CHD4 Mouse Monoclonal Antibody
- Known as:
- CHD4 Mouse Monoclonal Antibody
- Catalog number:
- BIN-001108-M01
- Product Quantity:
- 0.05mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CHD4 Mouse Monoclonal Antibody
Related genes to: CHD4 Mouse Monoclonal Antibody
- Gene:
- CHD4 NIH gene
- Name:
- chromodomain helicase DNA binding protein 4
- Previous symbol:
- -
- Synonyms:
- Mi-2b, Mi2-BETA
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2016-10-05
Related products to: CHD4 Mouse Monoclonal Antibody
Related articles to: CHD4 Mouse Monoclonal Antibody
- RNA guanine quadruplexes (rG4s) are noncanonical nucleic acid structures that contribute to diverse cellular functions and disease mechanisms. Defining the proteins that interact with rG4s (rG4IPs) is essential for elucidating their biological roles. Here, we build on the RNA-protein interaction detection (RaPID) platform to develop G4-RaPID, a tailored chemoproteomic strategy for the unbiased profiling of rG4IPs in living cells. Using G4-RaPID, we identified 105 candidate rG4IPs that were commonly enriched across three distinct rG4 sequences. Biochemical analyses confirmed that recombinant hnRNPA0, CHD4, and IGF2BP1 proteins directly bind rG4 structures . In addition, CLIP-seq experiments revealed significant enrichment of hnRNPA0 binding at endogenous rG4 loci. Luciferase reporter assays further demonstrated that hnRNPA0 engages the rG4 in the 5' UTR of mRNA to negatively regulate its translation. Together, these results establish G4-RaPID as a robust approach for mapping rG4-protein interactions in living cells and document hnRNPA0-rG4 recognition as a regulatory mechanism controlling mRNA translation. - Source: PubMed
Publication date: 2026/04/17
Tang FengLiang XiaochenPorter Douglas FMiao WeiliMaehlmann KevinYuan JunKhavari Paul AWang Yinsheng - Opioid and methamphetamine use disorders (OUD and MUD) are characterized by enduring neural adaptations within brain reward circuitry, yet the cell-type-specific post-transcriptional mechanisms underlying these changes remain poorly understood. While microglia are essential for maintaining central nervous system homeostasis and modulating neuroinflammatory responses to drugs of abuse, their alternative splicing (AS) programs have not been defined in the context of addiction. This study characterized the microglial AS landscape in the mouse dorsal striatum during morphine and methamphetamine intravenous self-administration (IVSA), as well as following a 21-day period of abstinence. Analysis of RNA-sequencing data using rMATS and DEXSeq revealed that both drugs significantly dysregulate core splicing machinery, with skipped exons (SE) emerging as the most prevalent splicing event. Notably, morphine exposure induced a robust persistent splicing signature, comprising 736 exonic regions in 221 genes that remained altered through abstinence, whereas methamphetamine-induced changes were primarily reversible. Functional annotation predicted that approximately 27.5% of these events induce frameshifts, potentially impacting critical microglial pathways such as autophagy (), chromatin remodeling (), and RNA processing (). These findings identify previously unrecognized post-transcriptional neuroimmune mechanisms and suggest that persistent splicing dysregulation in microglia may contribute to the long-term pathophysiology of OUD. - Source: PubMed
Publication date: 2026/04/05
Margetts Alexander VBystrom Lauren LVilca Samara JTuesta Luis M - Skeletal muscle fiber-type composition is key determinant of systemic metabolism and health. However, how fiber-type-specific gene expression patterns are established and maintained to specify myofiber identity remains unclear. Here we show that BRD4 is a crucial regulator for muscle fiber identity and metabolism. In humans, BRD4 expression correlates with muscle contractile properties, and is notably altered in individuals with obesity. In mice, HFD feeding elevates BRD4 protein levels, preceding body weight changes, while muscle-specific Brd4 deletion induces a slow-oxidative fiber shift, enhances energy expenditure, and protects against diet-induced obesity and insulin resistance. Mechanistically, BRD4 cooperates with MEF2 and CHD4 to regulate fast-twitch myofiber gene expression. CHD4 deletion mirrors the metabolic benefits seen with BRD4 loss. Importantly, BRD4 inhibition with JQ1 replicates these effects in mice and human myotubes. These findings establish BRD4 axis as a critical determinant of myofiber identity and metabolism, offering a potential therapeutic strategy for metabolic disorders. - Source: PubMed
