Plants are constantly challenged by a wide range of pathogens and have therefore evolved an array of mechanisms to defend against them. In response to these defense systems, pathogens have evolved strategies to avoid recognition and suppress plant defenses (Brown and Tellier, 2011). Three recent reports dealing with the resistance of rice to have added a new twist to our understanding of this fascinating co-evolutionary arms race (Ji et al., 2016; Read et al., 2016; Triplett et al., 2016). They show that pathogens also develop sophisticated effector mimics to trick recognition.
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http://dx.doi.org/10.3389/fpls.2017.00431 | DOI Listing |
Adv Sci (Weinh)
January 2025
Institute of Plant Protection, Jiangsu Academy of Agricultural Sciences, Jiangsu Key Laboratory for Food and Safety-State Key Laboratory Cultivation Base of Ministry of Science and Technology, Nanjing, 210014, China.
Plants activate defense machinery when infested by herbivorous insects but avoid such costs in the absence of herbivory. However, the key signaling pathway regulators underlying such flexibility and the mechanisms that insects exploit these components to disarm plant defense systems remain elusive. Here, it is reported that immune repressor 14-3-3e in rice Oryza sativa (OsGF14e) regulates immune homeostasis.
View Article and Find Full Text PDFBiol Open
January 2025
Department of Pulmonary Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Epithelial cell cohesion and barrier function critically depend on α-catenin, an actin-binding protein and essential constituent of cadherin-catenin-based adherens junctions. α-catenin undergoes actomyosin force-dependent unfolding of both actin-binding and middle domains to strongly engage actin filaments and its various effectors; this mechanosensitivity is critical for adherens junction function. We previously showed that α-catenin is highly phosphorylated in an unstructured region that links the mechanosensitive middle and actin-binding domains (known as the P-linker region), but the cellular processes that promote α-catenin phosphorylation have remained elusive.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Clinical Cooperation Unit Applied Tumor Immunity, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Reduced expression of adhesion molecules in tumor vasculature can limit infiltration of effector T cells. To improve T cell adhesion to tumor endothelial cell (EC) antigens and enhance transendothelial migration, we developed bispecific, T-cell engaging antibodies (bsAb) that activate T cells after cross-linking with EC cell surface antigens. Recombinant T-cell stimulatory anti-VEGFR2-anti-CD3 and costimulatory anti-TIE2-anti-CD28 or anti-PD-L1-anti-CD28 bsAb were engineered and expressed.
View Article and Find Full Text PDFJ Inflamm Res
December 2024
School of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, People's Republic of China.
Objective: The main objective of this study was to elucidate the effector material basis of Cimicifugae Rhizoma (CR) for the treatment of acute pneumonia (AP) and to explore the potential mechanisms underlying the anti-AP effects of these active components in a lipopolysaccharide (LPS)-induced inflammation model of lung epithelial cells.
Methods: Chemical components were identified using ultra-performance liquid chromatography-quadrupole-time-of-flight tandem mass spectrometry (UPLC-TOF-MS), and a CR component library was subsequently established based on a combination of databases and available literature. Bioinformatics techniques were used to construct "component-target" and "protein-protein interaction (PPI)" networks, and the potential active components and core targets screened according to degree value, followed by molecular docking and in vitro experiments for verification.
Int J Biol Macromol
January 2025
Department of Diagnostic Ultrasound and Echocardiography, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, China. Electronic address:
Immunogenetic cell death (ICD) is widely participated in tumor immune therapy. However, the stress responses triggered by individual ICD inducers are typically not strong enough to effectively kickstart an ICD effect and successful ICD necessitates a high level of ICD stimulus, which may be linked to dose-related toxicity. In this research, we developed a drug-free "artificial beacon" ATP/CSO@ECM that mimics the ICD cascade system to kickstart an immune response with cationic chitosan (CSO) as a bridge, which participated in integrating tumor antigens and functional damage-associated molecular patterns (DAMPs) into one effector by electrostatic interaction.
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