TRIM25 / RNF147 Clone 'N3C3 antibody
- Known as:
- TRIM25 / RNF147 Clone 'N3C3 (anti-)
- Catalog number:
- 'GTX116209
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- TRIM25 / RNF147 Clone 'N3C3 antibody
Related genes to: TRIM25 / RNF147 Clone 'N3C3 antibody
- 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 / RNF147 Clone 'N3C3 antibody
Related articles to: TRIM25 / RNF147 Clone 'N3C3 antibody
- 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 - SARS-CoV-2 3CL protease (3CL) plays crucial role in the viral life cycle by releasing different non-structural proteins from viral polyproteins. It also interacts with several host factors and orchestrates different host cell pathways by cleaving key cellular factors involved in immune modulation, cellular metabolism and cell death. Several host factors have been identified as high confidence substrates of 3CL which regulates host cellular environment both in an enzyme-dependent and enzyme-independent manner. Degradation of RIG-I, TRIM25 and NLRP12 by 3CL downregulates the innate immune response while enzyme-independent interaction with host factors like MAVS promote both its degradation and upregulation. Cellular transcription and translation are altered by interaction of 3CL with host proteins. It affects cell-death by interacting with factors like Gal-8, NDP52 and GSDMD. Post-COVID neurodegenerative disorders have been observed due to the downregulation of neuronal factors like NEMO and UBE3A. The spectrum of 3CL interaction with the key host factors indicates the alternate role of viral protease that modulates host response during infection. Several 3CL targets and their cleavage sites on the target proteins have been identified. This review highlights the crosstalk between 3CL and different host factors as possible alternate therapeutic targets to inhibit the viral propagation as well as address the post COVID clinical issues. - Source: PubMed
Publication date: 2026/06/10
Sanyal DebosmitaChaubey Binay - Vesicular stomatitis virus is a zoonotic rhabdovirus that infects livestock and can cause economically important disease. Tripartite motif-containing 25 (TRIM25) is an E3 ubiquitin ligase involved in innate antiviral signaling, but its role in pigs during vesicular stomatitis virus infection is unclear. - Source: PubMed
Cao YingZhang JinxiaYoo DongwanZhang HaowenJiang DandanHu YueCong XiaoyanLi JuntongWu XiangjuDu YijunQi JingHuang Juan - Chronic inhalation of crystalline silica precipitates silicosis, a progressive fibrotic lung pathology for which effective therapeutic strategies are currently lacking. Sophoricoside, a bioactive isoflavone glycoside derived from the seeds of Sophora japonica, possesses documented antioxidant and anticoagulant activities; however, its potential antifibrotic efficacy remains ill-defined. Accordingly, the present investigation seeks to systematically evaluate the protective effects of Sophoricoside against pulmonary fibrosis and to decipher the molecular mechanisms governing its action. - Source: PubMed
Publication date: 2026/06/01
Qian JiazhenLi SiyuanDeng LangWang XingchenRen LuHu YanZhou YuxingXie WeixiTang SiyuanZhang LuLi XinLiu YazhuoLiu Wei