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Cadmium (Cd) toxicity causes oxidative stress damage in plant cells. Glutaredoxins (GRXs), a type of small oxidoreductase, play a crucial role in modulating thiol redox states. However, whether GRXs act in Cd stress remains to be identified. Here, we reveal that Arabidopsis GRX480, a member of the CC-type family, enhances plant Cd stress tolerance. The mutants exhibit enhanced sensitivity to Cd stress, manifested by shortened root, reduced biomass, lower chlorophyll and proline levels, and decreased photosynthetic efficiency compared with the wild type. The Cd concentration in mutants is higher than the wild type, resulting from the inhibition of Cd efflux and transport genes transcription. Lower levels of GSH were detected in Cd-treated mutants than in the wild type, indicating that regulates plant Cd tolerance by influencing the balance between GSH and GSSG. Furthermore, the hyperaccumulation of reactive oxygen species (ROS) is associated with decreased expression of HO scavenging genes in Cd-treated mutants. Additionally, more toxic reactive carbonyl species (RCS), produced during oxidative stress, accumulate in Cd-treated mutants than in wild type. Overall, our study establishes a critical role of GRX480 in response to Cd stress, highlighting its multifaceted contributions to detoxification and the maintenance of redox homeostasis.
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http://dx.doi.org/10.3390/ijms252111455 | DOI Listing |
BMC Mol Cell Biol
September 2025
School of Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, UK.
Retinitis pigmentosa (RP) affects around 1 in 4000 individuals and represents approximately 25% of cases of vision loss in adults, through death of retinal rod and cone photoreceptor cells. It remains a largely untreatable disease, and research is needed to identify potential targets for therapy. Mutations in 94 different genes have been identified as causing RP, including AGBL5 which encodes the main deglutamylase that regulates and maintains functional levels of cilia tubulin glutamylation, which is essential to initiate ciliogenesis, maintain cilia stability and motility.
View Article and Find Full Text PDFActa Neuropathol
September 2025
Department of Pathology and Laboratory Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, NH, USA.
Nat Commun
September 2025
Shanghai Yao Yuan Biotechnology Ltd (Drug Farm), Shanghai, China.
ROSAH (retinal dystrophy, optic nerve edema, splenomegaly, anhidrosis, and headache) syndrome is a rare genetic disease caused by variants in alpha-kinase 1 (ALPK1) resulting in downstream pro-inflammatory signaling mediated by the TIFA/TRAF6/NF-κB pathway. Here, we report the design of an ALPK1 inhibitor, DF-003, with pharmacokinetic properties suitable for daily oral dosing. In biochemical assays, DF-003 potently inhibits human ALPK1 (IC = 1.
View Article and Find Full Text PDFAm J Transplant
September 2025
Center for Transplantation Sciences, Massachusetts General Hospital, Harvard Medical School; Department of Surgery, Massachusetts General Hospital, Harvard Medical School; Department of Surgery, Hospital of the University of Pennsylvania, Perelman School of Medicine at the University of Pennsylvania
Achieving immune tolerance is a key goal in organ transplantation, as it eliminates the need for long-term immunosuppression. Regulatory B cells (Bregs) present a promising strategy for inducing tolerance. Our previous findings demonstrate that the adoptive transfer of ex vivo-expanded murine splenic B regulatory cells, referred to as TLR-Bregs (TLR9/TLR4 stimulation), induces tolerance to allografts.
View Article and Find Full Text PDFCancer Lett
September 2025
State Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Department of Radiology, Department of Clinical Research and Translational Medicine, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou,
The tumor microenvironment (TME) plays a pivotal role in cancer progression, though the molecular regulators governing its immunosuppressive properties remain incompletely characterized. In this study, we identify Makorin-2 (MKRN2) as a novel modulator of TME remodeling through integrated analyses of genetically engineered mouse models and human clinical data. Utilizing MKRN2 knockout mice, we observed significantly accelerated tumor growth compared to wild-type control, which was associated with profound alterations in immune cell composition, especially M2 macrophages.
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