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Bmi1 acts immediately downstream of CCAAT enhancer binding protein-alpha (show CEBPA Proteins) to regulate the survival and self-renewal of hematopoietic stem cells and contribute to the erythropoietic dysplasia.
Thus, VEGFA (show VEGFA Proteins) stimulates ovarian cancer stem-like cells through Src (show SRC Proteins)-DNMT3A (show DNMT3A Proteins)-driven miR (show MLXIP Proteins)-128-2 methylation and Bmi1 upregulation.
Loss of BMI1 enhanced ribonuclease activity of polynucleotide phosphorylase and reduced mtRNA stability
These findings uncover a previously unrecognized role for MUC1 (show MUC1 Proteins)-C in driving BMI1 expression and in directly interacting with this stem cell factor (show KITLG Proteins), linking MUC1 (show MUC1 Proteins)-C with function of the PRC1 (show PRC1 Proteins) in epigenetic gene silencing.
Results show that the expression of BMI1 is elevated in human HBV-related hepatocellular carcinoma tissues.
BMI1 is a downstream target of GSK3 signaling.
According to our data, significant elevation of the expression of miR (show MLXIP Proteins)-218 and downregulation of BMI1 were observed in clinical breast cancer specimens compared with normal tissues ( p < 0.0001).
MCM4 (show MCM4 Proteins) and MCM7 (show MCM7 Proteins) expression is significantly correlated with Ki-67 (show MKI67 Proteins), Bmi1, and cyclin E (show CCNE1 Proteins) expression in esophageal adenocarcinoma, squamous cell carcinoma and precancerous lesions.
newly identified miR (show MLXIP Proteins)-376c/BMI1 pathway provides an insight into cervical cancer progression
Molecular mechanism studies confirmed that Bmi-1 mediated these effects of miR (show MLXIP Proteins)-495 on MSCs. Taken together, our data demonstrated that miR (show MLXIP Proteins)-495 induced senescence of MSCs may be involved in the pathogenesis of pre-eclampsia (PE)
miR (show MLXIP Proteins)-139-5p expression also blocked self-renewal of bladder cancer stem cells by inhibiting Bmi1. In summary, our study supports that miR (show MLXIP Proteins)-139-5p acts as a tumor suppressor in bladder cancer development and suppresses cancer stem cell property of bladder cancer. Our study also suggests that miR (show MLXIP Proteins)-139-5p has the potential to be used as a therapeutic molecule for bladder cancer treatment.
The retinal phenotype of Bmi1(-/-) mice was characterized by loss of heterochromatin, activation of tandem repeats, oxidative stress and Rip3-associated necroptosis.
Inducible fate mapping demonstrates that BMI1 is expressed in vivo by multipotent Olfactory epithelium progenitors. expression of BMI1 and other Polycomb (show CBX2 Proteins) proteins not previously identified in olfactory basal cells are essential for self-renewal.
We conclude that silencing of Bmi1 by miR (show MLXIP Proteins)-27b relieves repression of the presynaptic transcriptome and supports neurotransmission in cortical networks.
a full complement of Bmi-1 is required for the intestinal proliferative effects of GLP-2 in both the physiological and pathological setting
Our work revealed that MOZ and BMI1 regulate HSCs in a synergistic manner by acting on distinct processes required to maintain HSCs.
Bmi-1 played a critical role in the protection from acute tubular necrosis by maintaining mobilization of renal stem cells and would be a novel therapeutic target for preventing the progression of ATN
Bmi1 deletion could substitute for Gata4 (show GATA4 Proteins) during iCM reprogramming. Thus, Bmi1 acts as a critical epigenetic barrier to iCM production. Bypassing this barrier simplifies iCM generation and increases yield, potentially streamlining iCM production for therapeutic purposes.
Cardiac Bmi1 progenitor cells respond to cardiac injury, contributing to the generation of de novo cardiomyocytes in the adult mouse heart.
Bmi1 is a potential driver oncogene (show RAB1A Proteins) of bladder cancer, and it may become a potential treatment target for human bladder cancer.
Component of a Polycomb group (PcG) multiprotein PRC1- like complex, a complex class required to maintain the transcriptionally repressive state of many genes, including Hox genes, throughout development. PcG PRC1 complex acts via chromatin remodeling and modification of histones\; it mediates monoubiquitination of histone H2A 'Lys-119', rendering chromatin heritably changed in its expressibility. In the PRC1 complex, it is required to stimulate the E3 ubiquitin-protein ligase activity of RNF2/RING2 (By similarity).
BMI1 polycomb ring finger oncogene
, B lymphoma Mo-MLV insertion region 1 homolog
, polycomb complex protein BMI-1-A
, polycomb group RING finger protein 4-A
, polycomb group ring finger 4
, murine leukemia viral (bmi-1) oncogene homolog
, polycomb complex protein BMI-1
, polycomb group RING finger protein 4
, polycomb group protein Bmi1
, ring finger protein 51
, B lymphoma Mo-MLV insertion region 1
, B lymphoma Mo-MLV insertion region