Expressions of Axl and Tyro-3 receptors are under regulation of nerve growth factor and are involved in differentiation of PC12 cells

Wang, Qi; Lu, Qingjun; Xiao, Bing; Zheng, Yi; Wang, Xiaomin

doi:10.1007/s12264-011-1042-4

Cited by 10 publications

(6 citation statements)

References 18 publications

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“…Studies were performed to investigate the role of TAMs in AD, overall point to a protective effect against progression, probably acting on both neuronal survival and amyloid deposition. It was showed that the nerve growth factor, which may counteract AD-related neurodegeneration of cholinergic neurons [131], induced both Tyro3 and Axl expression in differentiating embryogenic cells and protecting them against apoptosis [132]. Moreover, a study on the role of Tyro3 in amyloid precursor protein (APP) processing and amyloid deposition in the hippocampus of AD models, showed that the overexpression of Tyro3 significantly decreased amyloid beta plaques burden from cell lines, while in Tyro3 knockdown transgenic AD mice the number of amyloid plaques increased in the hippocampus [133].…”

Section: The Role Of Tams In Neurodegenerative and Neuroinflammatomentioning

confidence: 99%

TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration

2019

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Increasing evidence suggests that pathogenic mechanisms underlying neurodegeneration are strongly linked with neuroinflammatory responses. Tyro3, Axl, and Mertk (TAM receptors) constitute a subgroup of the receptor tyrosine kinase family, cell surface receptors which transmit signals from the extracellular space to the cytoplasm and nucleus. TAM receptors and the corresponding ligands, Growth Arrest Specific 6 and Protein S, are expressed in different tissues, including the nervous system, playing complex roles in tissue repair, inflammation and cell survival, proliferation, and migration. In the nervous system, TAM receptor signalling modulates neurogenesis and neuronal migration, synaptic plasticity, microglial activation, phagocytosis, myelination, and peripheral nerve repair, resulting in potential interest in neuroinflammatory and neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and Multiple Sclerosis. In Alzheimer and Parkinson diseases, a role of TAM receptors in neuronal survival and pathological protein aggregate clearance has been suggested, while in Multiple Sclerosis TAM receptors are involved in myelination and demyelination processes. To better clarify roles and pathways involving TAM receptors may have important therapeutic implications, given the fine modulation of multiple molecular processes which could be reached. In this review, we summarise the roles of TAM receptors in the central nervous system, focusing on the regulation of immune responses and microglial activities and analysing in vitro and in vivo studies regarding TAM signalling involvement in neurodegeneration.

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Section: The Role Of Tams In Neurodegenerative and Neuroinflammatomentioning

confidence: 99%

TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration

2019

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“…Protection from serum starvation-induced apoptosis is through both the PI3K/Akt and ERK pathways [ 228 ]. Furthermore, nerve growth factor (NGF) can regulate the expression and localization of Tyro3 and Axl, contributing to induction of neuronal differentiation [ 229 ]. Differential expression of Axl and Mer may also be responsible for the differential activity of Gas6 in early- and late-phase maturation of chondrocytes in the growth plate [ 95 ].…”

Section: Tissue and Cell Type-specific Roles For Axlmentioning

confidence: 99%

Axl as a mediator of cellular growth and survival

2014

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The control of cellular growth and proliferation is key to the maintenance of homeostasis. Survival, proliferation, and arrest are regulated, in part, by Growth Arrest Specific 6 (Gas6) through binding to members of the TAM receptor tyrosine kinase family. Activation of the TAM receptors leads to downstream signaling through common kinases, but the exact mechanism within each cellular context varies and remains to be completely elucidated. Deregulation of the TAM family, due to its central role in mediating cellular proliferation, has been implicated in multiple diseases. Axl was cloned as the first TAM receptor in a search for genes involved in the progression of chronic to acute-phase leukemia, and has since been established as playing a critical role in the progression of cancer. The oncogenic nature of Axl is demonstrated through its activation of signaling pathways involved in proliferation, migration, inhibition of apoptosis, and therapeutic resistance. Despite its recent discovery, significant progress has been made in the development of effective clinical therapeutics targeting Axl. In order to accurately define the role of Axl in normal and diseased processes, it must be analyzed in a cell type-specific context.

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“…TAM receptors promote neural stem cell survival, proliferation, and neuron differentiation (30). Nerve growth factor (NGF) regulates the expression of Axl and Tyro-3 receptors and has a role in the differentiation of PC12 cells (31). Tyro3 of Axl expression in PC12 cells are induced by Nerve growth factor (NGF) (32).NGF collaborates with TrkA to promote neuronal differentiation and survival (32).…”

Section: Introductionmentioning

confidence: 99%

Zika Virus Enters Soma of Neuron through NGF/TrkA-Like Endosomal Signaling Pathway

Liu

2021

Preprint

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Infection with the Zika virus results in severe neurological disease in adults or congenital Zika syndrome in newborns. We employed the domain search strategy to study the Zika virus glycoprotein E in this work. The results revealed that immature E contains a NGF domain (“MNKCYIQIMDLGHMCDATMSYECPMLDEGVEPDDVDCWCNTTSTWVVYGTCHH”) and is capable of interacting with TrkA. The E/TrkA complex increased E's interaction with receptors such as Axl and facilitated Zika virus endocytosis via clathrin. Rab5 retrograded transmission of Zika virus-containing E/TrkA endosomal signals to neuronal soma. Rab7 helped dissociation of E/TrkA in late acidic endosomes, and then E became mature after the NGF domain was cut. After membrane fusion with the endosome, the Zika virus was released into the neuron cell body. It showed only the immature E protein of Zika had NGF activity. The retrograde trafficking of endosomal signals (E/TrkA) similar to NGF/TrkA enabled Zika virus to infect neuronal cells. E's interference with the TrkA signal impaired neuronal cell growth and results in neuronal cell apoptosis.

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Expressions of Axl and Tyro-3 receptors are under regulation of nerve growth factor and are involved in differentiation of PC12 cells

Cited by 10 publications

References 18 publications

TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration

TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration

Axl as a mediator of cellular growth and survival

Zika Virus Enters Soma of Neuron through NGF/TrkA-Like Endosomal Signaling Pathway

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