ACID RED 33 (C.I. NO. 17200)
- Known as:
- ACID RED 33 (C.I. NO. 17200)
- Catalog number:
- A-00256
- Product Quantity:
- 25 gm
- Category:
- -
- Supplier:
- Oxford Lab
- Gene target:
- ACID RED 33 (.. . 17200)
Related genes to: ACID RED 33 (C.I. NO. 17200)
- Gene:
- MED25 NIH gene
- Name:
- mediator complex subunit 25
- Previous symbol:
- -
- Synonyms:
- ARC92, ACID1, TCBAP0758, DKFZp434K0512
- Chromosome:
- 19q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-09
- Date modifiied:
- 2019-04-23
Related products to: ACID RED 33 (C.I. NO. 17200)
Related articles to: ACID RED 33 (C.I. NO. 17200)
- DNA methylation has been proposed as a predictive biomarker. Cervical intraepithelial neoplasia grade 2 (CIN2) was historically the cut-off for surgical treatment, however it is increasingly managed with active surveillance, while there is currently no accurate way to predict which lesions will regress. - Source: PubMed
Publication date: 2026/04/11
Ellis Laura BurneyBowden Sarah JParaskevaidi MariaLyons DeirdreParaskevaidis EvangelosMoscicki Anna-BarbaraFlanagan James MKyrgiou Maria - Mediator is a central transcriptional coactivator that connects sequence-specific transcription factors with RNA polymerase II to control inducible gene expression in plants. MED16 is a Mediator tail module subunit that functions as a context-dependent integrator, helping coordinate developmental programs with environmental adaptation. This review summarizes current evidence for MED16 function from structural and evolutionary perspectives to physiological outputs, with emphasis on how MED16 interacts with transcription factors and other Mediator subunits to shape RNA polymerase II engagement at target loci. In terms of development, MED16 contributes to organ growth and root system architecture, and comparative studies have revealed that it plays conserved roles in lineage-specific wiring. Under abiotic stress, MED16 supports the efficient activation of stress-inducible transcription, including cold acclimation and nutrient stress responses such as phosphate starvation-dependent root remodeling. In immunity, MED16 modulates salicylic acid- and jasmonate/ethylene-associated defence outputs and can be targeted by plant viruses, which is consistent with its role in antiviral transcriptional responses. Mechanistically, MED16 participates in cooperative and competitive interactions within the Mediator complex that tune hormone-responsive outputs, exemplified by MED25-related competition in abscisic acid signalling. We highlight key limitations and future directions, including the need for mechanistic validation beyond , clearer models of dosage control in crops, improved understanding of context-dependent tail configurations, and high-resolution mapping of MED16 interaction interfaces. - Source: PubMed
Publication date: 2026/03/07
Li LuyiQi Shu-LiShen ChunxiuZhi Tian-TianZou JieChen Gang - Hypoxia significantly impacts plant metabolism and growth by disrupting mitochondrial respiration, and oxygen sensing plays a vital role in regulating responses to low-oxygen conditions. Plants sense oxygen through the N-degron pathway, involving Plant Cysteine Oxidases (PCOs) that oxidize the Ethylene Response Factors belonging to group VII (ERF-VII), leading to their degradation under normoxia. Under hypoxic conditions, PCO activity decreases, stabilizing ERF-VII proteins and activating the transcription of Hypoxia-Responsive Genes (HRGs) to adapt to oxygen limitation. Recent research highlights additional factors, including the MBR1/MED25 complex, ERF-VII phosphorylation, and the integration of energy and oxygen signals via the Target of Rapamicin (TOR) pathway, which fine-tune the hypoxic response. Upon reoxygenation, PCOs restore activity and degrade ERF-VII, but this degradation is delayed, possibly due to reactive oxygen species (ROS) inhibiting PCO function. Repressive factors such as HRA1 and ORA59 also modulate ERF-VII activity to suppress HRG expression. The plant's response to hypoxia also involves a sophisticated network of molecular signals, including calcium signaling and the redox-modulatory role of phytoglobins and nitric oxide. Despite significant progress, much remains unknown about plant hypoxia, as its complex, spatiotemporal nature affects not only environmental adaptation but also development and plant-microbe interactions, necessitating intricate regulatory mechanisms. - Source: PubMed
