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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 09 Dec 2014.

BMI1 polycomb ring finger oncogene

Top mentioned proteins: Polycomb, CAN, p16, EZH2, c-Myc
Papers using Bmi-1 antibodies
The Polycomb group protein EZH2 impairs DNA repair in breast epithelial cells
Hendzel Michael J. et al., In The Journal of Cell Biology, 2004
... Control and one of two different BMI1 shRNA plasmids were obtained from OriGene.
Papers on Bmi-1
SMURF1 silencing diminishes a CD44-high cancer stem cell-like population in head and neck squamous cell carcinoma.
Dickerson et al., In Mol Cancer, 03 Jan 2015
RESULTS: Populations of enriched CSC-like cells displayed decreased levels of pSMAD1/5/8 and BMP signaling target gene ID1 while SMURF1, CD44, and BMI1 were highly expressed when compared to non-CSC populations.
miR-203 inhibits melanoma invasion and stemness by targeting the polycomb group gene BMI1.
Lian et al., Beijing, China. In Biochem Biophys Res Commun, 02 Jan 2015
In this study, we revealed a miR-203-BMI1 axis that regulated melanoma metastasis.
209 cloned embryonic development and gene expression of spontaneously immortalized porcine skin fibroblasts.
Lee et al., Seoul, South Korea. In Reprod Fertil Dev, 31 Dec 2014
The BMI1 gene has been used to immortalize human and murine somatic cells, and we confirmed that BMI1 increased cell-life span of porcine skin fibroblasts and had no detrimental effect on pre-implantational development after somatic-cell nuclear transfer (SCNT; unpublished data).
Global histone H3 lysine 27 triple methylation levels are reduced in vessels with advanced atherosclerotic plaques.
van den Elsen et al., Leiden, Netherlands. In Life Sci, 01 Dec 2014
MATERIALS AND METHODS: 28 peri-renal aortic tissue patches covering the entire spectrum of atherosclerotic plaque development were evaluated by immunohistochemistry for the levels of H3K27Me3, EZH2, JMJD3 and BMI1.
The Notch Delta-4 ligand helps to maintain the quiescence and the short-term reconstitutive potential of haematopoietic progenitor cells through activation of a key gene network.
Lauret et al., Paris, France. In Stem Cell Res, 13 Nov 2014
Both effects are directly correlated with the decrease of cell cycle genes transcription such as CYCLIN-D1, -D2, and -D3, and the upregulation of stemness related genes transcription such as BMI1, GATA2, HOXB4 and C-MYC.
A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer.
Zhang et al., Philadelphia, United States. In Cancer Cell, Oct 2014
FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A.
FAL1ing inside an amplicon.
Huarte et al., Pamplona, Spain. In Cancer Cell, Oct 2014
FAL1 acts as an oncogene by stabilizing BMI1, which results in the repression of CDKN1A expression.
Expandable megakaryocyte cell lines enable clinically applicable generation of platelets from human induced pluripotent stem cells.
Eto et al., Kyoto, Japan. In Cell Stem Cell, May 2014
This approach involves the establishment of stable immortalized megakaryocyte progenitor cell lines (imMKCLs) from PSC-derived hematopoietic progenitors through the overexpression of BMI1 and BCL-XL to respectively suppress senescence and apoptosis and the constrained overexpression of c-MYC to promote proliferation.
Self-renewal as a therapeutic target in human colorectal cancer.
O'Brien et al., Toronto, Canada. In Nat Med, Jan 2014
Here we demonstrate that tumor formation and, more specifically, human colorectal CIC function are dependent on the canonical self-renewal regulator BMI-1.
The role of BMI1 as a biomarker of cancer stem cells in head and neck cancer: a review.
Puzzo et al., Catanzaro, Italy. In Oncology, Dec 2013
Emerging studies show that BMI1 (B cell-specific Moloney murine leukemia virus integration site 1) has an important function as a biomarker of cancer stem cells (CSCs), i.e. cells with self-renewal characteristics, capable of tumor initiation, progression, invasion, metastasis, tumor recurrence and resistance to chemotherapy and radiotherapy.
Genetic Modeling of PIM Proteins in Cancer: Proviral Tagging and Cooperation with Oncogenes, Tumor Suppressor Genes, and Carcinogens.
Blanco-Aparicio et al., Madrid, Spain. In Front Oncol, Dec 2013
The use of retroviral insertional mutagenesis and refined approaches such as complementation tagging has allowed the identification of myc, pim, and a third group of genes (including bmi1 and gfi1) as complementing genes in lymphomagenesis.
Relevance of cancer initiating/stem cells in carcinogenesis and therapy resistance in oral cancer.
Bhutia et al., India. In Oral Oncol, Sep 2013
Oral CSCs populations show upregulation of the stem cell related genes Oct-4, Nanog, Nestin, CK19, BMI-1, CD117 (c-kit), CD44 and CD133 with sunken expression of involucrin and CK13.
Unraveling tumor suppressor networks with in vivo RNAi.
Hemann et al., Cambridge, United States. In Cell Stem Cell, Jul 2013
BMI1 is a known oncogenic transcriptional repressor in glioblastoma stem-like cells, but its downstream mediators are poorly understood.
What is the clinical value of cancer stem cell markers in gliomas?
Kristensen et al., Odense, Denmark. In Int J Clin Exp Pathol, 2012
Using the Pubmed database, twenty-seven CSC studies looking at membrane markers (CD133, podoplanin, CD15, and A2B5), filament markers (nestin), RNA-binding proteins (Musashi-1) and transcription factors (BMI1, SOX2, Id1 and Oct-4) qualified for this review.
Mechanism and method for generating tumor-free iPS cells using intronic microRNA miR-302 induction.
Ying et al., Santa Fe Springs, United States. In Methods Mol Biol, 2012
Additionally, miR-302 also silenced BMI-1, a cancer stem cell marker gene, to promote the expression of two senescence-associated tumor suppressor genes, p16Ink4a and p14/p19Arf.
Bmi1 is required for regeneration of the exocrine pancreas in mice.
Hebrok et al., San Francisco, United States. In Gastroenterology, 2012
Bmi1 contributes to regeneration of the exocrine pancreas after cerulein-induced injury through cell autonomous mechanisms, in part by regulating Cdkn2a expression, and non-cell autonomous mechanisms.
Prognostic relevance of c-Myc and BMI1 expression in patients with glioblastoma.
Larocca et al., Roma, Italy. In Am J Clin Pathol, 2012
We found that overexpression of c-Myc was significantly associated with that of BMI1, and that patients who harbored glioblastomas overexpressing c-Myc and BMI1 showed significantly longer overall survival.
Bmi1 facilitates primitive endoderm formation by stabilizing Gata6 during early mouse development.
Azuara et al., London, United Kingdom. In Genes Dev, 2012
Bmi1 overlaps with the nascent Gata6 and Nanog protein from the eight-cell stage onward before it preferentially cosegregates with Gata6 in primitive endoderm progenitors
Bmi1 confers resistance to oxidative stress on hematopoietic stem cells.
Iwama et al., Chiba, Japan. In Plos One, 2011
overexpression of Bmi1 confers resistance to stresses, particularly oxidative stress, onto hematopoietic stem cells. This enhances their regenerative capacity and suggests that Bmi1 is located downstream of ROS signaling and negatively regulated by it.
Bmi-1 siRNA inhibited ovarian cancer cell line growth and decreased telomerase activity.
Jin et al., Harbin, China. In Br J Biomed Sci, 2011
Bmi-1 siRNA has a role in inhibiting ovarian cancer cell line growth and decreasing telomerase activity
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