Publication date: 2026/04/09
Zhou ZhengLiu LinXu ZhishengZhou DanxiaLiu AnqiYuan JiachenShen GonghaoGuo QiqiYin YujingMao YanSun WanpingXiao LiweiLv ChengKiram AbdukaharYang LikunJia YuhuanKe LuFang LeiLi WeiqinFu TingtingGan Zhenji - Chromodomain helicase DNA‑binding protein 4 (CHD4) is a core adenosine triphosphate (ATP)‑dependent chromatin‑remodeling factor of the nucleosome‑remodeling and deacetylase (NuRD) complex. It plays a crucial role in chromatin structure regulation, gene expression regulation, and DNA damage response. It has been demonstrated that CHD4 has context‑dependent functions in tumor development and progression. It can influence tumor progression via such mechanisms as regulating tumor‑related signaling pathways, maintaining the silencing of tumor suppressor genes, and promoting metabolic adaptation; it can also exert tumor‑suppressive effects in specific transcriptional regulatory environments. Additionally, during DNA damage response, CHD4 participates in chromatin remodeling at damage sites, in cell cycle recovery, and in repair pathway selection. It is also involved in the development of tumor treatment resistance through mechanisms that include regulation of DNA repair, cell cycle progression, drug efflux, the tumor immune microenvironment, and replication fork stability. It has also been shown that various non‑coding RNAs participate in the functional regulation of CHD4 by modulating its expression, localization, and protein stability. In summary, as a key node connecting chromatin regulation, genome stability, and tumor treatment response, CHD4 holds significant importance in tumor progression and treatment. - Source: PubMed
Publication date: 2026/04/03
Li ShuoMa QuanLian KeyingJiang ZhishengMa Yun - GLI1-rearranged tumors of the gynaecologic tract are rare, but likely under-recognised, neoplasms, which have recently been reported in the ovary and uterus. It is important to identify these neoplasms due to their malignant potential and possible responsiveness to tyrosine kinase inhibition in the metastatic setting. We present the largest series to date of GLI1-rearranged tumours of the gynaecologic tract with comprehensive clinicopathologic analysis. Ten cases (7 primary ovarian tumors and 3 primary uterine corpus tumours) with GLI1 rearrangements were identified in the case files of the contributing authors, and clinical findings, histomorphology, and immunophenotype were reviewed. Patients ranged in age from 26 to 60 years of age. Three of the 10 tumours in our series recurred, including one late recurrence 180 months postoperatively. The 10 cases, in keeping with previous reports in the literature, showed 2 main morphologic patterns: (i) variable admixture of trabecular, nested and tubular/microfollicular growth, akin to sex cord-stromal morphology; and (ii) cytologically bland, elongated spindle cells with abundant admixed blood vessels and variably myxoid matrix, morphologically suggestive of a low-grade mesenchymal neoplasm such as low-grade endometrial stromal sarcoma. In both scenarios, the immunophenotype was not supportive of the morphologic impression (with the sex cord-like tumours typically showing negative staining for calretinin, inhibin, and WT-1, whereas the tumours resembling low-grade endometrial stromal sarcomas were consistently hormone receptor-negative), and the diagnosis was ultimately made after next-generation sequencing. GLI1 fusion partners included PTCH1 (4 cases), ACTB (4 cases), CHD4 (1 case), and TXNIP (1 case). Morpho-molecular correlation suggested that tumours with PTCH1::GLI1 fusions were enriched in sex cord-like morphology, whereas tumours with ACTB::GLI1 fusions were enriched in low-grade endometrial stromal sarcoma-like morphology. Given that our cases were identified in a relatively short time period, it is likely that GLI1-rearranged tumours are more common in the female genital tract than is realised and a high index of suspicion is required to initiate appropriate testing and establish the diagnosis. In the absence of readily available appropriate molecular testing, GLI1 immunohistochemistry can serve as an acceptably accurate surrogate biomarker for GLI1 rearrangement, since we found that GLI1 immunohistochemistry showed strong, diffuse nuclear staining in 6 GLI1-rearranged gynaecologic tumours stained for this study, whereas this was consistently negative, or at most weak/focal, in an array of 135 morphologic mimics. - Source: PubMed
Publication date: 2026/04/03
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