Supplementary Fig. 3a, b) when obesity had not yet become evident.
	0.97	FoxM1 deficiency completely suppressed HFD-induced upregulations of both cell cycle-related genes and the Mki67 gene (Supplementary Fig. 3c).
	0.96	Foxm1, its target genes, and that of Mki67 (Fig. 2c).
	0.91	FoxM1 target genes and that of the Mki67 gene in islets.
	0.59	FoxM1 target genes or that of the Mki67 gene, indicating a minimal role of GRP.
30546054	0.98	Foxm1 and cell cycle-related genes downstream from FoxM1, such as Cdk1, Ccna2, and Plk1, as well as a cell proliferation marker, Mki67, by several dozen to 100-fold on postoperative days 2 and 3 (Fig. 2a and Supplementary Fig. 1g).
	0.98	Foxm1 and its target genes, as well as Mki67 after PHx were significantly blocked by atropine treatment (Fig. 4c).
	0.98	Foxm1, its target genes, and Mki67 (Fig. 7a).
	0.97	Foxm1 and its target cell cycle-related genes, as well as Mki67 on day 2 after PHx were markedly suppressed in anti-IL-6 antibody-treated mice (Fig. 7c).
	0.95	FoxM1 and its target genes as well as Mki67 (Supplementary Fig. 5b).
	0.92	Foxm1 and Mki67 gene expressions in the cultured hepatocytes (Supplementary Fig. 4a).
	0.75	FoxM1 or its target genes, nor that of Mki67 (Supplementary Fig. 3b).
32092075	0.98	marker of proliferation Ki-67 (Mki67), and forkhead box M 1 (Foxm1) (Fig 7I), which are critical cell cycle regulators for beta cell proliferation.
22885335	0.97	Ki-67 antigen and phosphorylated histone H3 (PH3) was reduced (Fig. 1C-D), and total numbers of epithelial cells undergoing the cell cycle were significantly decreased in CCSP-Foxm1-/- airways compared to the bronchiolar epithelium of control mice (Fig. 1F-G).
	0.87	Ki-67-positive Clara cells was reduced in CCSP-Foxm1-/- mice compared to controls (F and J).
	0.76	Foxm1 (E), Ki-67 (F) and PH3 (G) in CCSP-Foxm1-/- bronchioles (Br).
24853430	0.97	FoxM1 hepatocyte expansion was induced by the activation of pathway relative to Ki67 and PCNA, but not Cyclin D1.
	0.94	FoxM1 enhanced hepatocyte proliferation during liver repopulation was through both PCNA and Ki67 involved signaling pathway, but not cyclin D1 involved one.
	0.60	Ki67+ cells in total FoxM1+ hepatocytes were significantly higher than those in WT hepatocytes after 30 h of culture.
20816795	0.97	Ki-67 expression was observed in airway regions expressing FoxM1-DeltaN (Fig. 8D and 8F) and CCSP protein (Fig. 8H).
	0.94	FoxM1-DeltaN (C-D), Ki-67 (E-F) and CCSP (G-H) showed expression of these proteins in hyperplastic airway regions of Dox-treated epFoxM1 mice (arrows).
19835856	0.94	Foxm1fl/fl and smMHC-Cre-GFPtg/- embryos, Ki-67 positive cells were readily detected in endothelial and smooth muscle layers of the developing aorta, as well as in all layers of the developing esophagus (Fig. 6A).
29642003	0.93	Ki-67- and FOXM1-positive cells in myoFoxf1 KO lungs (Figure 4C).
28011860	0.92	FoxM1 (F) and Id1 (I) overexpression and Jnk3 inhibitor (Ji) treatment were able to increase CM proliferation as measured by the alpha-MHC+/Ki67+ population (Fig 3C).
31072351	0.92	FOXM1 + sh-KIF4A than in FOXM1 + sh-Control mice (Fig. 6b, c), and FOXM1 + sh-KIF4A xenografts expressed lower levels of KIF4A as well as the proliferation marker Ki67 (Fig. 6e), as determined by immunohistochemistry and western blotting (Fig. 6d).
29740591	0.88	Ki67, Aurkb), pro-proliferation markers (Bub1, Cdk1, Foxm1, Nrg1) and decreased expression of proliferation inhibitors (Nox4, Sfrp).
19887554	0.80	Ki67 staining (marker for proliferation) showed a significant 39% and 38% reduction in tumors treated with JWH-133 and WIN-55,212-2, respectively, relative to control tumors (Fig. 3D).
23144938	0.77	FOXM1 protein and mRNA in juvenile cardiomyocytes, there was no difference in the percentage of Ki-67-positive cells at P7 (Figure 1D & I).
	0.70	Foxm1 mRNA and protein at P7, there was no change in the percentage of Ki-67-positive cardiomyocytes in alphaMHC-Cre/Foxm1fl/fl hearts.
26251404	0.60	FoxM1HI endocrine cells expressed the proliferation marker Ki67 (Fig. 7G), as did all FoxM1-expressing acinar cells (Fig. 7H).