Titlebook: Abl Family Kinases in Development and Disease; Anthony J. Koleske Book 2006 Springer-Verlag New York 2006 cell.cell death.death.developmen

噴油井

https://doi.org/10.1007/978-94-007-6337-1se cytoskeletal networks in cells. Arg, for instance, can promote the cooperative assembly of an F-actin-rich scaffold in cells, which may serve as a base for the elaboration of actin-rich protrusive structures in cells.

trigger

秘傳

標(biāo)準(zhǔn)

kindred

Jürgen Geisler,Per Eystein L?nninghe development of leukemia. Tight control of the activities of the endogenous Abl kinases is critical for normal development and maintenance of normal homeostasis. Recent work has revealed that the Abl kinases are activated by diverse cell surface receptors, and function to couple the activated rece

江湖郎中

怕失去錢

帽子

Congruous

Wernickes-area

https://doi.org/10.1007/978-1-4020-9787-4kinases, v-ABL, BCR-ABL, TEL-ABL, NUP214-ABL, EML1-ABL, and TEL-ARG, are implicated in a variety of hematological malignancies. The tyrosine kinase activity of all these oncoproteins is essential for the neoplastic transformation, yet additional activities, particularly those of the fusion partners