posted on 2019-07-25, 14:38authored byMiran Rada, Nickolai Barlev, Salvador Macip
Many genes of the human genome display pleiotropic activity, playing an important role in two or more unrelated pathways. Surprisingly, some of these functions can even be antagonistic, often letting to divergent functional outcomes depending on microenviromental cues and tissue/cell type-dependent parameters. Lately, the Bruton's tyrosine kinase (BTK) has emerged as one of such pleiotropic genes, with opposing effects in cancer pathways. While it has long been considered oncogenic in the context of B cell malignancies, recent data shows that BTK can also act as a tumour suppressor in other cells, as an essential member of the p53 and p73 responses to damage. Since BTK inhibitors are already being used clinically, it is important to carefully review these new findings in order to fully understand the consequences of blocking BTK activity in all the cells of the organism.
Funding
N.B. acknowledges the grant support from the Russian Government Program for the Recruitment of the leading scientists into the Russian Institutions of Higher Education 14.W03.31.0029.
History
Citation
Cell Death & Disease, 2018, 9, Article number: 1064
Author affiliation
/Organisation/COLLEGE OF LIFE SCIENCES/Biological Sciences/Molecular & Cell Biology
Version
VoR (Version of Record)
Published in
Cell Death & Disease
Publisher
Springer Nature for Associazione Differenziamento e Morte Cellulare