Role of the Flt-1 receptor tyrosine kinase in regulating the assembly of vascular endothelium

Nature ◽  
1995 ◽  
Vol 376 (6535) ◽  
pp. 66-70 ◽  
Author(s):  
Guo-Hua Fong ◽  
Janet Rossant ◽  
Marina Gertsenstein ◽  
Martin L. Breitman
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Vascular Endothelium

scholarly journals TRIM31 facilitates K27-linked polyubiquitination of SYK to regulate antifungal immunity

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Xueer Wang ◽  
Honghai Zhang ◽  
Zhugui Shao ◽  
Wanxin Zhuang ◽  
Chao Sui ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Fungal Pathogen ◽  
Essential Role ◽  
Molecular Mechanisms ◽  
Systemic Infection ◽  
Lectin Receptors ◽  
Innate And Adaptive Immunity ◽  
Cytokines And Chemokines

AbstractSpleen tyrosine kinase (SYK) is a non-receptor tyrosine kinase, which plays an essential role in both innate and adaptive immunity. However, the key molecular mechanisms that regulate SYK activity are poorly understood. Here we identified the E3 ligase TRIM31 as a crucial regulator of SYK activation. We found that TRIM31 interacted with SYK and catalyzed K27-linked polyubiquitination at Lys375 and Lys517 of SYK. This K27-linked polyubiquitination of SYK promoted its plasma membrane translocation and binding with the C-type lectin receptors (CLRs), and also prevented the interaction with the phosphatase SHP-1. Therefore, deficiency of Trim31 in bone marrow-derived dendritic cells (BMDCs) and macrophages (BMDMs) dampened SYK-mediated signaling and inhibited the secretion of proinflammatory cytokines and chemokines against the fungal pathogen Candida albicans infection. Trim31−/− mice were also more sensitive to C. albicans systemic infection than Trim31+/+ mice and exhibited reduced Th1 and Th17 responses. Overall, our study uncovered the pivotal role of TRIM31-mediated K27-linked polyubiquitination on SYK activation and highlighted the significance of TRIM31 in anti-C. albicans immunity.

The role of Ret receptor tyrosine kinase in dopaminergic neuron development

Neuroscience ◽  
2006 ◽  
Vol 142 (2) ◽  
pp. 391-400 ◽  
Author(s):  
L. Li ◽  
Y. Su ◽  
C. Zhao ◽  
H. Zhao ◽  
G. Liu ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Dopaminergic Neuron ◽  
Neuron Development

scholarly journals Oncogenic role of TYRO3 receptor tyrosine kinase in the progression of pancreatic cancer

2020 ◽  
Vol 470 ◽  
pp. 149-160 ◽  
Author(s):  
Masaki Morimoto ◽  
Yosuke Horikoshi ◽  
Kazuhiro Nakaso ◽  
Tatsuyuki Kurashiki ◽  
Yoshinori Kitagawa ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase

scholarly journals The Role of Hypoxia and SRC Tyrosine Kinase in Glioblastoma Invasiveness and Radioresistance

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2860 ◽  
Author(s):  
Filippo Torrisi ◽  
Nunzio Vicario ◽  
Federica M. Spitale ◽  
Francesco P. Cammarata ◽  
Luigi Minafra ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Poor Prognosis ◽  
High Rate ◽  
Crucial Importance ◽  
Src Tyrosine Kinase ◽  
Complete Surgical Resection ◽  
Radiation Induced ◽  
Proliferation And Invasion

Advances in functional imaging are supporting neurosurgery and radiotherapy for glioblastoma, which still remains the most aggressive brain tumor with poor prognosis. The typical infiltration pattern of glioblastoma, which impedes a complete surgical resection, is coupled with a high rate of invasiveness and radioresistance, thus further limiting efficient therapy, leading to inevitable and fatal recurrences. Hypoxia is of crucial importance in gliomagenesis and, besides reducing radiotherapy efficacy, also induces cellular and molecular mediators that foster proliferation and invasion. In this review, we aimed at analyzing the biological mechanism of glioblastoma invasiveness and radioresistance in hypoxic niches of glioblastoma. We also discussed the link between hypoxia and radiation-induced radioresistance with activation of SRC proto-oncogene non-receptor tyrosine kinase, prospecting potential strategies to overcome the current limitation in glioblastoma treatment.

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