Target Validation Information
Target ID T99740
Target Name mRNA of Myb proto-oncogene protein
Target Type
Clinical Trial
Action against Disease Model LR3001 Neuroblastoma cell proliferation was inhibited to a greater extent by GD2-targeted liposomes containing c-myb asODNs (including LR3001) than by nontargeted liposomes or free asODNs. GD2-targeted liposomes containing c-myb asODNs specifically reduced xpression of c-Myb protein by neuroblastoma cells. Enhanced liposome binding and asODN uptake, as well as the antiproliferative [552211] Drug Info
The Effect of Target Knockout, Knockdown or Genetic Variations The myb gene family consists of three members, named A, B and c-myb which encode nuclear proteins that function as transcriptional transactivators. Proteins encoded by these three genes exhibit a tripartate structure with an N-terminal DNA-binding domain, a central transactivation domain and a C-terminal regulatory domain. These proteins exhibit highest homology in their DNAbinding domains and appear to bind DNA with overlapping sequence specificities. Transactivation by myb gene family varies considerably depending on cell type and promoter context suggesting a dependence on interaction with other cell type specific co-factors. While the C-terminal domains of A-Myb and c-Myb proteins exert a negative regulatory effect on their transcriptional transactivation function, the C-terminal domain of B-Myb appears to function as a positive regulator of this activity. One or more of these proteins interact with other transcription factors such as Ets-2, CEBP and NF-M. In addition, expression of these genes is cell cycle-regulated and inhibition of their expression with antisense oligonucleotides has been found to affect cell cycle-progression, cell division and/or differentiation. Members of the myb gene family exhibit different temporal and spatial expression patterns suggesting a distinctive function for each of these genes. Gene knockout experiments show thatthese genes play an essential role in development. Loss of c-myb function results in embryonic lethality due to failure of fetal hepatic hematopoiesis. A-myb null mutant mice, on the other hand are viable but exhibit growth abnormalities, and defects in spermatogenesis and female breast development. While the role of c-myb in oncogenesis is well established, future experiments are likely to provide further clues regarding the role of A-myb and B-myb in t uMorigenesis. [552211]
References
Ref 552211Delivery of c-myb antisense oligodeoxynucleotides to human neuroblastoma cells via disialoganglioside GD(2)-targeted immunoliposomes: antitumor effects. J Natl Cancer Inst. 2000 Feb 2;92(3):253-61.

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