Year: 2017
Type: article
Abstract: JAK2 inhibition, a combinatorial therapeutic approach in need of further study for chronic myeloid malignancies.As mentioned earlier, the most wellcharacterized role of the enzymatic activity of mutant CBL is ubiquitinylating receptor tyrosine kinases for proteasome degradation as part of the negative feedback mechanism after cytokine stimulation. 10This model now provides a platform to identify the effects of CBL mutations on the proteome in specific subsets of primary cells, including rare cell types such as stem cells.This effort, in turn, may identify novel downstream substrates of mutant CBL that mediate its leukemogenic effects and might serve as novel therapeutic targets themselves.Overall, the model generated by Nakata et al represents one of the most faithful genetically engineered murine models of human CMML to date, as well as a valuable reagent to expand our understanding of CMML pathogenesis.
Source: Blood
Author: Valder R. Arruda
Language: English
Subfield: Genetics
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2607028513