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Validated All-in-One™ qPCR Primer for BMI1(NM_005180.8) Search again
Product ID:
HQP017234
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
FLVI2/BMI1, PCGF4, RNF51, flvi-2/bmi-1
Gene Description:
BMI1 proto-oncogene, polycomb ring finger
Target Gene Accession:
NM_005180.8(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.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- The Bmi-1 oncogene induces telomerase activity and immortalizes human mammary epithelial cells.
- Bmi-1 extends the replicative life span of human fibroblasts by suppressing the p16-dependent senescence pathway
- BMI-1 binds the MLL repression domain. Recruitment of BMI-1 to the MLL protein may be able to modulate its function.
- E2a-Pbx1 and Bmi-1 are likely to play a role in the pathogenesis of human lymphoid leukemias through downregulation of the INK4A-ARF gene
- modulation of Bmi-1 protein might be involved in human colorectal carcinogenesis by repressing the INK4a/ARF proteins
- BMI-1 is transiently localized with the centromeric region in interphase.
- BMI1 overexpression is an alternative or additive mechanism in the pathogenesis of medulloblastomas
- Activation or overexpression of MAPKAP kinase 3pK resulted in phosphorylation of Bmi1 and other PcG members and their dissociation from chromatin
- Altered expression is associated with therapy failure and death in patients with multiple types of cancer.
- a subgroup of M0 patients has a high expression level of polycomb group gene BMI-1, which may contribute to leukemogenesis
- CALM-AF10+ T-ALL associatd with elevated expression of subset of HOXA genes and some of there transcriptional and functional regulators, as well as specific overexpression of oncogene BMI1
- EZH2 is essential for BMI1 recruitment to the polycomb bodies.
- Critical for the short-term survival of cancer cells, and inhibition has minimal effect on the survival of normal cells.
- p16(INK4a) expression was regulated by the Polycomb group repressor Bmi-1, which is shown as a direct transcriptional target of c-Myc.
- Bmi-1-Ring1B complex stabilizes the interaction of the ubiquitin ligase complex.
- Bmi1 is required for H2A ubiquitylation; H2A ubiquitylation regulates Bmi1-mediated gene expression
- BMI-1 is expressed in gastrointestinal stem cells and may have a role protein in cellular differentiation and stem cell maintenance
- bmi1 expression caused by oxidative stress may be involved in the pathogenesis of cellular senescence of biliary epithelial cells in primary biliary cirrhosis.
- Advanced cell- & animal imaging, expression profiling, stable siRNA-gene targeting, and TMAs of experimental and clinical samples indicate that activation of the BMI1 oncogene-associated PcG pathway plays an essential role in metastatic prostate cancer.
- Bmi-1 regulates the differentiation and clonogenic self-renewal of I-type neuroblastoma cells
- PcG protein BMI1 is associated with adverse pathological features and clinical PSA recurrence of prostate cancer.
- The oncogenic role of Bmi-1 in human primary breast carcinomas is not determined by its capacity to inhibit INK4a/ARF proteins(p16INK4a, p14ARF, or h-TERT) or to induce telomerase activity.
- Bmi1 overexpression was correlated with the malignant grades of human digestive precancerous tissues, which suggests that advanced Bmi1 dysregulation might predict malignant progression.
- ERK5 probably mediates HOXB9 expression by repressing BMI1 in Hodgkin lymphoma cell lines
- Bmi-1 and LMP1 down-regulate the ataxia telangiectasia-mutated (ATM) tumor suppressor and conclude that Bmi-1 contributes to LMP1-induced oncogenesis in Hodgkin lymphoma
- Our data suggest that Mel-18 regulates Bmi-1 expression during senescence via down-regulation of c-Myc.
- Our results provide new information on the roles of Bmi-1 and HPV-16 E6 in the multi-step process of oral epithelial carcinogenesis.
- The Bmi-1 may act through p16(INK4A)-independent pathways to regulate cellular proliferation during oral cancer progression.
