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Outd7b facilitates T cell activation and inflammatory responses by regulating Zap70 ubiquitination
( Hongbo Hu ),( Hui Wang ),( Yichuan Xiao ),( Jin Jin ),( Jae Hoon Chang ),( Qiang Zou ),( Xiaopin Xie ),( Xuhong Cheng ),( Shao Cong Sun ) 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Signal transduction from the T ceII receptor (TCR) is crucial for T cell-mediated immune responses and, when deregulated, also contributes to the development of autoimmunity. How TCR signaling is regulated is incompletely understood. In this study, we demonstrate a ubiquitin-dependent mechanism in which the deubiquitinase Otud7b has a crucial role in facilitatinq TCR signaling. Upon TCR ligation, Olud7b is rapidly recruited to the tyrosine kinase Zap70, a central mediator of TCR-proximal signaling. Otud7b deficiency attenuates the activation of Zap70 and its downstream pathways and impairs T cell activation and differentiation, rendering mice refractory to T cell-mediated autoimmune and inflammatory responses. Olud7b facilitated Zap70 activation by deubiquitinating Zap70, thus preventing the association of Zap70 with the negative-regulatory phosphatases SIs1 and Sts2. These findings establish Otud7b as a positive requlator of TCR-proximal signaling and T cell activation. highlighting the importance of deubiquitination in regulaling Zap70 function.
OTUD7B controls non-canonical NF-kB activation through deubiquitination of TRAF3
( Hongbo Hu ),( George C Brittain ),( Jae Hoon Chang ),( Nahum Puebla Osorio ),( Jin Jin ),( Anna Zal ),( Yichuan Xiao ),( Xuhong Cheng ),( Mikyoung Chang ),( Yang Xin Fu ),( Tomasz Zal ),( Chengming 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
The non-canonical NF-κB pathway forms a major arm of NF-κB signalling that mediates important biological functions, including lymphoid organogenesis, B-lymphocyte function, and cell growth and survival. Activation of the non-canonical NF-κB pathway involves degradation of an inhibitory protein, TNF receptor-associated factor 3 (TRAF3), but how this signalling event is controlled is still unknown. Here we have identified the deubiquitinase OTUD7B as a pivotal regulator of the non-canonical NF-κB pathway. OTUD7B deficiency in mice has no appreciable effect on canonical NF-κB activation but causes hyperactivation of non-canonical NF-κB. In response to non-canonical NF-κB stimuli, OTUD7B binds and deubiquitinates TRAF3, thereby inhibiting TRAF3 proteolysis and preventing aberrant non-canonical NF-κB activation. Consequently, the OTUD7Bdeficiency results in B-cell hyper-responsiveness to antigens, lymphoid follicular hyperplasia in the intestinal mucosa, and elevated host-defence ability against an intestinal bacterial pathogen, Citrobacter rodentium. These findings establish OTUD7B as a crucial regulator of signal-inducednon-canonical NF-κB activation and indicate a mechanism of immune regulation that involves OTUD7B-mediated deubiquitination and stabilization of TRAF3.
Youmei Xiao,Zhanxue Xu,Yuan Cheng,Rufan Huang,Yuan Xie,Hsiang‑i Tsai,Hualian Zha,Lifang Xi,Kai Wang,Xiaoli Cheng,Yanfeng Gao,Changhua Zhang,Fang Cheng,Hongbo Chen 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00
Background Ferroptosis, iron-dependent cell death, is an established mechanism for cancer suppression, particularly in hepatocellular carcinoma (HCC). Sorafenib (SOR), a frontline drug for the treatment of HCC, induces ferroptosis by inhibiting the Solute Carrier family 7 member 11 (SLC7A11), with inadequate ferroptosis notably contributing to SOR resistance in tumor cells. Methods To further verify the biological targets associated with ferroptosis in HCC, an analysis of the Cancer Genome Atlas (TCGA) database was performed to find a significant co-upregulation of SLC7A11 and transferrin receptor (TFRC), Herein, cell membrane-derived transferrin nanovesicles (TF NVs) coupled with Fe3+ and encapsulated SOR (SOR@TF-Fe3+ NVs) were established to synergistically promote ferroptosis, which promoted the iron transport metabolism by TFRC/TF-Fe3+ and enhanced SOR efficacy by inhibiting the SLC7A11. Results In vivo and in vitro experiments revealed that SOR@TF-Fe3+ NVs predominantly accumulate in the liver, and specifically targeted HCC cells overexpressing TFRC. Various tests demonstrated SOR@TF-Fe3+ NVs accelerated Fe3+ absorption and transformation in HCC cells. Importantly, SOR@TF-Fe3+ NVs were more effective in promoting the accumulation of lipid peroxides (LPO), inhibiting tumor proliferation, and prolonging survival rates in HCC mouse model than SOR and TF- Fe3+ NVs alone. Conclusions The present work provides a promising therapeutic strategy for the targeted treatment of HCC.
