ETK2 receptor tyrosine kinase promotes survival of factor-dependent FDC-P1 progenitor cells

Darby, C; Giannola, Diane; Couzens, Matthew S.; Emerson, Stephen G.

doi:10.1016/s0301-472x(00)00162-4

Cited by 6 publications

(1 citation statement)

References 27 publications

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“…They appear to connect to different nodes of transforming pathways. In some cell types, they induce cell proliferation, but in most others, they are antiapoptotic and mediate cell adhesion and migration (8,10,14,23). Activation of phosphoinositide 3Ј-kinase (PI3K)/AKT and extracellular signal-regulated kinase (ERK) pathways is often associated with activation of this family of kinases.…”

Section: Introductionmentioning

confidence: 99%

Signal Pathways in Up-regulation of Chemokines by Tyrosine Kinase MER/NYK in Prostate Cancer Cells

Robinson

Kung

2004

Cancer Research

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Section: Introductionmentioning

confidence: 99%

Signal Pathways in Up-regulation of Chemokines by Tyrosine Kinase MER/NYK in Prostate Cancer Cells

Robinson

Kung

2004

Cancer Research

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The TAM family: phosphatidylserine-sensing receptor tyrosine kinases gone awry in cancer

et al. 2014

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The TYRO3, AXL (also known as UFO) and MERTK (TAM) family of receptor tyrosine kinases (RTKs) are aberrantly expressed in multiple haematological and epithelial malignancies. Rather than functioning as oncogenic drivers, their induction in tumour cells predominately promotes survival, chemoresistance and motility. The unique mode of maximal activation of this RTK family requires an extracellular lipid–protein complex. For example, the protein ligand, growth arrest-specific protein 6 (GAS6), binds to phosphatidylserine (PtdSer) that is externalized on apoptotic cell membranes, which activates MERTK on macrophages. This triggers engulfment of apoptotic material and subsequent anti-inflammatory macrophage polarization. In tumours, autocrine and paracrine ligands and apoptotic cells are abundant, which provide a survival signal to the tumour cell and favour an anti-inflammatory, immunosuppressive microenvironment. Thus, TAM kinase inhibition could stimulate antitumour immunity, reduce tumour cell survival, enhance chemosensitivity and diminish metastatic potential.

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Gas6 and protein S

2006

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Gas6 and protein S are two homologous secreted proteins that depend on vitamin K for their execution of a range of biological functions. A discrete subset of these functions is mediated through their binding to and activation of the receptor tyrosine kinases Axl, Sky and Mer. Furthermore, a hallmark of the Gas6–Axl system is the unique ability of Gas6 and protein S to tether their non receptor‐binding regions to the negatively charged membranes of apoptotic cells. Numerous studies have shown the Gas6–Axl system to regulate cell survival, proliferation, migration, adhesion and phagocytosis. Consequently, altered activity/expression of its components has been detected in a variety of pathologies such as cancer and vascular, autoimmune and kidney disorders. Moreover, Axl overactivation can equally occur without ligand binding, which has implications for tumorigenesis. Further knowledge of this exquisite ligand–receptor system and the circumstances of its activation should provide the basis for development of novel therapies for the above diseases.

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ETK2 receptor tyrosine kinase promotes survival of factor-dependent FDC-P1 progenitor cells

Cited by 6 publications

References 27 publications

Signal Pathways in Up-regulation of Chemokines by Tyrosine Kinase MER/NYK in Prostate Cancer Cells

Signal Pathways in Up-regulation of Chemokines by Tyrosine Kinase MER/NYK in Prostate Cancer Cells

The TAM family: phosphatidylserine-sensing receptor tyrosine kinases gone awry in cancer

Gas6 and protein S

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