New Insights into Tyrosine Kinase Alterations in Human Diseases
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".
Deadline for manuscript submissions: 31 March 2024 | Viewed by 7873
Special Issue Editors
Interests: angiogenesis; membrane receptor; tumors; imaging; metabolism; bioscaffold for tissue regeneration
Special Issues, Collections and Topics in MDPI journals
Interests: mechanisms of tumorigenesis; cancer metabolism; tumor angiogenesis; receptor tyrosine kinases; novel anti-cancer agents
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Tyrosine kinases are pleiotropic enzymes that mediate the signaling cascades occurring in response to both external and internal stimuli. They regulate critical cellular processes including cell survival, proliferation and differentiation; cell cycle control; cell metabolism; and cell migration. The activation mechanism for tyrosine kinases is highly conserved in evolution, which is expected for proteins exerting such critical roles. Genetic alterations of tyrosine kinases or abnormalities that alter their activity, abundance, regulation or spatiotemporal distribution are found in numerous human diseases. For example, the aberrant activation of tyrosine kinases has been causally linked to cancer, metabolic disorders, inflammation, arteriosclerosis and angiogenesis. On these bases, tyrosine kinase inhibitors have been developed to block their detrimental effects. However, a broad range of tyrosine kinases remain poorly characterized, and completing the picture is a major challenge for the future. Moreover, many orphan genetic alterations of tyrosine kinases may hide potential druggable targets. Additionally, obtaining mechanistic insights into the spatiotemporal regulation of the tyrosine kinase-mediated signaling network and its crosstalk with other signaling cascades is critical for developing effective treatments for human diseases driven by altered tyrosine kinases. This Special Issue aims to summarize the current knowledge and cutting-edge research on tyrosine kinases in human diseases. Reports can address both receptor and nonreceptor tyrosine kinases. In the latter case, we ask authors to focus on receptor crosstalk with other membrane proteins and heterodimerization as mechanisms for determining signaling specificity. Translational studies are particularly welcome. We also encourage authors to present noncanonical views in opinion papers or reviews.
Prof. Dr. Stefania Mitola
Guest Editor
Dr. Elisabetta Grillo
Co-Guest Editor
Manuscript Submission Information
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Keywords
- mechanism of tyrosine kinase activation/inactivation in human diseases
- mutations of tyrosine kinases in cancer
- tyrosine kinases as therapeutic targets
- novel therapeutic approaches to target tyrosine kinases
Planned Papers
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: A non-canonical role for the glycosyltransferase enzyme UGT2B17 as a novel constituent of B cell receptor signalosome
Author: Guillemette
Highlights: An elevated UGT2B17 expression identifies a subgroup of patients with shorter survival and poor drug response.
UGT2B17 affects the pro-survival BCR signalosome and forms a complex with multiple BCR effector kinases.
Findings reveal for the first time a potential therapeutic vulnerability in high-risk UGT2B17HI CLL that can be targeted with a tyrosine kinase inhibitor for personalized therapy.