29F6 preferentially associates with several distinct heterochromatic domains in tumor cell lines. In both primary and tumor cell lines a marked cell cycleregulation of Pc-G-chromatin interaction is observed.
纯化方法
Purified
免疫原
Recombinant Bmi1 protein corresponding to residues 1-202 of Mouse Bmi-1 acterial fusion protein of membrane proximal non repeat domain of Human episialin.
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
储存条件
4 °C,-20 °C
储存方法
Store undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing. Shelf life: one year from despatch.
有效期
12 months
抗原
BMI1
(BMI1 Polycomb Ring Finger Oncogene (BMI1))
别名
bmi-1,rnf51
背景
BMI1 polycomb ring finger oncogene, also known as BMI1, is a protein which in humans is encoded by the BMI1 gene. 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 is rapidly recruited to sites of DNA damage and it sustains for over than 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. Bmi1 is also thought to inhibit ageing in neurons through the suppression of p53. In primary and tumor cells, nuclear BMI1 shows a fine-grain distribution over chromatin, usually dense in interphase nuclei and significantly weaker along mitotic chromosomes. In addition, BMI1 preferentially associates with several distinct heterochromatic domains in tumor cell lines. Bmi1 seems to play an important role in several types of cancer, such as bladder, skin, prostate, breast, ovarian, colorectal as well as hematological malignancies. Its amplification and overexpression is especially pronounced in mantle cell lymphomas. In both primary and tumor cell lines a marked cell cycle regulation of Pc-G-chromatin interaction is observed: nuclear BMI1-staining dissipates in late S phase and is reestablished early in G1-phase. Chromatin-association of BMI1 inversely correlates with its phosphorylation status in a cell cycle-dependent fashion: at G1/S, hypophosphorylated. BMI1 is specifically retained in the chromatin-associated nuclear protein fraction, whereas during G2/M, phosphorylated BMI1 is not chromatin bound.