Human Apelin 36,AP36 ELISA Kit
- Known as:
- Human Apelin 36,AP36 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2038
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Apelin 36 AP36 ELISA Kit
Related genes to: Human Apelin 36,AP36 ELISA Kit
- Gene:
- MED4 NIH gene
- Name:
- mediator complex subunit 4
- Previous symbol:
- VDRIP
- Synonyms:
- HSPC126, DRIP36, TRAP36
- Chromosome:
- 13q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-23
- Date modifiied:
- 2016-10-05
Related products to: Human Apelin 36,AP36 ELISA Kit
Related articles to: Human Apelin 36,AP36 ELISA Kit
- Long-term survival in breast cancer is often limited by metastatic recurrence arising from disseminated cancer cells that persist in a dormant state. The mechanisms that enable these dormant cells to survive and subsequently reawaken remain incompletely understood. Here an unbiased genome-scale genetic screen identified Med4 as a cancer cell-intrinsic gatekeeper in metastatic reactivation. Correspondingly, MED4 haploinsufficiency was found to be prevalent in metastatic breast cancer and associated with poorer clinical outcomes. Syngeneic mouse metastasis models revealed that MED4 enforces metastatic dormancy. Mechanistically, and unexpectedly given the canonical role of the Mediator complex in transcriptional activation, MED4 suppresses enhancer priming (H3K4me1) and activation (H3K27ac). Loss of a single Med4 allele disrupts enhancer poise, leading to extracellular matrix remodelling and integrin-mediated mechanotransduction programmes that ultimately drive metastatic outgrowth. Together, these findings establish MED4 as a key regulator of breast cancer cell dormancy and nominate MED4 haploinsufficiency as a potential predictive biomarker for patients at high risk of metastatic relapse. - Source: PubMed
Publication date: 2026/06/22
Bae Seongyeon SLing Hsiang-HsiZhang JiankangChen YiChen HongKumar DhirajSaw Ajay KRai KunalViny Aaron DDePinho Ronald AGiancotti Filippo G - Multiple epiphyseal dysplasia (MED) is a clinically and genetically heterogeneous group of disorders characterized by a waddling gait, joint pain, and early-onset osteoarthritis. The aim of this study was to compare the genetic characteristics and long-term clinical follow-up findings of 22 patients with MED from 17 unrelated families. Molecular diagnosis was performed using clinical exome analysis and exome sequencing. Seventeen children were followed for a median of 5.5 years. Eighteen disease-related variants were identified: 47% in , 11.8% each in and in a monoallelic state, 17.6% in , and 11.8% each in and in a biallelic state. Some mutations previously identified in pseudoachondroplasia, an allelic disorder of MED1, were shown in our study to exhibit a typical MED1 or intermediate phenotype. In contrast, it was confirmed that certain mutations in lead to MED4 phenotype. Furthermore, it has been observed that biallelic variants in may be associated with the MED5 phenotype. In patients with MED2 and MED3, the knee joint is affected, while in other types, the hip joint is predominantly affected. In 15 children followed until ages 11-18, height decreased slightly as they grew older but remained normal or at the lower limit, and slow progression was observed in the waddling gait and joint pain, except in the intermediate form. This study reveals the frequency of disease-related variants, including seven novel ones, in genes leading to MED1-5 and 7 phenotypes, and expands the spectrum of genetic and clinical phenotypes. - Source: PubMed
Publication date: 2026/04/15
Taner Hasan EmirUludağ Alkaya DilekKalyoncu Uçar AyşeŞeker AliCentel TuncayYıldırım TimurGüneş NilayTüysüz Beyhan - Bacteriophage auxiliary metabolic genes (AMGs) alter host metabolism by hijacking reactions, but previous studies mostly inferred their roles from annotations, ignoring system-wide impacts and phage production. Here we integrate AMGs and phage assembly into a genome-scale metabolic model of MED4 infected by P-HM2. We show that 17 directly hijacked reactions substantially affect more than 30% of the reactions in MED4 metabolism, including carbon fixation, photosynthesis, and nucleotide synthesis, distinguishing these AMGs as either phage aligned-shifting feasible reaction velocities in accordance with maximal phage production-or phage antialigned. Pareto optimization reveals that phage-aligned reactions alter phage-host growth trade-offs, while phage-antialigned reactions do not. We experimentally validate our predictions of system-level AMG impacts by measuring the N-dependent effect of P-HM2 expression on growth in a model relative of the genetically intractable MED4, . We also show that AMGs' indirect impacts are synergistically and antagonistically coupled, providing systems-level insight into AMG perturbations and highlighting how nontrivial cascading effects shape host metabolism. - Source: PubMed
