TRIM25 Pre-design Chimera RNAi
- Known as:
- TRIM25 Pre-design Chimera RNAi
- Catalog number:
- H00007706-R01
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- TRIM25 Pre-design Chimera RNAi
Related genes to: TRIM25 Pre-design Chimera RNAi
- Gene:
- TRIM25 NIH gene
- Name:
- tripartite motif containing 25
- Previous symbol:
- ZNF147
- Synonyms:
- EFP, RNF147
- Chromosome:
- 17q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-16
- Date modifiied:
- 2015-09-01
Related products to: TRIM25 Pre-design Chimera RNAi
Related articles to: TRIM25 Pre-design Chimera RNAi
- Ribophagy is a crucial mechanism that maintains ribosome homeostasis in the cell by directing nonfunctional ribosomes to degradation via macroautophagy/autophagy. Impaired ribophagy may lead to ribosome quality control disorders and may consequently be associated with various diseases known as ribosomopathies. This topic has been actively studied over the past decade, but the complete mechanism of ribophagy is not fully understood. To study the mechanism of ribophagy, we performed a genome-wide CRISPR-Cas9-based screening using a fluorescent ribophagy reporter, which is a cell line with ribosomes carrying RPL29 fused with mCherry and GFP fluorescent proteins. Using the genome-wide Brunello library of guide RNAs, we identified the most promising targets for further study, including the ubiquitin ligase TRIM25, for which we have shown specific binding to the ribosome during ribophagy induction, leading to ubiquitination of the ribosome on the nascent peptide chain and degradation of the whole ribosome. Our findings also demonstrated that poly(I:C) treatment, which mimics viral infection, activates ribophagy in a TRIM25-dependent manner, suggesting the ribophagy pathway could be an antiviral defense mechanism. Taken together, we discovered a novel regulator of ribophagy, TRIM25, which provides new insights into the regulation of selective autophagy in the context of ribosomopathies. - Source: PubMed
Publication date: 2026/07/13
Golubeva JuliaMikhailov AlexeyShepelev NikitaPleshko ElizavetaGuseva EkaterinaSidorova VeraShagimardanova ElenaAndrianova NadezdaPlotnikov EgorKarpov DmitryNovikova SvetlanaZgoda VictorRubtsova MariaDontsova OlgaSergiev Petr - Sepsis-associated acute liver injury (SALI) is an independent risk factor that significantly worsens sepsis prognosis, underscoring the need for mechanistic insights to guide targeted therapy. Accordingly, we established a sepsis mouse model via cecum ligation and puncture (CLP) and performed in vitro experiments using murine hepatic Kupffer cells stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Here, we found that growth arrest and DNA damage 45A (GADD45A) was highly expressed in liver tissues of CLP-induced septic mice, and its knockdown ameliorated liver injury and systemic inflammation. Mechanistically, GADD45A knockdown upregulated ATP synthase F1 subunit alpha (ATP5A1) expression by disrupting the interaction between tripartite motif-containing 25 (TRIM25) and ATP5A1, thereby suppressing pyroptosis and pro-inflammatory cytokine secretion in LPS+ATP-stimulated murine Kupffer cells. Additionally, Aly/REF export factor (ALYREF), a 5-methylcytosine (mC) reader, was upregulated in septic liver tissues and LPS+ATP-treated Kupffer cells. ALYREF likely stabilized GADD45A mRNA in an mC-dependent manner, thereby promoting its expression. ALYREF knockdown inhibited NLRP3 inflammasome-dependent macrophage pyroptosis and alleviated SALI, likely by modulating the GADD45A/TRIM25/ATP5A1 axis. Notably, the increased expression of ALYREF in SALI appeared to be driven by activated STAT3 signaling. In conclusion, ALYREF, likely driven by activated STAT3 signaling, appears to activate the GADD45A/TRIM25/ATP5A1 axis in an mC-dependent manner to promote NLRP3 inflammasome-dependent macrophage pyroptosis, thereby contributing to the development of SALI and suggesting a promising therapeutic strategy for targeted SALI intervention. - Source: PubMed
Publication date: 2026/07/09
