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首頁 /藥靶模型 /激酶靶點 /NTRKs /ETV6-NTRK3 [G696A]/BaF3

ETV6-NTRK3 [G696A]/BaF3

CBP73209

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I. Introduction
Cell Line Name: ETV6-NTRK3 [G696A]/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+2 ug/ml puromycin
Mycoplasma Status: Negative
 
II. Background
ETV6-NTRK3 gene fusion is the translocation of genetic material between the ETV6 gene located on the short arm (designated p) of chromosome 12 at position p13.2 (i.e. 12p13.2) and the NTRK3 gene located on the long arm (designated q) of chromosome 15 at position q25.3 (i.e. 15q25.3) to create the (12;15)(p13;q25) fusion gene, ETV6-NTRK3. This new gene consists of the 5' end of ETV6 fused to the 3' end of NTRK3. ETV6-NTRK3 therefore codes for an chimeric oncoprotein consisting of the helix-loop-helix (HLH) protein dimerization domain of the ETV6 protein fused to the tyrosine kinase (i.e. PTK) domain of the NTRK3 protein. The ETV6 gene codes for the transcription factor protein, ETV6, which suppresses the expression of, and thereby regulates, various genes that in mice are required for normal hematopoiesis as well as the development and maintenance of the vascular network. NTRK3 codes for Tropomyosin receptor kinase C a NT-3 growth factor receptor cell surface protein that when bound to its growth factor ligand, neurotrophin-3, becomes an active tyrosine kinase that phosphorylates tyrosine residues on, and thereby stimulates, signaling proteins that promote the growth, survival, and proliferation of their parent cells. The tyrosine kinase of the ETV6-NTRK3 fusion protein is dysfunctional in that it is continuously active in phophorylating tyrosine residues on, and thereby continuously stimulating, proteins that promote the growth, survival, and proliferation of their parent cells. In consequence, these cells take on malignant characteristics and are on the pathway of becoming cancerous. Indeed, the ETV6-NTRK3 fusion gene appears to be a critical driver of several types of cancers. It was originally identified in congenital fibrosarcoma and subsequently found in secretory breast cancer (also termed juvenile breast cancer), Mammary analogue secretory carcinoma of salivary glands (also termed MASC or MASCSG), congenital fibrosarcoma, congenital mesoblastic nephroma, rare cases of acute myelogenous leukemia, ALK-negative Inflammatory myofibroblastic tumour, and radiation-induced papillary thyroid carcinoma.
 
III. Representative Data

1. WB of  ETV6-NTRK3-G696A/BaF3 expression

2. Sanger of ETV6-NTRK3 [G696A]/BaF3

Figure 2. SNP of  ETV6-NTRK3-G696A/BaF3

Figure 3. Breakpoint of  ETV6-NTRK3-G696A/BaF3

3. Anti-proliferation assay

Figure 4. CCK8 Proliferation Assay of ETV6-NTRK3 G696A.

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藥靶模型聯(lián)系方式: 華東銷售經(jīng)理(上海):18240630236 華東銷售經(jīng)理(上海、江蘇、安徽):15715191010 華中&華西銷售經(jīng)理:18071545918 華中&西南銷售經(jīng)理:13871580511 華北銷售經(jīng)理:18628311252 全國銷售經(jīng)理:13816461235
診斷標(biāo)準(zhǔn)品聯(lián)系方式: 華東銷售經(jīng)理:15000320447 華北銷售經(jīng)理:18628311252 華中&華西銷售經(jīng)理:18071545918 華中&西南銷售經(jīng)理:13871580511 全國銷售經(jīng)理:13816461235

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