Publication date: 2026/04/01
Rozum Jordan CSineath WilliamBohutskyi PavloQuenneville JordanKim Doo NamJohnson ConnahMehta Angad PEvans JamesPollock DavidQian Wei-JunCheung Margaret SWu RuonanFeng Song - Photosynthetic microorganisms rely on multiple pathways in central carbon metabolism to adapt to fluctuating light and energy availability across diel cycles. Mechanistic insight into the regulatory dynamics of this adaptation requires integrating processes spanning disparate timescales, from rapid redox-dependent post-translational modifications (PTMs) to slower changes in protein expression and metabolic pathway usage. To address this complexity beyond genome-based inference and traditional modeling, we develop a whole-cell four-dimensional (3D + time) model of the marine cyanobacterium MED4 that explicitly represents the spatial organization of enzymatic and molecular processes in central carbon metabolism under light perturbation. We employ a perturbation-based research design to experimentally generate time-series, multi-omics measurements that provide molecular descriptors and cryo-ET images as constraints for this dynamic 4D framework. The integration of experiments and modeling across defined light regimes enables quantitative validation of system-level responses and forecasting under distinct light disturbances. We test the hypothesis that light-dependent redox PTMs regulating the structural assembly of a protein megacomplex, the "dark complex," modulate metabolic flux at a conserved regulatory node of the Calvin-Benson cycle (CBC) in cyanobacteria. Our model shows that subcellular spatial organization buffers rapid light-induced changes in thylakoid reaction rates, which are followed by redox-PTM-mediated sequestration or release of CBC enzymes in the dark complex, ultimately impacting carbon fixation dynamics within carboxysomes. Comparison with an equivalently parameterized well-mixed stochastic model demonstrates that post-translational regulation not only buffers transcriptional noise and diffusion-driven fluctuations but also stabilizes phenotypic outcomes, underscoring the importance of spatial heterogeneity in phenotypic robustness. This ability to probe adaptive, spatiotemporally resolved mechanisms in photosynthetic machinery and central carbon metabolism addresses a critical gap in genotype-to-phenotype inference and expands modeling and design capabilities for understudied or genetically intractable autotrophs such as MED4. - Source: PubMed
Publication date: 2026/01/23
Johnson Connah G MChan AaronRozum JordanGeorge AugustParvate Amar DKim Doo NamFeng SongBohutskyi PavloJohnson ZacharySadler NatalieGarcia MarciLi XiaoluTrejo JesseWu RuonanSineath WilliamAnderson Lindsey NEvans James EMehta Angad PQian Wei-JunLuthey-Schulten ZaidaCheung Margaret S - The causal association between plasma proteomes and the risk of developing hepatocellular carcinoma (HCC) in human populations has not been fully elucidated. Mendelian randomization (MR) is an innovative epidemiological study design that enables the unbiased identification of causal relationships by utilizing genetic variants as instrumental variables. Consequently, we employed a two-sample MR approach to investigate the potential causal link between plasma protein levels and the incidence of HCC. A comprehensive bidirectional two-sample MR analysis was performed using genome-wide significant published genome-wide association studies of plasma proteomes (N: 35,559 healthy individuals) and HCC (168 cases and 372,016 controls). Sensitivity analyses were conducted for identified causal proteins. Furthermore, we pursued pathway exploration using Kyoto Encyclopedia of Genes and Genomes and gene ontology analyses. Protein-protein interaction network analysis provided insights into plasma protein-HCC interactions. We identified 17 plasma proteins causally associated with HCC risk (PIVW < .05). Sixteen proteins were positively associated, including TMCC3, METTL1, SNRPF, KRT19, MED4, RFNG, IL26, NRXN1, MSH2, CLCA2, AKT2, CRYZL1, RDH16, CSF3, CPA4 and COPS7B, while EPHA2 was inversely associated. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses implicated key gene correlations with JAK-STAT, PI3K-AKT and chemokine pathways. The protein-protein interaction network highlighted potential plasma protein-HCC relationships. Our genetics-based approach provides evidence supporting a causal role for specific plasma proteomes in influencing HCC risk. Results support causal effects on HCC for TMCC3, METTL1, SNRPF, KRT19, MED4, RFNG, IL26, NRXN1, MSH2, CLCA2, AKT2, CRYZL1, RDH16, CSF3, CPA4, EPHA2, and COPS7B. Experimental validation and mechanistic study are warranted to confirm findings. - Source: PubMed
Chen XueZheng ZhenHu JingYe ShuangLiu Kaitai