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Validated All-in-One™ qPCR Primer for FOXM1(NM_202002.3) Search again
Product ID:
HQP153911
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
FKHL16, FOXM1A, FOXM1B, FOXM1C, HFH-11, HFH11, HNF-3, INS-1, MPHOSPH2, MPP-2, MPP2, PIG29, TRIDENT
Gene Description:
forkhead box M1
Target Gene Accession:
NM_202002.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- hepatocyte nuclear translocation of the FoxM1B transgene protein was rapidly induced during the hepatic acute phase response
- Data show that forkhead box M1B (FoxM1B) transcriptional activity requires binding of Cdk-cyclin complexes to mediate efficient Cdk phosphorylation of the FoxM1B Thr 596 residue, which is essential for recruitment of p300/CBP coactivator proteins.
- Expression of FoxM1 is significantly elevated in primary breast cancer and microarray analysis shows that FoxM1 regulates genes that are essential for faithful chromosome segregation and mitosis.
- FoxM1 regulates transcription of cell cycle genes critical for progression into S-phase and mitosis.
- Foxm1-depleted A549 cells exhibit reduced expression of cell cycle-promoting cyclin A2 and cyclin B1 genes. These data show that Foxm1 stimulates the proliferation of tumor cells during progression of NSCLC.
- Cyclin-dependent kinases regulate the transcriptional activity of FOXM1c; a combination of three phosphorylation sites mediates the Cyclin E and Cyclin A/CDK2 effects.
- FoxM1 regulates the expression of Skp2 protein, which is known to promote degradation of the cell cycle regulator p27; results showed that FoxM1 is overexpressed in human glioblastomas and contributes to glioma tumorigenicity.
- Increased expression of SHh mRNA in human colonic adenocarcinomas and in a colorectal cell line with downstream increased expression of FOXM1 mRNA known to promote cell proliferation.
- FoxM1 and FoxO3a cooperate to regulate ERalpha gene transcription
- cyclin D1/Cdk4 converts FOXM1c from an almost inactive form into a strong transactivator in G1-phase, i.e., just at the time point at which the transcriptional activity of FOXM1 is required for stimulation of the G1/S-transition
- Human FoxM1 nkockout mousse lungs demonstrated impaired cell proliferation in association with sustained expression of p27(Kip1) and decreased expression of cyclin B1 and Cdc25C.
- interference with FoxM1 activity may contribute to the increase in mitotic errors seen in human diseases such as cancer and early onset of ageing diseases[review]
- These results identify a novel role for FoxM1 in the transcriptional response during DNA damage/checkpoint signaling and show a novel mechanism by which Chk2 protein regulates expression of DNA repair enzymes.
- FoxM1 down-regulation could be a novel approach for the inhibition of pancreatic tumor progression.
- Data show FoxM1 regulates growth factor-induced expression of kinase-interacting stathmin (KIS) to promote cell cycle progression.
- FOXM1 regulates genes that control G1/S-transition, S-phase progression, G2/M-transition and M-phase progression--{REVIEW}
- We found a positive correlation between FOXM1 expression and HER2 status, pointing to a potential role of FOXM1 as a new drug target in HER2 resistant breast tumour, as FOXM1 inhibitors for cancer treatment were described recently.
- FoxM1 is inactive in the G(1)/S transition through the action of the N-terminal autorepressor domain, while phosphorylation by cyclin A/cdk complexes in G(2) results in relief of inhibition by N terminus, activating FoxM1-mediated gene transcription.
- Whereas FOXM1 expression is extinguished in terminally differentiated cells, it has been found to be upregulated and/or required in a number of different cancers [commentary]
- TIS21 negatively regulated hepatocarcinogenesis in part by disruption of the FoxM1-cyclin B1 regulatory loop, thereby inhibiting proliferation of transformed cells developed in mouse and human livers.
- JNK1 is a critical transcriptional target of FoxM1 that contributes to FoxM1-regulated cell cycle progression, tumor cell migration, invasiveness, and anchorage-independent growth
- FoxM1 is one of the targets of Cdh1 in late M or early G(1) phase and that its proteolysis is important for regulated entry into S phase.
- Cdh1-dependent degradation of FoxM1 is required to shut down transcriptional activation of mitotic regulators during exit from mitosis.
- findings provide both clinical and mechanistic evidence that FoxM1 contributes to glioma progression by enhancing VEGF gene transcription and thus tumor angiogenesis
- HIF-1alpha directly bound to the promoter of FoxM1
- Plk1-dependent regulation of FoxM1 activity provides a positive-feedback loop ensuring tight regulation of transcriptional networks essential for orderly mitotic progression.