TRIM25 Pre-design Chimera RNAi
- Known as:
- TRIM25 Pre-design Chimera RNAi
- Catalog number:
- H00007706-R01
- Product Quantity:
- 10 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
- Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis often leads to severe kidney damage. To better understand ANCA-associated glomerulonephritis (AAGN) and identify potential new therapeutic targets, we performed comprehensive transcriptomic and compartmental proteomic analysis of kidney biopsies from 23 patients in the transcriptomic cohort, 10 in the proteomic cohort, and 5 healthy controls for each comparison. - Source: PubMed
Stojkic IvanaShapiro John PArazi ArnonSong HuijuanYan PearllyPuchulu-Campanella EstelaWang HubaoSmoyer William EFussner Lynn ASatoskar AnjaliWang XinParikh Samir VArdoin Stacy PKoboldt DanRovin Brad HAlmaani Salem - Circular RNAs (circRNAs) play crucial roles in cancer progression and metastasis. However, the expression profiles and biological roles of circRNAs in non-small cell lung cancer (NSCLC) remain unclear. In this study, we found a novel circRNA, hsa_circ_0001936(circBRWD3), in NSCLC and investigated the biological role of circBRWD3 in NSCLC progression in vitro and in vivo. qRT-PCR was used to quantify the expression of circBRWD3 in NSCLC tissues, serum and cells. Cell growth curves, colony formation, Edu assay and transwell assays were conducted to study the function of circBRWD3. Finally, the molecular mechanism of circBRWD3 was revealed by Bioinformatic analyses, RNA pull-down analysis, RNA Fluorescence in situ hybridization (FISH), RNA-Binding Protein Immunoprecipitation (RIP), western blot, dual-luciferase reporter gene assays and rescue experiments. Our results showed that circBRWD3 was upregulated in NSCLC tumor tissues, patient serum and cell lines. CircBRWD3 knockdown inhibited NSCLC cells' growth and metastasis both in vitro and in vivo, while circBRWD3 overexpression had the opposite effect. Mechanistically, circBRWD3 binds to the TRIM25 protein to enhance its stability and mediate ubiquitin degradation of the p53 protein. In addition, circBRWD3 acted as a sponge for miR-135a-5p and miR-135b-5p to regulate the expression of SPTBN2, which promoted NSCLC progression. Our findings uncovered a tumor oncogenic function of circBRWD3 in NSCLC through the regulation of TRIM25 protein stability and miR-135a-5p/miR-135b-5p/SPTBN2 axis. CircBRWD3 may act as a promising oncogenic biomarker and therapeutic target for NSCLC. - Source: PubMed
Publication date: 2026/07/16
Zhu YanhuaHe YuefengXiao MeiGuo LeiLiu XiaoChen XiLiu JiezhenChen XuZhang Yanliang - Chromosomal instability (CIN), a hallmark of malignancy, remains poorly understood in clear cell renal cell carcinoma (ccRCC). Here, we identify spindle and kinetochore-associated protein 3 (SKA3) as a critical regulator of CIN in ccRCC. BAP1 loss-of-function mutations, prevalent in ccRCC, drive aberrant SKA3 overexpression. Mechanistically, BAP1 deubiquitinates nuclear receptor co-repressor 1 (NCOR1) to enhance its recruitment to the SKA3 promoter, thereby repressing SKA3 transcription. Additionally, BAP1-mediated histone H2AK119 deubiquitination at the TRIM25 promoter activates the expression of TRIM25, facilitating ubiquitin-proteasome-mediated degradation of SKA3. BAP1 deficiency disrupts both regulatory pathways, leading to aberrant accumulation of SKA3, which fuels CIN and correlates with metastasis progression and poor prognosis. In conclusion, our findings establish dysfunction of the BAP1-SKA3 axis as a molecular driver of CIN in ccRCC and suggest SKA3 as a potential therapeutic target for BAP1-mutant ccRCC. - Source: PubMed
Publication date: 2026/07/15
Wang YueyangLai ChongWang LinglingDeng JingwenTian ZhouLiang ZhiyongZhang Honghe - Ankylosing Spondylitis (AS) is a chronic inflammatory autoimmune rheumatic disease that primarily affects the spine and sacroiliac joints. This study aimed to investigate the expression levels of immune response-related genes, including , , , , , , and , as well as the serum levels of CXCL10 and SIRPA proteins in patients with AS. In addition, the potential diagnostic performance of these molecular and serum biomarkers in distinguishing patients with AS from healthy controls was evaluated. A total of 45 patients with AS and 44 healthy controls were included in the study. Immune-related gene expression levels were analyzed using RT-PCR. In addition, serum CXCL10 and SIRPA protein levels were evaluated using ELISA. The expression levels of , , , , and were significantly increased in patients with AS compared to healthy controls ( < 0.05). In contrast, no significant differences were detected in the expression levels of and . In the ROC analysis, the highest diagnostic performance was obtained for (AUC = 0.741), (AUC = 0.720), and (AUC = 0.722). Serum CXCL10 and SIRPA levels were not significantly different between the groups. In AS, genes particularly associated with NF-κB and interferon signaling pathways (, , , , and ) were found to be significantly altered, and these genes may serve as potential molecular biomarkers for AS. In contrast, the diagnostic power of serum protein biomarkers is limited. These findings indicate that the potential of these genes as biomarkers for AS pathogenesis should be further supported by advanced studies evaluating their expression levels. - Source: PubMed
Publication date: 2026/06/27
Dogan Sevil CeyhanAgbektas TugbaAtas MertKabak GoncaTas AycaSilig Yavuz - Small nucleolar RNAs (snoRNAs) play crucial regulatory roles in various cancers. However, the mechanisms by which snoRNAs regulate N6-methyladenosine (mA) modifications in colorectal cancer (CRC) remain unclear. This study systematically deciphered the precise interaction mechanism between and the mA reader IMP2 in CRC. We demonstrate that specifically stabilizes IMP2 to activate the PIK3CD-CHKA-Kennedy pathway in an mA-dependent manner, promoting endoplasmic reticulum stress (ERS) and phosphatidylcholine (PC) biosynthesis, thereby driving CRC. Conversely, the -targeting antisense oligonucleotide (ASO), ASO-78, effectively suppresses ERS and PC levels, inhibiting CRC progression. Mechanistically, , relying on the "UAAUGA" element in its C-D box region, specifically binds to the Lys221 ubiquitination site of IMP2, blocking TRIM25-mediated degradation of IMP2 and maintaining its stability. IMP2 enhanced the stability and translation of the target mRNAs and by recognizing their corresponding mA positions, mA-3208 and mA-1619, respectively, to reshape the phosphatidylcholine metabolite profile in CRC cells. In terms of potential therapeutic strategies, the ASO-78 can significantly inhibit CRC cell proliferation, reduce ERS levels, and decrease phosphatidylcholine content. The combination of ASO-78 and IMP2 inhibitor IMP2-IN1, by dual blocking of the -IMP2 axis, exhibits an excellent proliferation-inhibiting effect in CRC organoids. This study not only reveals a mechanism by which the -IMP2 interaction regulates CRC occurrence and development but also provides theoretical basis for innovative therapeutic strategies for precise targeting of tumor snoRNA-mA reader interactions. - Source: PubMed
Publication date: 2026/07/14
Zhao YingqiHu XiaoyunLi YalunZhang JingGuo HaoZhang YuyingWu TingGuo JinyuPeng YiChe YingZhu XianglongChen QiuchenGrieve DavidWei MinjieWu Huizhe