- many human cell types undergo senescence by activation of the p16(INK4a)/Rb pathway, and that introduction of Bmi-1 can inhibit p16(INK4a) expression and extend the life span of human epithelial cells
- Study shows that the ability of the oncogene BMI1 to repress the INK4A-ARF locus requires its direct association and is dependent on the continued presence of the EZH2-containing Polycomb-Repressive Complex 2 complex.
- In a cohort of 64 CML patients, the level of BMI1 at diagnosis correlated with time to transformation to blast crisis, and the combination of low BMI1 and high proteinase-3 expression was associated with an improved overall survival
- These results suggest that Bmi-1 and Mel-18 may have overlapping functions in cancer cell growth.
- Bmi-1 seems to play a secondary role in chronic myeloid leukemia transformation
- Mel-18 and Bmi-1 may regulate the Akt pathway in breast cancer cells, and that Mel-18 functions as a tumor suppressor by repressing the expression of Bmi-1 and consequently down-regulating Akt activity.
- BMI1 is a target gene for SALL4 in leukemic cells.
- BMI-1 mediated repression of p16(ink4a) may contribute to an increased aggressive behavior of stem cell-like melanoma cells.
- Bmi-1 may promote maintenance of suprabasal keratinocyte survival to prevent premature death during differentiation.
- Elevated Bmi-1 is associated with breast cancer
- Bmi-1 could be a candidate biomarker for long-term survival in HCC
- Examination of various growth-regulatory pathways suggested that Bmi-1 overexpression together with H-Ras promotes human mammary epithelial cell transformation and breast oncogenesis by deregulation of multiple growth-regulatory pathways.
- BMI1 is an oncogenic candidate in a novel TCRB-associated chromosomal aberration in a patient with TCRgammadelta+ T-cell acute lymphoblastic leukemia
- BMI-1 antibody as a potential marker of nasopharyngeal carcinoma may be rational, and could have diagnostic and prognostic value.
- BMI1 is an intrinsic regulator of human stem/progenitor cell self-renewal.
- Bmi-1 expression associated with favorable overall survival only in estrogen receptor-positive breast cancer patients.
- loss of BMI-1 expression was associated with features of aggressive tumors. Low levels of BMI-1 expression were also significantly associated with decreased patient survival.
- Bmi-1 expression in non-small cell lung cancer (NSCLC) in respect to clinicopathological features and therapeutic outcomes
- Neither EGFR nor BMI-1 had significant prognostic impact for basal-like phenotype of breast cancer.
- BMI-1 is a novel independent prognostic marker in oligodendroglial tumours.
- study showed BMI-1 expression was inversely correlated with the differentiation grade of renal clear cell carcinoma; BMI-1 was strongly expressed in both papillary carcinomas and oncocytomas
- BMI1 gene is aberrant at the chromosomal level in a subset of gliomas, and possibly contributes to brain tumour pathogenesis
- Bmi-1 protein is highly expressed in ovarian epithelial cancer tissues, and its expression level correlates with histological grade and clinical phase of the patients.
- Bmi1 can induce multipotency in astrocytes.
- the results suggest that BMI1 does not play a significant prognosticator role ini astrocytic tumors
- Loss of BMI-1 seems to be associated with an aggressive phenotype in endometrial carcinomas.
- BMI-1 measured prior to allo-SCT can serve as a biomarker for predicting outcome in patients with CP-CML receiving allo-SCT
- overexpression associated with the malignant progression of hepatocellular carcinoma
- The relative expression of BMI1 in bladder tumor tissues is greater than 5 times that of nontumor samples and there is a statistically significant correlation between the level of BMI1 expression and the stage of the bladder tumors.
- BMI1 overexpression accompanied with 11q23 rearrangements is associated with acute myeloid leukemias.
- Overexpresion of BMI-1 is associated with ewing sarcoma tumorigenesis
- An important role for BMI1 in the maintenance of tumor-initiating side population cells in hepatocellular carcinoma.
- dysregulated BMI-1 could indeed lead to keratinocytes transformation and tumorigenesis, potentially through promoting cell cycle progression and increasing cell mobility.