Background: ETHYLENE RESPONSE FACTOR (ERF) 8 is a member of one of the largest transcription factor families in plants, the APETALA2/ETHYLENE RESPONSIVE FACTOR (AP2/ERF) superfamily. Members of this superfamily have been implicated in a wide variety of processes such as development and environmental stress responses.
Results: In this study we demonstrated that ERF8 is involved in both ABA and immune signaling. ERF8 overexpression induced programmed cell death (PCD) in Arabidopsis and Nicotiana benthamiana. This PCD was salicylic acid (SA)-independent, suggesting that ERF8 acts downstream or independent of SA. ERF8-induced PCD was abolished by mutations within the ERF-associated amphiphilic repression (EAR) motif, indicating ERF8 induces cell death through its transcriptional repression activity. Two immunity-related mitogen-activated protein kinases, MITOGEN-ACTIVATED PROTEIN KINASE 4 (MPK4) and MPK11, were identified as ERF8-interacting proteins and directly phosphorylated ERF8 in vitro. Four putative MPK phosphorylation sites were identified in ERF8, one of which (Ser103) was determined to be the predominantly phosphorylated residue in vitro, while mutation of all four putative phosphorylation sites partially suppressed ERF8-induced cell death in N. benthamiana. Genome-wide transcriptomic analysis and pathogen growth assays confirmed a positive role of ERF8 in mediating immunity, as ERF8 knockdown or overexpression lines conferred compromised or enhanced resistance against the hemibiotrophic bacterial pathogen Pseudomonas syringae, respectively.
Conclusions: Together these data reveal that the ABA-inducible transcriptional repressor ERF8 has dual roles in ABA signaling and pathogen defense, and further highlight the complex influence of ABA on plant-microbe interactions.
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http://dx.doi.org/10.1186/s12870-018-1402-6 | DOI Listing |
Background And Aim: The high rate of tumor growth results in an increased need for amino acids. As solute carriers (SLC) transporters are capable of transporting different amino acids, cancer may develop as a result of these transporters' over-expression due to their complex formation with other biological molecules. Therefore, this review investigated the role of SLC transporters in the progression of cancer.
View Article and Find Full Text PDFVet Res Forum
November 2024
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Docetaxel (DTX) is widely utilized in breast cancer treatment. However, cancer cell resistance has limited its anti-tumor efficacy. Some molecules called microRNAs (miRNAs), acting like fine-tuned switches, can influence how breast cancer develops and spreads.
View Article and Find Full Text PDFInt J Cardiol Heart Vasc
February 2025
Department of Geriatrics, Peking University Third Hospital, Beijing 100191, PR China.
Background: Ferroptosis is a cell death process that depends on iron and reactive oxygen species. It significantly contributes to cardiovascular diseases. However, its exact role in ischemic cardiomyopathy (ICM) is still unclear.
View Article and Find Full Text PDFDrug Des Devel Ther
January 2025
Department of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, People's Republic of China.
Introduction: The mechanism of remimazolam, a benzodiazepine that activates γ-aminobutyric acid a (GABAa) receptors, in cerebral ischemia/reperfusion (I/R) injury is not well understood. Therefore, we explored whether remimazolam activates protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β)/nuclear factor erythroid 2-related factor 2 (NRF2) to attenuate brain I/R injury in transcerebral I/R-injured rats and transoxygenic glucose deprivation/reperfusion (OGD/R)-injured SY5Y cells.
Material And Methods: Remimazolam was added at the beginning of cell and rat reperfusion, and the PI3K/AKT inhibitor LY294002 was added to inhibit the AKT/GSK-3β/NRF2 pathway 24 h before cellular OGD/R treatment and 30 min before rat brain I/R treatment.
Acta Pharm Sin B
December 2024
Infection Control Convergence Research Center, Chungnam National University College of Medicine, Daejeon 35015, Republic of Korea.
Combination therapy with checkpoint inhibitors blocks inhibitory immune cell signaling and improves clinical responses to anticancer treatments. However, continued development of innovative and controllable delivery systems for immune-stimulating agents is necessary to optimize clinical responses. Herein, we engineered to deliver recombinant granulocyte macrophage colony stimulating factor (GM-CSF) in a controllable manner for combination treatment with a programmed death-ligand 1 (PD-L1) inhibitor.
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