6_ROX, FREE ACID
- Known as:
- 6_ROX, FREE ACID
- Catalog number:
- 90013
- Product Quantity:
- 10 MG
- Category:
- -
- Supplier:
- Biotium
- Gene target:
- 6_ROX FREE ACID
Related genes to: 6_ROX, FREE ACID
- 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: 6_ROX, FREE ACID
Related articles to: 6_ROX, FREE ACID
- MED25-related developmental disorder (Basel-Vanagaite-Smirin-Yosef syndrome) is a rare autosomal recessive disorder, defined by severe neurodevelopmental delay, corpus callosum abnormalities, ocular involvement, epilepsy, and marked facial appearance. MED25 pathogenic variants interfere with the functioning of the Mediator complex, which is responsible for RNA polymerase II transcription. We report a 9-year-old girl who presents with significant global developmental delay, agenesis of the corpus callosum, congenital cataracts, epilepsy, hypotonia, musculoskeletal abnormalities, and typical craniofacial features. Trio-based whole-exome sequencing revealed compound heterozygous variants in MED25: a maternally transmitted truncating variant (c.1366 C > T; p.Gln456*) and a paternally inherited missense variant (c.430 C > T; p.Leu144Phe). The new classification of the missense variant as potentially pathogenic is supported by a systematic ACMG re-evaluation supported by segregation analysis, phenotypic specificity, computational prediction, and structural localization in the MED25 Activator Interaction Domain (ACID). Comparative phenotypic analyses show strong agreement with reported cases but add more data to fine-tune clinical spectrum. This article broadens the allelic and phenotypic spectrum of MED25-related developmental disorder and highlights the need for comprehensive evaluation across molecular, structural, and phenotypic pathways to elucidate variant signature in rare genetic disease models correctly. - Source: PubMed
Publication date: 2026/09/09
Yidi Camilo AndrésJiménez SofíaSolano Nataly AlejandraDe Jesús Rodríguez AsidPorras Alexandra - To explore the clinical features and genetic etiology of a child with Basel-Vanagaite-Smirin-Yosef syndrome (BVSYS). - Source: PubMed
Zhao YongLi NuoHan YuLi NannanLiu QiuliFu WenjieLuo GuanjunChen YizhaoWang NantianZhou YuanQian Xuguang - High-temperature stress severely limits the cultivation and ornamental quality of herbaceous peony, especially in low-latitude regions. The objective of this study was to reveal the potential mechanism involved in regulation of jasmonates on herbaceous peony heat tolerance through crosstalk between phytohormones and the reactive oxygen species (ROS) scavenging system. The study found that exogenous methyl jasmonate (MeJA) significantly improved thermotolerance of the low-latitude cultivar 'Hang Baishao' by enhancing antioxidase activities and modulating endogenous phytohormone levels. The MeJA-treated group exhibited markedly higher ratios of MeJA to zeatin riboside (ZR), gibberellic acid (GA), brassinolide (BR), and indole-3-acetic acid (IAA) compared with the control group; catalase (CAT) and superoxide dismutase (SOD) activities were significantly elevated relative to hydrogen peroxide (HO) content, with both ratios peaking at 36 h post-heat treatment. Transcriptomic results revealed that MeJA reshaped the expression of genes involved in jasmonic acid (JA) signaling and ROS scavenging, such as , , and and /, , and . Four modules including the hub genes / and were identified from the weighted gene co-expression network analysis (WGCNA), which may be key players in coordinating JA signaling and antioxidant defense. This study demonstrates that MeJA enhanced herbaceous peony thermotolerance by orchestrating a regulatory network involving phytohormonal crosstalk and activation of the ROS scavenging system, and offers candidate genes for future exploration of function and interactions. - Source: PubMed
Publication date: 2026/08/07
Shi XiaohuaZhou ZiyuShen YanChen XiaoxuanZhen QianziLi DanqingWang XiaobinXia YipingZhu KaiyuanLiu HuichunZhang Jiaping - In canonical jasmonate (JA) signaling, MYC2 activity is restrained by JA-inducible JAZ repressors that are rapidly degraded upon JA perception. However, it remains unclear how MYC2 is attenuated during prolonged developmental processes such as leaf senescence, where sustained repression is required independently of acute JA fluctuations. Here, we identify C-type cyclin 1;1 (CycC1;1) as a negative regulator of JA-induced leaf senescence in Arabidopsis. CycC1;1 physically interacts with MYC2 in the nucleus to inhibit MYC2-mediated transcriptional activation of senescence-associated genes (SAGs) by interfering with RNA polymerase II recruitment. Additionally, CycC1;1 interacts with the Mediator subunit MED25 to disrupt its association with MYC2. Disruption of CycC1;1 accelerates JA-dependent leaf yellowing, whereas loss of MYC2 or MED25 fully suppresses this premature-senescence phenotype. Unlike JAZ repressors, CycC1;1 expression and protein stability are uncoupled from JA signaling. Phylogenetic analyses suggest that the CycC1;1-MYC2 interaction may predate the emergence of JAZ repressors in aquatic ancestors, and CycC1;1 shows evolutionarily conserved ability to interact with and inhibit MYC2 across different plant species. Collectively, our findings uncover a CycC1;1-MED25-MYC2-regulatory module wherein CycC1;1 suppresses MYC2 activity by inhibiting MED25 binding to MYC2 and RNA polymerase II recruitment, downregulating SAG expression and thus delaying leaf senescence in plants. - Source: PubMed
Publication date: 2026/08/21
Liao Cai-YiHuang Xiao-LiLi LinLiu Guo-MaoLu Kai-KaiYang HongLi Song-QiJing Peng-WeiSong Ru-FengLiu Wen-Cheng - Direct chemical inhibition of transcription factor (TF)-cofactor interactions in plants remains challenging because their large protein-protein interfaces are poorly suited to conventional small molecules, while peptide-based inhibitors are limited by inefficient intracellular delivery. In our previous work, we demonstrated that peptide inhibitors can disrupt MYC transcription factor complexes in plants, but only at relatively high concentrations. Here, we show that a chemically defined chemocarrier overcomes this limitation and enables low-dose functional activity of peptide inhibitors in planta. To access TF-cofactor interfaces, we established a multi-step, target-guided screening platform that links in vitro high-throughput assays with functional validation in plants. This workflow integrates primary and secondary AlphaScreen assays using full-length and truncated MYC constructs with a tertiary assay targeting the interaction between MYCs and the MED25 coactivator. Screening of an approved-drug library followed by structure-activity optimization led to the identification of a low-toxicity aromatic derivative with potent cell-penetrating activity in Arabidopsis. Conjugation with this chemocarrier markedly enhanced the intracellular delivery and functional efficacy of multiple MYC-targeting peptide scaffolds, including cyclic and stapled peptides, resulting in over two orders of magnitude improvement in potency. This enabled robust inhibition of MYC-dependent transcriptional programs at substantially reduced concentrations, converting peptide-based inhibition from a high-dose proof-of-concept into a low-dose, functionally tractable strategy. These findings establish a practical chemical modality for accessing transcription factor-cofactor interfaces in plants. - Source: PubMed
Publication date: 2026/08/17
Liu RuiqiUehara YumaMino KoshikiIdei AkikoKimoto KazusaFujiwara DaisukeYoshida MinoruUeda MinoruTakaoka Yousuke