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抗Human FOXM1 抗体:
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抗Mouse (Murine) FOXM1 抗体:
Human Polyclonal FOXM1 Primary Antibody for ChIP, ICC - ABIN441006
Zhao, Siu, Jiang, Tam, Ngan, Le, Wong, Wong, Gomes, Bella, Khongkow, Lam, Cheung: Overexpression of forkhead box protein M1 (FOXM1) in ovarian cancer correlates with poor patient survival and contributes to paclitaxel resistance. in PLoS ONE 2014
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Dog (Canine) Polyclonal FOXM1 Primary Antibody for WB - ABIN2781166
Laoukili, Alvarez, Meijer, Stahl, Mohammed, Kleij, Heck, Medema: Activation of FoxM1 during G2 requires cyclin A/Cdk-dependent relief of autorepression by the FoxM1 N-terminal domain. in Molecular and cellular biology 2008
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Human Polyclonal FOXM1 Primary Antibody for IF (p), IHC (p) - ABIN749138
Liu, Zhang, Mao, Zhang, Zhang: Over-expression of FoxM1 is associated with adverse prognosis and FLT3-ITD in acute myeloid leukemia. in Biochemical and biophysical research communications 2014
The tumour suppressive roles of miR8765p overexpression in GBM cells were significantly reversed by FOXM1 reintroduction.
Data show that forkhead box protein M1 (FoxM1) enhanced carboplatin resistance in Y-79CR cells through directly up-regulating the transcription of ATP-binding cassette transporter C4 (ABCC4).
FoxM1 repression during human aging leads to mitotic decline and aneuploidy-driven full senescence.
TBX2 is a neuroblastoma core regulatory circuitry component enhancing MYCN/FOXM1 reactivation of DREAM targets.
Studies indicate that the oncogene forkhead box protein M1 (FoxM1) has emerged as an important molecule implicated in initiation, development and progression of cancer [Review].
These findings revealed the role of forkhead box M1 upregulation by manganese superoxide dismutase overexpression in maintaining lung cancer stem-like cell properties. Therefore, inhibition of forkhead box M1 upregulation by manganese superoxide dismutase overexpression may represent an effective therapeutic strategy for non-small cell lung cancer.
FoxM1 silenced cell induces G2/M cell cycle arrest and necrosis.
High FOXM1 expression is associated with invasion of renal cancer.
Analyses with phospho-defective and phospho-mimetic mutants of FoxM1b identified a critical role of the Plk1 phosphorylation sites in regulating the binding of FoxM1b to Rb and DNMT3b.
Study found that DLX1 was the direct target of FoxM1 in HCC. Downregulation of FoxM1 inhibits the proliferation, migration, and invasion of HCC cells by miR-214.
A significant over expression of forkhead box protein M1 (FOXM1), polo-like kinase 1 (PLK1) and centrosomal protein 55 (CEP55) was observed in tumor samples compared to adjacent and normal bladder tissues, suggesting they may be potential candidate's biomarkers for early diagnosis and targets for cancer therapy.
In conclusion, our findings indicated that FOXM1 was highly expressed in lung cancer cells after exposure to ionizing radiation (IR). We also found that FOXM1 promoted radioresistance, invasion, migration, and EMT of lung cancer cells after IR, partly through upregulating KIF20A.
The concurrent overexpression of FoxM1 and FoxP3 was evident in gastric cancer and inversely correlated with patient survival.
A better understanding of the mechanisms regulating the FOXO3-FOXM1 axis, as well as their downstream transcriptional targets and functions, may render these proteins reliable and early diagnostic/prognostic factors as well as crucial therapeutic targets for cancer treatment and importantly, for overcoming chemotherapeutic drug resistance.
CRNDE overexpression accelerated lipopolysaccharide-induced apoptosis and inflammation via up-regulation of FOXM1 in WI-38 cells.
In male breast cancer patients high forkhead box protein M1 (FOXM) expression is significantly associated with disease free survival (DFS). Median progression free survival under chemotherapy or Tamoxifen hormone therapy is shorter for the High FOXM1 expression group. High FOXM1 expression is significantly associated with chemotherapy and endocrine resistance.
High FoxM1 expression is associated with the development of prostate cancer.
FOXM1 promotes proliferation in human hepatocellular carcinoma cells by transcriptional activation of CCNB1.
