<unk>  (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.<unk>  knockout in mice results in defects in hematopoiesis, skeletal patterning, neurological functions, and development of the cerebellum. Recently it has been reported<unk>  is rapidly recruited to sites of DNA damage and it sustains for over 8h. Loss of<unk>  leads to radiation sensitive and impaired repair of DNA double-strand breaks by homologous recombination.<unk>  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. However, it is less important for the generation of differentiated progeny. Given that phenotypic changes in<unk>  knockout mice are numerous and that<unk>  has very broad tissue distribution, it is possible that it regulates the self-renewal of other types of somatic stem cells.<unk>  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.
BMI1
Body fat percentage
BodyKom
Body adiposity index
Weight and height percentile
Lean body mass
Baseline 
Body surface area