ZNF395 antibody - middle region (ARP33163_P050)
- Known as:
- ZNF395 (anti-) - middle region (ARP33163_P050)
- Catalog number:
- arp33163_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF395 antibody - middle region (ARP33163_P050)
Related genes to: ZNF395 antibody - middle region (ARP33163_P050)
- Gene:
- ZNF395 NIH gene
- Name:
- zinc finger protein 395
- Previous symbol:
- -
- Synonyms:
- PRF-1, HDBP2, PBF, DKFZp434K1210
- Chromosome:
- 8p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-30
- Date modifiied:
- 2016-10-05
Related products to: ZNF395 antibody - middle region (ARP33163_P050)
Related articles to: ZNF395 antibody - middle region (ARP33163_P050)
- Clear cell renal cell carcinoma (ccRCC) remains poorly understood at the genetic level. In this study, 12 GEO microarray datasets were combined, and meta-analysis and multiparameter gene prioritization were used to reveal candidate diagnostic biomarkers. Improved preprocessing and analysis were used to identify differentially expressed genes (DEGs), which led to 4651 DEGs enriched in metabolic pathways, immune response, and kidney development. Key transcription factors (TFs), including ZNF692, ZNF395, and ZNF582, were identified. Utilizing WGCNA, 21 hub genes were identified, and diagnostic potential was determined via ROC analysis. Seventeen of the genes with AUC > 0.7 were validated as diagnostic hub genes, including ALDH2, ACADM, KIF11, and PTPRC. Nine of these genes showed significant prognostic relevance. The current work identifies key biomarkers that can enhance ccRCC diagnosis and guide future therapy. - Source: PubMed
Publication date: 2026/02/02
Namdari HaidehRezaei FarhadKaramigolbaghi Maryam - Hypoxia signaling induced by VHL deficiency fuels growth but also imposes metabolic stress on clear cell renal cell carcinomas (ccRCC). Many ccRCC cells depend on glutamine as the primary source of tricarboxylic acid (TCA) anaplerosis. Hypoxia-inducible factor α (HIFα) governs glycolysis but does not directly regulate glutamine metabolism; instead, the factor responsible for orchestrating glutamine metabolism and mitochondrial adaptations to hypoxia remains elusive. In this study, we showed that ZNF395 is a hypoxia-responsive factor that regulates glutamine metabolism in the mitochondria. When activated by a HIF2α-modulated superenhancer, ZNF395 facilitated the transcription of enzymes essential for glutaminolysis, including glutaminase (GLS) and isocitrate dehydrogenase 2. Functionally, ZNF395 depletion resulted in reduced TCA cycle intermediates and their derivatives, including amino acids, glutathione, and pyrimidine nucleotides, leading to impaired mitochondrial respiration. Restoration of mitochondrial complex I function and GLS expression partially rescued the effects of ZNF395 depletion on ccRCC tumor growth. Together, this study underscores the coordinated role of HIFα and ZNF395 in shaping metabolic adaptations in response to hypoxia in VHL-deficient ccRCCs. - Source: PubMed
Koh JoannaLiao ChenghengNg Michelle Shu WenHong Jing HanHeng Hong LeeGui Dan YWang ZhenxunChua Benjamin Yan-JiangLi ZhimeiSobota Radoslaw MLee Lye SiangIqbal JabedLim Kevin JunliangBezwada DivyaDeBerardinis Ralph JSteger GertrudChing JianhongTan PatrickTeh Bin TeanZhang QingYao Xiaosai - Cancer-associated fibroblasts (CAFs) play important roles in the progression of hepatocarcinoma, while the mechanism underlying the pro-invasive transformation of normal fibroblasts (NFs) to CAFs remains poorly defined. lncDILC is a long non-coding RNA previously identified to be downregulated in liver cancer stem cells. Here, we found that lncDILC was also significantly downregulated in liver cancer CAFs compared with NFs. Knockdown of lncDILC in NFs facilitated their conversion into CAFs, and enhanced the ability to promote the migration and invasion of liver cancer cells. Conversely, overexpression of lncDILC in CAFs ameliorated their invasive characteristics, and suppressed cancer cell metastasis. Moreover, we found miR-6071 acted as a target of lncDILC, and functioned as a transcriptive suppressor of zinc finger protein 395 (ZNF395), which exhibited an inhibitory effect on the pro-invasive conversion of fibroblasts. Overexpression of ZNF395 reversed the pro-invasive effects induced by lncDILC knockdown. These results elucidate a pathway of lncDILC-miR-6071-ZNF395 that suppresses the NF-CAF conversion, suggesting new therapeutic targets for the strategies for the treatment of liver cancer. - Source: PubMed
