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Bmi1 acts immediately downstream of CCAAT enhancer binding protein-alpha (show CEBPA ELISA Kits) to regulate the survival and self-renewal of hematopoietic stem cells and contribute to the erythropoietic dysplasia.
We found that BMI1 showed increased expression in hypoxic-cultured hUCB-MSCs, and the further knock-down of BMI1 in hypoxic cells induced decreased proliferative and immunomodulatory abilities in hUCB-MSCs, along with COX-2 (show COX2 ELISA Kits)/PGE2 down-regulation. More importantly, we identified BMI1 as a direct repressor of MAP kinase phosphatase-1 (MKP-1 (show DUSP1 ELISA Kits))/DUSP1 (show DUSP1 ELISA Kits), which suppresses p38 MAP kinase (show MAPK14 ELISA Kits) activity.
Collectively, the data establish a hitherto unknown liaison among MDR1, BMI1 and TIP60 (show KAT5 ELISA Kits) and provide mechanistic insights into cisplatin-induced MDR1 expression resulting in acquired cross-resistance against paclitaxel, doxorubicin and likely other anticancer drugs.
Thus, VEGFA (show VEGFA ELISA Kits) stimulates ovarian cancer stem-like cells through Src (show SRC ELISA Kits)-DNMT3A (show DNMT3A ELISA Kits)-driven miR (show MLXIP ELISA Kits)-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 ELISA Kits)-C in driving BMI1 expression and in directly interacting with this stem cell factor (show KITLG ELISA Kits), linking MUC1 (show MUC1 ELISA Kits)-C with function of the PRC1 (show PRC1 ELISA Kits) 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 (show GSK3b ELISA Kits) signaling.
According to our data, significant elevation of the expression of miR (show MLXIP ELISA Kits)-218 and downregulation of BMI1 were observed in clinical breast cancer specimens compared with normal tissues ( p < 0.0001).
MCM4 (show MCM4 ELISA Kits) and MCM7 (show MCM7 ELISA Kits) expression is significantly correlated with Ki-67 (show MKI67 ELISA Kits), Bmi1, and cyclin E (show CCNE1 ELISA Kits) expression in esophageal adenocarcinoma, squamous cell carcinoma and precancerous lesions.
newly identified miR (show MLXIP ELISA Kits)-376c/BMI1 pathway provides an insight into cervical cancer progression
KLF4 (show KLF4 ELISA Kits) modulates development of BMI1-expressing intestinal stem cell-derived lineage following gamma-radiation-induced gut (show GUSB ELISA Kits) injury in mice.
The retinal phenotype of Bmi1(-/-) mice was characterized by loss of heterochromatin, activation of tandem repeats, oxidative stress and Rip3 (show MPRIP ELISA Kits)-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 ELISA Kits) proteins not previously identified in olfactory basal cells are essential for self-renewal.
We conclude that silencing of Bmi1 by miR (show MLXIP ELISA Kits)-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 (show MYST3 ELISA Kits) 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 ELISA Kits) 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.
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).
B lymphoma Mo-MLV insertion region 1 homolog
, 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
, BMI1 polycomb ring finger oncogene
, B lymphoma Mo-MLV insertion region 1
, polycomb group ring finger 4
, polycomb complex protein BMI-1-A
, polycomb group RING finger protein 4-A
, B lymphoma Mo-MLV insertion region
, Polycomb group RING finger protein 4-B
, polycomb complex protein BMI-1-B
, polycomb group RING finger protein 4-B
, oncoprotein BMI-1