Src family kinases (SFKs) play important roles in a variety of signal transduction pathways. Abnormal SFK activation can lead to diseases such as cancer, blood and bone pathologies. C-terminal Src kinase (CSK) and CSK homologous kinase (CHK) are SFK negative regulators that phosphorylate and inactivate SFKs. A unique feature of CHK is its ability to inactivate SFKs via a non-catalytic mechanism. Most recently, the discovery of colon cancers caused by hypermethylation of CHK promoter demonstrated the critical roles of novel CSK/CHK regulation in disease pathogenesis. Although studies have shown that dysregulation of CHK and CSK is present in diseases other than cancers, the underlying mechanisms remain unknown. Increasing evidence shows that CHK and CSK are not functionally redundant and may interact in disease development. Moreover, recent research suggests that, in addition to the CHK/CSK-SFK axis, there may be novel pathways or targets of CHK/CSK, as well as novel modes of regulation of SFKs.
For these reasons, we will summarize recent advances in this field, and invite submissions of novel discoveries related. This Research Topic aims to uncover novel regulatory mechanisms and molecules of the CHK/CSK pathways that can be targeted or used as biomarkers for disease diagnosis and treatment.
We welcome Original Research, Brief Research Reports, important Case Reports, Reviews, and Mini-Review articles focusing on, but not limited to, the following subtopics:
• The regulation of CHK or CSK, including genetic, epigenetic, translational, posttranslational modifications, and their functional roles in health or cancer;
• Identification of novel molecular targets of CHK or CSK, and their biological roles;
• Novel regulation of SFKs (key targets of CHK and CSK), including mutations and other new regulation mechanisms, and their effects in the development of various cancers;
• Dysregulation and roles of CHK and CSK signaling in other diseases may also be considered.
Topic Editor Dr. Octavian Bucur is the co-Founder and CEO of QPathology, Boston, MA, United States. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Src family kinases (SFKs) play important roles in a variety of signal transduction pathways. Abnormal SFK activation can lead to diseases such as cancer, blood and bone pathologies. C-terminal Src kinase (CSK) and CSK homologous kinase (CHK) are SFK negative regulators that phosphorylate and inactivate SFKs. A unique feature of CHK is its ability to inactivate SFKs via a non-catalytic mechanism. Most recently, the discovery of colon cancers caused by hypermethylation of CHK promoter demonstrated the critical roles of novel CSK/CHK regulation in disease pathogenesis. Although studies have shown that dysregulation of CHK and CSK is present in diseases other than cancers, the underlying mechanisms remain unknown. Increasing evidence shows that CHK and CSK are not functionally redundant and may interact in disease development. Moreover, recent research suggests that, in addition to the CHK/CSK-SFK axis, there may be novel pathways or targets of CHK/CSK, as well as novel modes of regulation of SFKs.
For these reasons, we will summarize recent advances in this field, and invite submissions of novel discoveries related. This Research Topic aims to uncover novel regulatory mechanisms and molecules of the CHK/CSK pathways that can be targeted or used as biomarkers for disease diagnosis and treatment.
We welcome Original Research, Brief Research Reports, important Case Reports, Reviews, and Mini-Review articles focusing on, but not limited to, the following subtopics:
• The regulation of CHK or CSK, including genetic, epigenetic, translational, posttranslational modifications, and their functional roles in health or cancer;
• Identification of novel molecular targets of CHK or CSK, and their biological roles;
• Novel regulation of SFKs (key targets of CHK and CSK), including mutations and other new regulation mechanisms, and their effects in the development of various cancers;
• Dysregulation and roles of CHK and CSK signaling in other diseases may also be considered.
Topic Editor Dr. Octavian Bucur is the co-Founder and CEO of QPathology, Boston, MA, United States. All other Topic Editors declare no competing interests with regards to the Research Topic subject.