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聯(lián)系人：蔣經(jīng)理
電話：4008750250
號(hào)碼：
手機(jī)：18066071954
地址：南京市棲霞區(qū)緯地路9號(hào)
Email： zhangxiangwen@cobioer.com

CBP73323
I. Introduction
Cell Line Name：	BCR-ABL1 [M351T]/BaF3
Host Cell:	Ba/F3
Stability:	16 passages (in-house test, that not means the cell line will be instable beyond the passages we tested.)
Application:	Anti-proliferation assay and PD assay
Freeze Medium:	90% FBS+10% DMSO
Complete Culture Medium:	RPMI-1640+10%FBS
Mycoplasma Status:	Negative

II.Background
Presence of a BCR-ABL1 fusion gene is necessary for the pathogenesis of CML. In up to 95% of cases, a t(9;22) (q34;q11) translocation results in the BCR-ABL1 fusion gene (Faderl et al. 1999). This translocation results in the Philadephia chromosome. In rare CML cases lacking the traditional t(9;22) translocation, other translocations result in the creation of the BCR-ABL1 fusion gene, which sometimes involve multiple chromosomes. ABL1 is a tyrosine kinase, and, in normal cells, it plays a role in cellular differentiation and regulation of the cell cycle. The BCR-ABL1 fusion gene creates a constitutively active tyrosine kinase, which leads to uncontrolled proliferation.

III. Representative Data
1.WB of BCR-ABL1 [M351T]/BaF3
2.Sanger of BCR-ABL1 [M351T]/BaF3 Figure 2. BCR-ABL1 [M351T]/BaF3 Figure 3. BCR-ABL1 [M351T]/BaF3 Fusion
3. Anti-proliferation assay Figure 4. CTG Proliferation Assay of BaF3 BCR-ABL1 M351T Cells (C3).