Pei YanfangTan ZhengCao YanZhou WeiGeng YanZhu CuiCao CaiwenXu JingNie LingjingYu FangFan MaiyingHan XiaotongPeng Haiping - The genomes of human adenoviruses (HAdVs) are double-stranded DNA bound with viral nucleocapsid protein VII. During HAdV infection, host RNA polymerase can produce viral-associated RNAs (VA RNAs) that are recognized by retinoic acid-inducible gene I (RIG-I). However, it remains unclear whether and how HAdV, as a DNA virus, can evade RNA sensors. Here, we show that nucleocapsid protein VII from HAdV can inhibit type I interferon (IFN) production by antagonizing RIG-I. It is found that protein VII precursor of HAdV/C5 (C5preVII) could impede tripartite motif-containing protein 25 (TRIM25)-mediated K63 ubiquitination of RIG-I by preventing TRIM25 oligomerization. Importantly, we provide in vitro and in vivo evidence that cytoplasm-oriented C5preVII is responsible for TRIM25 inactivation. Moreover, the preVII proteins from diverse HAdVs show evolutionarily conserved immunosuppressive functions. Collectively, our study illustrates the function of HAdV preVII in retinoic acid-inducible gene I-like receptor (RLR) signaling and uncovers an evolutionally conserved mechanism of DNA viruses to evade host RNA sensors. - Source: PubMed
Publication date: 2026/07/09
Yu Pei-HongZhang Li-MinGu QianLiu Jia - Osteoporosis (OP) is a gradual metabolic bone disease characterized by decreased bone mass and degradation of bone microarchitecture. It affects hundreds of millions of people globally and places considerable pressure on healthcare systems. Current pharmacological treatments, such as bisphosphonates, selective estrogen receptor modulators, and anabolic agents, can reduce fracture risk; however, their prolonged use is limited by significant adverse effects, elevated treatment costs, and a lack of sustained disease remission. Their constraints have intensified interest in restorative approaches utilizing mesenchymal stem cells (MSCs). In the past 20 years, MSCs have emerged as attractive treatment options for OP due to their capacity to differentiate into osteoblasts, modulate immune responses, and exert paracrine effects. Bone marrow-MSCs are the best characterized; nevertheless, MSCs obtained from adipose tissue, umbilical cord, and dental pulp have distinct benefits. Preclinical data demonstrate that direct MSC transplantation enhances bone mineral density, promotes osteoblast production, and reestablishes the equilibrium of bone remodeling in many OP models, including Ovariectomy, glucocorticoid-induced OP, and diabetic OP. Nonetheless, significant obstacles persist: insufficient targeting of osteoporotic bone surfaces, suboptimal cell viability and integration, donor heterogeneity, and unresolved safety concerns. The discovery that the secretome and exosomes (EXOs) produced from MSCs recapitulate several therapeutic advantages of the original cells has initiated a transition toward cell-free methodologies. EXOs produced from MSCs include osteogenic microRNAs (including miR-150-3p and miR-21), inhibit NLRP3 inflammasome activation in osteoclasts, promote macrophage polarization toward an M2 phenotype via TRIM25/TREM1 signaling, and facilitate angiogenesis through the activation of the PI3K/Akt pathway. Furthermore, nanoparticle engineering and combinatorial medicines are advancing to enhance targeting and therapeutic efficacy. - Source: PubMed
Publication date: 2026/06/22
Ardah Mustafa TAbdulsahib Waleed KNaji Hasanain AmerRekha M MPatro Pradeepta SekharNanda AnimaSharma VipashaChauhan Ashish SinghAlimova ZebinisoYazdi Farzaneh - Japanese encephalitis virus (JEV) is a neurotropic flavivirus that causes a substantial threat to human health and livestock; however, the epitranscriptomic mechanisms that support its replication remain poorly defined. Here, we identify a proviral host factor CH zinc-finger protein ZNF33B that promotes JEV infection through coupling N-methyladenosine (mA) RNA modification to autophagy regulation. Mechanistically, ZNF33B recruits METTL14 to stabilize the METTL3-METTL14 methyltransferase complex, thereby increasing global mA deposition. Multi-omics analyses reveal that ZNF33B selectively binds mA-modified sites within the antiviral transcript Trim25 (c.1567 and c.1669 bp) to accelerate its decay. We further demonstrate that TRIM25 functions as an E3 ubiquitin ligase that catalyzes K48-linked ubiquitination of ATG7 at lysines 389 and 423, leading to its proteasomal degradation and ultimately suppressing autophagic flux. In contrast, ZNF33B-mediated Trim25 degradation counteracts its inhibitory effect on autophagy, creating a favorable environment for viral replication. In vivo, adeno-associated virus (AAV)-mediated ZNF33B delivery increases mouse brain mA levels, decreases TRIM25 expression, elevates ATG7 abundance, exacerbates JEV-induced neuropathology, and accelerates mouse mortality. Together, these findings reveal a previously uncharacterized ZNF33B-mA-TRIM25-autophagy axis that JEV hijacks to evade host antiviral responses, providing new insights into flaviviral pathogenesis and potential therapeutic targets. - Source: PubMed
Publication date: 2026/06/18
Du JianLi ChunweiLuo JiyuanZhang HuizhiZhang JinyanWang SuyaChen HuanchunXu HongliLi XiangminQian Ping