A5068691968- Cell death mechanisms and regulation
- NF-κB Signaling Pathways
- Immune Response and Inflammation
- Flow Measurement and Analysis
- Phagocytosis and Immune Regulation
- Autophagy in Disease and Therapy
- Immune cells in cancer
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- interferon and immune responses
- Chinese history and philosophy
- Cancer-related Molecular Pathways
- Fluid Dynamics and Mixing
- Cytokine Signaling Pathways and Interactions
- Advanced Sensor Technologies Research
- Retinoids in leukemia and cellular processes
- Nuclear Receptors and Signaling
- MicroRNA in disease regulation
- RNA Interference and Gene Delivery
- Fluid Dynamics and Vibration Analysis
- Wind and Air Flow Studies
- Remote Sensing and Land Use
- Regional Development and Environment
- Glioma Diagnosis and Treatment
- Advanced Algorithms and Applications
- Fluid Dynamics and Turbulent Flows
Center for Cancer Research
2014-2025
National Institutes of Health
2014-2025
National Cancer Institute
2014-2025
Chinese Academy of Sciences
2010-2025
Dalian Institute of Chemical Physics
2024-2025
Dalian National Laboratory for Clean Energy
2024
Beijing Information Science & Technology University
2023
Shandong University
2006-2022
Guizhou University
2021
Liaoning Technical University
2005-2015
Tumor necrosis factor (TNF) is an important inflammatory cytokine and induces many cellular responses, including inflammation, cell proliferation, apoptosis, necrosis. It known that receptor interacting protein (RIP) kinases, RIP1 RIP3, are key effectors of TNF-induced necrosis, but little about how these two RIP kinases mediate this process, although reactive oxygen species (ROS) generation JNK activation have been suggested to be downstream events kinases. Here we report the identification...
Differentiation to different types of macrophages determines their distinct functions. Tumor-associated (TAMs) promote tumorigenesis owing proangiogenic and immune-suppressive functions similar those alternatively activated (M2) macrophages. We report that reactive oxygen species (ROS) production is critical for macrophage differentiation inhibition superoxide (O(2-)) specifically blocks the M2 found when monocytes are triggered differentiate, O(2-) generated needed biphasic ERK activation,...
The mechanism of tumor necrosis factor (TNF)-induced nonapoptotic cell death is largely unknown, although the TNF-induced apoptosis has been studied extensively. In wild-type mouse embryonic fibroblast cells under a caspase-inhibited condition, TNF effectively induced that morphologically resembled necrosis. this study, we utilized gene knockout fibroblasts and found receptor (TNFR) I mediates necrotic death, RIP, FADD, TRAF2 are critical components signaling cascade death. Inhibitors NF-κB...
Necroptosis, known as programmed necrosis, is a form of caspase-independent, finely regulated cell death with necrotic morphology. Tumor foci death, occurs in advanced solid tumors and often associated poor prognosis cancer patients. While it well documented that apoptosis plays key role tumor regression the inactivation pivotal to development, necroptosis tumorigenesis still not fully understood recent studies have reported both tumor-promoting tumor-suppressing effects necroptosis. In this...
Abstract Tumor necrosis happens commonly in advanced solid tumors. We reported that necroptosis plays a major role tumor necrosis. Although several key regulators including receptor interacting protein kinase 1 (RIPK1) have been identified, the regulation of during development remains elusive. Here, we report Z-DNA-binding (ZBP1), not RIPK1, mediates preclinical cancer models. found ZBP1 expression is dramatically elevated necrotic Importantly, ZBP1, deletion blocks and inhibits metastasis....
The death domain kinase, receptor interacting protein (RIP), is one of the major components tumor necrosis factor 1 (TNFR1) complex and plays an essential role in (TNF)-mediated nuclear κB (NF-κB) activation. activation NF-κB protects cells against TNF-induced apoptosis. Heat-shock proteins (Hsps) are chaperone molecules that confer stability help to restore native folding following heat shock other stresses. most abundant Hsp, Hsp90, also involved regulating function a number cell-signaling...
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) (Apo2 [Apo2L]) is a member of the TNF superfamily and has been shown to have selective antitumor activity. Although it known that TRAIL (Apo2L) induces apoptosis activates NF-κB Jun N-terminal kinase (JNK) through receptors such as TRAIL-R1 (DR4) TRAIL-R2 (DR5), components its signaling cascade not well defined. In this report, we demonstrated death domain RIP essential for TRAIL-induced IκB (IKK) JNK activation. We found...
Tumour necrosis factor α (TNF-α) binds to its receptor (TNFR1) and activates both death- inflammation/survival-related signalling pathways. The inflammation survival-related cascade results in the activation of transcription factor, nuclear κB (NF-κB) requires recruitment receptor-interacting protein (RIP) TNFR1. indispensable role RIP TNF-induced NF-κB has been demonstrated RIP-/- mice cell lines derived from such mice. In present study, we show that TNF-α-induced accumulation...