Bmi1 Recombinant Rabbit Monoclonal Antibody [JJ093-3] (ET1701-89)

UNIPROT #

P35226

PROTEIN NAME

Bmi1

SYNONYMS

B lymphoma Mo MLV insertion region (mouse) antibody;B lymphoma Mo MLV insertion region 1 homolog antibody;Bmi 1 antibody;BMI1 antibody;BMI1 polycomb ring finger oncogene antibody;BMI1_HUMAN antibody;Flvi 2/bmi 1 antibody;FLVI2/BMI1 antibody;MGC12685 antibody;Murine leukemia viral (bmi 1) oncogene homolog antibody;Oncogene BMI 1 antibody;PCGF 4 antibody;PCGF4 antibody;Polycomb complex protein BMI 1 antibody;Polycomb complex protein BMI-1 antibody;Polycomb group protein Bmi1 antibody;Polycomb group ring finger 4 antibody;Polycomb group RING finger protein 4 antibody;RING finger protein 51 antibody;RNF 51 antibody;RNF51 antibody

POST-TRANSLATIONAL MODIFICATION

Monoubiquitinated (By similarity). May be polyubiquitinated; which does not lead to proteasomal degradation.

SUBCELLULAR LOCATION

Nucleus, Cytoplasm.

FUNCTION

BMI1 (B lymphoma Mo-MLV insertion region 1 homolog) has been reported as an oncogene by regulating p16 and p19, which are cell cycle inhibitor genes. Bmi1 knockout in mice results in defects in hematopoiesis, skeletal patterning, neurological functions, and development of the cerebellum. Recently it has been reported BMI1 is rapidly recruited to sites of DNA damage and it sustains for over 8h. Loss of BMI1 leads to radiation sensitive and impaired repair of DNA double-strand breaks by homologous recombination. Bmi1 is necessary for efficient self-renewing cell divisions of adult hematopoietic stem cells as well as adult peripheral and central nervous system neural stem cells.[5][6] However, it is less important for the generation of differentiated progeny. Given that phenotypic changes in Bmi1 knockout mice are numerous and that Bmi1 has very broad tissue distribution, it is possible that it regulates the self-renewal of other types of somatic stem cells. Bmi1 is also thought to inhibit ageing in neurons through the suppression of p53. The Bmi-1 expression interacts with several signaling containing Wnt, Akt, Notch, Hedgehog and receptor tyrosine kinase (RTK) pathway. In Ewing sarcoma family of tumors (ESFT), the knockdown of BMI-1 gene would greatly influence the Notch and Wnt signaling pathway which are important for ESFT formation and development. Bmi-1 was shown to mediate the effect of Hedgehog signaling pathway on mammary stem cell proliferation.[Bmi-1 also regulates multiple downstream factors or genes. It represses p19Arf and p16Ink4a. Bmi-1-/- neural stem cells and HSCs have high expression level of p19Arf and p16Ink4a which diminished the proliferation rate.Bmi-1 is also indicated as a key factor in controlling Th2 cell differentiation and development by stabilizing GATA transcription factors.