DGCR8 Antibody (Center)
- Known as:
- DGCR8 Antibody (Center)
- Catalog number:
- AP8933c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- DGCR8 Antibody (Center)
Related genes to: DGCR8 Antibody (Center)
- Gene:
- DGCR8 NIH gene
- Name:
- DGCR8 microprocessor complex subunit
- Previous symbol:
- C22orf12
- Synonyms:
- DGCRK6, Gy1, pasha
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-29
- Date modifiied:
- 2019-01-25
Related products to: DGCR8 Antibody (Center)
Related articles to: DGCR8 Antibody (Center)
- DiGeorge syndrome critical region gene 8 (DGCR8) is best known as the RNA-binding subunit of the microprocessor complex required for canonical microRNA (miRNA) biogenesis. Whether DGCR8 also exerts a direct, microprocessor-independent function in the RNA polymerase II (Pol II) transcription cycle remains unclear. Here, we combined rapid protein degradation with nascent transcription profiling to examine the immediate role of DGCR8 in transcriptional regulation in mouse embryonic stem cells (mESCs). We found that DGCR8 broadly occupies promoters and transcription start sites (TSSs) with limited co-occupancy by its catalytic microprocessor partner DROSHA. Acute DGCR8 depletion triggered a rapid genome-wide reduction in nascent RNA synthesis as measured by TT-seq, whereas PRO-seq revealed only modest changes in Pol II occupancy and no significant alteration in promoter-proximal pausing, suggesting that DGCR8 primarily supports transcriptional output rather than Pol II pausing. Consistently, TT-seq/PRO-seq ratios were broadly reduced following DGCR8 depletion, whereas acute DROSHA depletion produced the opposite effect. Mechanistically, proteomic and biochemical analyses identified DGCR8 interactions with Enhancer of Rudimentary Homolog (ERH) and the elongation factor SPT5. DGCR8 depletion reduced ERH and SPT5 chromatin occupancy, while acute ERH depletion similarly diminished SPT5 chromatin association and nascent transcription. Together, these findings identify a non-canonical DGCR8-ERH-SPT5 regulatory module that sustains global nascent transcription independently of the canonical DGCR8-DROSHA Microprocessor complex. - Source: PubMed
Publication date: 2026/08/01
Wang JinCai YingWang DuanduanShen HongjieXu Wenqi - Chronic stress contributes to hippocampal neuronal apoptosis and neural circuit dysfunction in major depressive disorder (MDD), but the epitranscriptomic mechanisms regulating stress-responsive microRNAs remain unclear. This study investigated whether methyltransferase-like 3 (METTL3)-mediated N6-methyladenosine (m6A) modification promotes miR-140-3p maturation and neuronal apoptosis through the OTX2/Wnt/β-catenin axis under chronic stress. - Source: PubMed
Publication date: 2026/08/04
Zhang YuanxiangDu XinFu MengxueHu HaitaoLu JuanPan TongshuaiYuan LiliWu YigaoTong Jiucui - Cardiometabolic diseases remain a major global health burden, and current therapies only partially address the persistent residual risk driven by chronic inflammation, hypoxia, metabolic overload, and mechanical stress. A critical need is to understand how these diverse stress signals are integrated at the cellular and molecular levels to determine whether tissues adapt or undergo pathological remodeling. This review presents a comprehensive framework of kinase-microRNA (miRNA) crosstalk as an emerging regulatory axis in cardiometabolic disease. We discuss how stress-activated kinase pathways, including ERK, p38/JNK, PI3K-Akt-mTOR/S6K2, AMPK, GSK-3, and EGFR, reprogram miRNA output through phosphorylation of key components of the miRNA machinery, including DROSHA/DGCR8, DICER-TRBP, and AGO2. These phosphorylation-dependent mechanisms influence miRNA processing, substrate selection, RISC assembly, and target repression in a context-dependent manner. We further highlight the reciprocal regulation whereby miRNAs modulate kinase signaling pathways, establishing feedback networks that regulate inflammation, apoptosis, fibrosis, angiogenesis, and metabolic adaptation across cardiac, vascular, and immune cells. Emerging technologies, including AGO2 eCLIP, phosphoproteomics, CRISPR-based perturbations, and single-cell/spatial profiling, allow causal mapping of kinase-miRNA networks. Collectively, these advances establish kinase-miRNA crosstalk as a promising mechanistic framework and therapeutic target for precision intervention in heart failure, atherosclerosis, diabetic cardiomyopathy, and related cardiometabolic diseases. - Source: PubMed
Publication date: 2026/07/22
Ahmad FirdosKarim AsimaKannan MeganathanQaisar Rizwan - Enterovirus 71 (EV71) is the main causative agent of severe hand, foot, and mouth disease (HFMD) in children. Dysregulation of microRNAs (miRNAs) has been associated with HFMD progression, but the underlying regulatory mechanisms remain incompletely characterized. - Source: PubMed
Publication date: 2026/07/01
Hu QuanmanChen LongLu SaiweiJi WangquanLong JinzhaoYang HaiyanJin YuefeiChen ShuaiyinDuan Guangcai - A high genetic predisposition for neuropsychiatric disorders, such as schizophrenia and autism spectrum disorders (ASDs), is 22q11.2 deletion syndrome (22q11DS), caused by a hemizygous microdeletion in the q-arm of human chromosome 22. The deletion most often spans a 3 Mb region, with variable breakpoints ranging from 1.5 to 3 Mb. Experimental studies on 22q11DS have revealed several aspects of the pathophysiology of neuropsychiatric disorders and also identified various interventional and rescue strategies. Herein, we review these strategies by grouping the studies into three main mechanistic categories: (i) microRNA (miR)-mediated, (ii) mitochondrial, and (iii) neural circuit deficits in polygenic deletion, and also briefly describe a few other monogenic mechanisms implicated. Haploinsufficiency of Dgcr8, a 22q11DS gene involved in miR processing, forms the center of miR-mediated mechanisms and rescuing consequent pathophysiology rely on age-dependent, brain region-specific or global replenishment of miRs or their targets. Seven genes in the 22q11.2 genomic region encode mitochondrial proteins and approaches to mitigate these gene deficiencies concentrate on the respective mitochondrial functions affected. We briefly describe other potential monogenic mechanisms for intervention including transcriptional regulation, synaptic release, catecholamine metabolism, and cell-cell adhesion, represented by Tbx1, Sept5, Comt, Arvcf, and Cldn5. We also give examples of how the multifaceted pathophysiological mechanisms and rescue strategies can have convergent effects at the molecular, synaptic, cellular and circuit levels. Based on the experimental interventions identified in the 22q11DS studies, we inform on the supportive therapies possible now and the future potential of curative interventions. - Source: PubMed
Publication date: 2026/06/26
Devaraju Prakash