Publication date: 2025/10/30
Li YawenLiu JilongTai ShentaoTong DandanWang BifengLu DingbingShi GuoqingLiu Xuemei - Several studies have suggested that allele-specific expression (ASE)plays a critical role in cancer initiation and progression. However, little is known about genome-wide ASE and monoallelic expression of genes in non-small cell lung cancer (NSCLC). We analysed 11,422 genes that had either at least two Single Nucleotide Variations (SNVs) or a high-confidence single SNV (depth ≥10) in metastatic NSCLC samples, and found that approximately 43 % (4935 genes) exhibited monoallelic expression in at least one sample. On average 21% of genes in each sample showed monoallelic expression. These genes were involved in key cancer hallmarks, including tumour growth, metastasis, maintenance of tumour microenvironment, and cell proliferation. Several important NSCLC driver genes, such as CDH1, STK11, MYH9, ZNF395, TP53, EGFR, JAK2, RB1, CREBBP, FAT4, APC, CTNNB1, and TFRC, were identified in our monoallelically expressed (MAE) gene panel. This suggests that monoallelic expression plays a significant role in how these genes influence NSCLC growth and progression. In addition to the driver genes, the monoallelically expressed gene panel was enriched with imprinted genes. Of the 4935 unique MAE genes 52 genes were either known imprinted or predicted to be imprinted. Interestingly, individual-specific monoallelic expression of genes was predominantly observed, although, 134 genes exhibited consistent monoallelic expression across the samples, indicating that a significant proportion of MAE genes are individual-specific. These consistent MAE genes were found to interact with both MAE and non-MAE genes, highlighting a well-connected network of MAE genes. Overall, these findings could contribute to the development of effective diagnostic and prognostic models and support efforts in implementing tailored treatment strategies and vaccines for NSCLC. - Source: PubMed
Publication date: 2025/06/26
Niharika Asthana ShailendraYadav Harlokesh NarayanSharma NanaochaSingh Vijay Kumar - Human cytomegalovirus (HCMV) is a herpes virus with a long replication cycle. HCMV encoded long non-coding RNA termed RNA2.7 is the dominant transcript with a length of about 2.5kb, accounting for 25% of total viral transcripts. Studies have shown that HCMV RNA2.7 inhibits apoptosis caused by infection. The effect of RNA2.7 on other forms of cell death is still unclear. In this work, we found that RNA2.7 deletion significantly decreased the viability of HCMV-infected cells, while treatment with ferroptosis inhibitor Fer-1 rescued the infection-induced cell death, demonstrating an anti-ferroptosis role of RNA2.7. The results further showed that RNA2.7 inhibited ferroptosis via enhancing Ferritin Heavy Chain 1 (FTH1) and Solute Carrier Family 7 Member 11 (SLC7A11) expression in Erastin treated cells without involving other viral components. Pooled Genome-wide CRISPR screening revealed zinc finger protein 395 (ZNF395) as a new regulator repressing the expression of FTH1 and SLC7A11. HCMV RNA2.7 promoted proteasome-mediated degradation of ZNF395 that resulted in upregulation of FTH1 and SLC7A11 to inhibit ferroptosis, therefore maintain survival in host cells and complete replication of virus. - Source: PubMed
Publication date: 2024/12/26
Xu MingyiRuan ShanSun JingxuanLi JianmingChen DanMa YanpingQi YingLiu ZhongyangRuan QiangHuang Yujing