Peli1 promotes microglia-mediated CNS inflammation by regulating Traf3 degradation
( Yichuan Xiao ),( Jin Jin ),( Mikyoung Chang ),( Jae Hoon Chang ),( Hongbo Hu ),( Xiaofei Zhou ),( George C Brittain ),( Christine Stansberg ),( Qivind Torkildsen ),( Xiaodong Wang ),( Robert Brink ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
Microglia are crucial for the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). Here we show that the E3 ubiquitin ligase Peli1 is abundantly expressed in microglia and promotes microglial activation during the course of EAE induction. Peli1mediates the induction of chemokines and proinflammatory cytokines in microglia and therebypromotes recruitment of T cells into the central nervous system. The severity of EAE is reduced inPeli1-deficient mice despite their competent induction of inflammatory T cells in the peripheral lymphoid organs. Notably, Peli1 regulates Toll-like receptor (TLR) pathway signaling by promoting degradation of TNF receptor-associated factor 3 (Traf3), a potent inhibitor of mitogen-activated protein kinase (MAPK) activation and gene induction. Ablation of Traf3 restores microglial activation and CNS inflammation after the induction of EAE in Peli1-deficient mice. These findings establish Peli1 as a microglia-specific mediator of autoimmune neuroinflammation and suggest a previously unknown signaling mechanism of Peli1 function.
Construction of a Ginsenoside Content-predicting Model based on Hyperspectral Imaging
Ning, Xiao Feng,Gong, Yuan Juan,Chen, Yong Liang,Li, Hongbo Korean Society for Agricultural Machinery 2018 바이오시스템공학 Vol.43 No.4
Purpose: The aim of this study was to construct a saponin content-predicting model using shortwave infrared imaging spectroscopy. Methods: The experiment used a shortwave imaging spectrometer and ENVI spectral acquisition software sampling a spectrum of 910 nm-2500 nm. The corresponding preprocessing and mathematical modeling analysis was performed by Unscrambler 9.7 software to establish a ginsenoside nondestructive spectral testing prediction model. Results: The optimal preprocessing method was determined to be a standard normal variable transformation combined with the second-order differential method. The coefficient of determination, $R^2$, of the mathematical model established by the partial least squares method was found to be 0.9999, while the root mean squared error of prediction, RMSEP, was found to be 0.0043, and root mean squared error of calibration, RMSEC, was 0.0041. The residuals of the majority of the samples used for the prediction were between ${\pm}1$. Conclusion: The experiment showed that the predicted model featured a high correlation with real values and a good prediction result, such that this technique can be appropriately applied for the nondestructive testing of ginseng quality.
TRAF3 regulates the effector function of regulatory T cells and humoral immune responses
( Jae Hoon Chang ),( Hongbo Hu ),( Jin Jin ),( Nahum Puebla Osorio ),( Yichuan Xiao ),( Brian E Gilbert ),( Robert Brink ),( Stephen E Ullrich ),( Shao Cong Sun ) 영남대학교 약품개발연구소 2014 영남대학교 약품개발연구소 연구업적집 Vol.24 No.0
Regulatory T cells (Treg cells) control different aspects of immune responses, but how the effector functions of Treg cells are regulated is incompletely understood. Here we identified TNF receptor-associated factor 3 (TRAF3) as a regulator of Treg cell function. Treg cell-specific ablation of TRAF3 impaired CD4 T cell homeostasis, characterized by an increase in the Th1 type of effector/memory T cells. Moreover, the ablation of TRAF3 in Treg cells resulted in increased antigen-stimulated activation of follicular T helper cells (TFH cells), coupled with heightened formation of germinal centers and production of high-affinity IgG antibodies. Although the loss of TRAF3 did not reduce the overall frequency of Treg cells, it attenuated the antigen-stimulated production of follicular Treg cells (TFR cells). TRAF3 signaling in Treg cells was required to maintain high level expression of inducible co-stimulator (ICOS), which in turn was required for TFR cell generation and inhibition of antibody responses. These findings establish TRAF3 as a mediator of Treg cell function in the regulation of antibody responses and suggest a role for TRAF3 in mediating ICOS expression in Treg cells.