Publication date: 2026/02/24
Castellana SimoneOlmi EmmaBrunello LucaLoreti ElenaPerata Pierdomenico - MEDIATOR 25 (MED25) is a key component of the universally conserved multi-subunit mediator complex. In plants, MED25 regulates diverse biological processes, including flowering, seed germination, cell proliferation, defense responses, and phytohormone signaling, largely through interactions with transcription factors. However, its role in specialized metabolism remains poorly understood. MED25 is a crucial component of the jasmonate (JA) signaling pathway, and JA is a major elicitor of specialized metabolites such as terpenoid indole alkaloids (TIAs) in Madagascar periwinkle (Catharanthus roseus) and flavonoids in Arabidopsis (Arabidopsis thaliana). Using C. roseus and Arabidopsis as models, we investigated the regulatory role of MED25 in these 2 distinct metabolic pathways. RNAi-mediated silencing of CrMED25 in C. roseus hairy roots significantly altered the expression of TIA biosynthetic genes and reduced TIA accumulation. We demonstrated that CrMED25 interacts with CrMYC2 and C. roseus jasmonate ZIM domain 1 (CrJAZ1), key regulators of the TIA pathway. Additionally, CrMED25 silencing suppressed the expression of flavonoid pathway genes in C. roseus hairy roots and flowers. Parallel analysis in Arabidopsis showed that the med25 mutant exhibited strong repression of flavonoid pathway genes and regulators. Protein-protein interaction assays revealed that AtMED25 interacts with GLABRA3 (GL3), MYB12, and MYB111, well-established regulators of flavonoid biosynthesis. These findings establish MED25 as a conserved co-activator of specialized metabolism, integrating JA signaling with transcriptional programs governing alkaloid and flavonoid biosynthesis. This work uncovers a previously unrecognized regulatory role of MED25 and highlights molecular entry points for engineering pharmaceutically important plant metabolites. - Source: PubMed
Singleton Joshua JSchluttenhofer CraigPatra BarunavaSingh Sanjay KWu XiaLyu RuiqingPattanaik SitakantaYuan Ling - Modern agriculture relies heavily on chemical inputs to sustain productivity, yet their intensive use poses environmental and health risks. Sustainable strategies based on biostimulants have emerged as promising alternatives to reduce agrochemical dependence. Among these compounds, humic substances (HS) stand out for their ability to modulate plant growth and activate defense responses. This study aimed to evaluate the effects of HS from different sources-vermicompost (Vc) and peat (Pt)-on the salicylic acid (SA)-mediated defense pathway in tomato plants ( cv. Micro-Tom) infected with sp. The HS were characterized by solid-state C CPMAS NMR to determine the relative distribution of carbon functional groups and structural domains, including alkyl, O-alkyl, aromatic, and carbonyl carbon fractions, as well as hydrophobicity-related indices. Enzymatic activities of lipoxygenase, peroxidase, phenylalanine ammonia lyase, and beta 1,3-glucanase were determined spectrophotometrically, and RT-qPCR quantified gene transcription levels involved in SA signaling and defense (, , , , , , , , , , , , , , , , , ). Both HS significantly reduced disease severity and activated key SA-related defense genes, including the regulatory gene and the effector genes , and , with Pt providing greater protection. Notably, HS amplified defense-related gene expression and enzymatic activities specifically under infection, showing a stronger induction than in non-infected plants. These results demonstrate that structural differences among HS drive distinct and enhanced defense responses under pathogen challenge, highlighting their potential as sustainable tools for improving plant immunity in agricultural systems. - Source: PubMed
Publication date: 2025/12/17
Silva Rakiely MMussi-Dias VicenteOlivares Fábio LPeres Lázaro E PCanellas Luciano P