Anti-BMI1 Antibody, Rabbit Polyclonal (Rabbit Polyclonal antibody) General Information
Anti-BMI1 Antibody, Rabbit Polyclonal
Reacts with: Human Predicted to React with:
Mouse (Species predicted to react based on 100% sequence homology)
A synthetic peptide corresponding to the C-terminus of the Human BMI1
Produced in rabbits immunized with a synthetic peptide corresponding to the C-terminus of the Human BMI1, and purified by antigen affinity chromatography.
Polyclonal Rabbit IgG
Protein A & Antigen Affinity
0.2 μm filtered solution in PBS
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.
Immunofluorescence staining of BMI1 in HepG2 cells. Cells were fixed with 4% PFA, permeabilzed with 0.3% Triton X-100 in PBS,blocked with 10% serum, and incubated with rabbit anti-human BMI1 polyclonal antibody (1:1000) at 4℃ overnight. Then cells were stained with the Alexa Fluor®594-conjugated Goat Anti-rabbit IgG secondary antibody (red).Positive staining was localized to cytoplasm and nucleus.
Immunochemical staining of human BMI1 in human skeletal muscle with rabbit polyclonal antibody (1:1000, formalin-fixed paraffin embedded sections).
Polycomb group member protein BMI1 is involved in maintaining cell identity, proliferation, differentiation and human oncogenesis. BMI1 mRNA expression in whole blood might represent a new biomarker for the diagnosis and prognosis of NSCLC. In human myoblasts, BMI1 overexpression increases mitochondrial activity, leading to an enhanced energetic state with increased ATP production and concomitant protection against DNA damage both in vitro and upon xenografting in a severe dystrophic mouse model. BMI1 inhibition suppressed proliferation of leukemia cells through NOTCH signaling which functions downstream of BMI1, suggesting that BMI1 inhibitors can be candidate targeted drugs against leukemia. BMI1 decreases ATR activation through a mechanism that involves binding to TOPBP1 and/or ATR. BMI1 over-expression may be useful in identifying patients who might benefit from novel therapies directed at reversing the chromatin-modifying functions of BMI1.
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