The Kinase TBK1 controls lgA class switching by negatively regulating noncanonical NF-kF dignaling
( Jin Jin ),( Yichuan Xiao ),( Jae Hoon Chang ),( Jiayi Yu ),( Hongbo Hu ),( Robyn Starr ),( George C Brittain ),( Mikyoung Chang ),( Xuhong Cheng ),( Shao Cong Sun ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
Immunoglobulin class switching is crucial for the generation of antibody diversity in humoral immunity and, when deregulated, also has severe pathological consequences. How the magnitude of immunoglobulin isotype switching is controlled is still poorly understood. Here we identify thekinase TBK1 as a pivotal negative regulator of class switching to the immunoglobulin A (IgA) isotype. B cell-specific ablation of TBK1 in mice resulted in uncontrolled production of IgA and the development of nephropathy-like disease signs. TBK1 negatively regulated IgA class switchingby attenuating noncanonical signaling via the transcription factor NF-κB, an action that involved TBK1-mediated phosphorylation and subsequent degradation of the NF-κB-inducing kinase NIK. Our findings establish TBK1 as a pivotal negative regulator of the noncanonical NF-κB pathway and identify a unique mechanism that controls IgA production.
A new equivalent friction element for analysis of cable supported structures
Renzhang Yan,Xiaodun Wang,Zhihua Chen,Hongbo Liu,Xiao Xiao 국제구조공학회 2015 Steel and Composite Structures, An International J Vol.18 No.4
An equivalent friction element is proposed to simulate the friction in cable-strut joints. Equivalent stiffness matrixes and load vectors of the friction element are derived and are unified into patterns for FEM by defining a virtual node specially to store internal forces. Three approaches are described to verify the rationality of the new equivalent friction element: applying the new element in a cable-roller model, and numerical solutions match well with experimental results; applying the element in a continuous sliding cable model, and theoretical values, numerical and experimental results are compared; and the last is applying it in truss string structures, whose results indicate that there would be a great error if the cable of cable supported structures is simulated with discontinuous cable model which is usually adopted in traditional finite element analysis, and that the prestress loss resulted from the friction in cable-strut joints would have adverse effect on the mechanical performance of cable supported structures.
Genome-wide analysis and environmental response profiling of SOT family genes in rice (Oryza sativa)
Rongjun Chen,Yunyun Jiang,Jiali Dong,Xin Zhang,Hongbo Xiao,Zhengjun Xu,Xiaoling Gao 한국유전학회 2012 Genes & Genomics Vol.34 No.5
Sulphotransferase (SOT) catalyses the transfer of a sulphonate group from 3'-phosphoadenosine 5'-phosphosulphate (PAPS)to an appropriate hydroxyl group of various substrates with the parallel formation of 3'-phosphoadenosine 5'-phosphate (PAP). Although several SOTs have been identified and characterized in mammalian, their role in plant is still unclear. In this study, we report genome-wide comprehensive expression analysis of 35 putative SOT genes in rice. The 35 OsSOTs were tandemly arranged into six clusters. The phylogenetic analysis showed that there were 7 subfamilies of OsSOTs and 11 putatively conserved motifs. Six OsSOTs might be pseudogenes,25 have the two motifs which were involved in PAPS binding regions I and IV. Microarray data indicated that all the OsSOTs were expressed almost at the same level but with different patterns: most OsSOTs were expressed exclusively in stigma and ovary and induced by IAA and BAP, several genes were induced by tZ and DMSO and 11 OsSOTs were response to abiotic stress. Further analysis showed that these 11 genes contained cis-regulatory elements responding to abiotic stresses.
Te Hu,Yuchang Su,Ian R. Baxendale,Jiang Tan,Hongbo Tang,Lihua Xiao,Feng Zheng,Ping Ning 한국물리학회 2017 Current Applied Physics Vol.17 No.4
Antimony-tin-doped indium oxide (IATO) as transparent conducting oxide (TCO) exhibits significant optical property on blocking UV and Infrared(IR) for wavelengths less ~400 nm and over ~1400 nm as well as appropriate transmissivity on visible wavelength in our work that can be as an optional idea optical material applying in shielding film or nanocomposite to achieve desired optical application. We have successfully developed an optimal synthesis system which allows for a single hydrothermal oxidation directly synthesizing IATO nanoparticles without high-temperature calcination. These nanoparticles show superior size, crystallinity, agglomeration and are free of intermediates In(OH)3 and InOOH. We also have demonstrated they give scope to desired optical property as a result of an altered IATO band gap energy. We highlight this approach due to the shortened preparation time, the reduced energy consumption and the decreased chemical usage which dramatically save on production costs and protect environment.