Upregulation of FOXM1 in a subset of relapsed myeloma results in poor outcome.
We first reported that the FOMX1 pathway is the most upregulated and the PPARalpha pathway is the most downregulated pathway in Triple Negative Breast Cancers (TNBCs). These two pathways could be simultaneously targeted in further studies. Also the pathway classifier we performed in this study provided insight into the TNBC heterogeneity.
Vagal signals activate the forkhead box M1 (FoxM1) pathway in beta-cells, resulting in compensatory beta-cell proliferation. Inducible beta-cell-specific FoxM1 deficiency also blocks compensatory beta-cell proliferation.
Disrupting LXRalpha phosphorylation promotes FoxM1 expression and modulates atherosclerosis by inducing macrophage proliferation
Upregulated ROS induced by FABP4 was of significance in activating FoxM1 leading to airway inflammation and epithelial barrier dysfunction.
Interactions between the Wnt/beta-catenin and the Kras/ERK/Foxm1 pathways are essential to restrict SOX9 expression in basal cells during pulmonary branching morphogenesis
YAP cooperates with FOXM1 to contribute to chromosome instability in hepatocellular carcinoma.
RCM-1 blocked the nuclear localization and increased the proteasomal degradation of Forkhead box M1 (FOXM1), a transcription factor critical for the differentiation of goblet cells from airway progenitor cells.
These data implicate the insulin-FoxM1/PLK1/CENP-A pathway-regulated mitotic cell-cycle progression as an essential component in the beta cell adaptation to delay and/or prevent progression to diabetes.
EGF promotes FoxM1 expression through the ERK signal pathway
FoxM1 induction in the pulmonary vasculature was inhibited by a p110gamma-selective inhibitor and in Pik3cg(-/-) mice after LPS challenge. Defective vascular repair in Pik3cg-/- mice results from impaired FoxM1 expression
we suggest that proper regional decidualization and polyploidy development requires FoxM1 signaling downstream of Hoxa10 and cyclin D3.
FOXM1 and CENPF are master regulators of prostate cancer malignancy, and can serve as drug response markers for antineoplastic drugs efficiency.
Both gain-of-function and loss-of-function TP53 mutations contribute to overexpression of FoxM1 in high-grade serous ovarian cancer.
MicroRNA-802 suppresses breast cancer proliferation through down-regulation of FoxM1.
FoxM1 expression correlates with proliferation, invasion and migration in mouse hepatocellular carcinoma cell lines.
null mice have reductions in both the somatotrope and gonadotrope cell populations.
activated FoxM1 increases beta-cell replication while simultaneously enhancing insulin secretion and improving glucose homeostasis, making FoxM1 an attractive therapeutic target for diabetes.
Data indicate transcription factor Foxm1 as a critical regulator of the quiescence and self-renewal of hematopoietic stem cells (HSCs).
SPDEF inhibits prostate carcinogenesis by disrupting a positive feedback loop in regulation of the Foxm1 oncogene.
FoxM1 might play an important role during the process of mouse embryo implantation.
Foxm1 influences pulmonary inflammatory responses to hyperoxia, inhibiting neutrophil-derived enzymes and enhancing monocytic responses that limit alveolar injury and remodeling in neonatal lungs.
the sequence and expression pattern of FoxM1 (fork head box M1) transcription factor in Xenopus laevis embryos are described
Results suggest that FoxM1 functions to link cell division and neuronal differentiation in early Xenopus embryos.
The protein encoded by this gene is a transcriptional activator involved in cell proliferation. The encoded protein is phosphorylated in M phase and regulates the expression of several cell cycle genes, such as cyclin B1 and cyclin D1. Several transcript variants encoding different isoforms have been found for this gene.
Forkhead, drosophila, homolog-like 16
, HNF-3/fork-head homolog 11
, M-phase phosphoprotein 2
, MPM-2 reactive phosphoprotein 2
, forkhead box protein M1
, forkhead-related protein FKHL16
, hepatocyte nuclear factor 3 forkhead homolog 11
, transcription factor Trident
, winged-helix factor from INS-1 cells
, INS-1 winged helix
, forkhead box M1
, forkhead box protein M1-like
, forkhead homolog 16
, winged-helix transcription factor Trident