FUBP1 antibody - N-terminal region (ARP35703_T100)
- Known as:
- FUBP1 (anti-) - N-terminal region (ARP35703_T100)
- Catalog number:
- arp35703_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FUBP1 antibody - N-terminal region (ARP35703_T100)
Related genes to: FUBP1 antibody - N-terminal region (ARP35703_T100)
- Gene:
- FUBP1 NIH gene
- Name:
- far upstream element binding protein 1
- Previous symbol:
- FUBP
- Synonyms:
- FBP
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-06
- Date modifiied:
- 2019-04-23
Related products to: FUBP1 antibody - N-terminal region (ARP35703_T100)
Related articles to: FUBP1 antibody - N-terminal region (ARP35703_T100)
- Cisplatin (DDP) is a commonly used chemotherapeutic drug for oral squamous cell carcinoma (OSCC) clinical treatment. However, DDP resistance often brings about treatment failure. This study aims to demonstrate the mechanism of JARID1B in DDP-resistance of OSCC cells. Tissue specimens of OSCC and adjacent normal tissues were collected and OSCC cell lines resistant to DDP were established, followed by measurement of JARID1B, H3K4me3, miR-495-3p and FUBP1 levels. CCK-8 was used to detect the IC value. Cell proliferation and apoptosis were assayed. The enrichment of JARID1B and H3K4me3 on the miR-495-3p promoter was assayed via ChIP. The binding between miR-495-3p and FUBP1 was confirmed via dual-luciferase reporter assay. Results showed that JARID1B and FUBP1 were highly expressed in OSCC, while miR-495-3p was lowly expressed. After inhibiting JARID1B expression in OSCC cells, cell proliferation was decreased, apoptosis was increased, and cell resistance to DDP was reduced. JARID1B downregulation increased H3K4me3 levels and promoted miR-495-3p expression, which promoted the binding of miR-495-3p to FUBP1, thus downregulating FUBP1 transcription. FUBP1 overexpression or miR-495-3p downregulation partially reversed the inhibitory effect of JARID1B downregulation on DDP resistance of OSCC cells. In conclusion, JARID1B-mediated H3K4me3 demethylation promotes DDP resistance in OSCC cells through the miR-495-3p/FUBP1 axis. - Source: PubMed
Publication date: 2026/05/21
Mao JixiongXu Lei - Colitis-associated colorectal cancer (CAC) is a serious complication of inflammatory bowel disease. As stress-responsive membraneless organelles, stress granules (SGs) are involved in modulating inflammatory suppression and promoting tumorigenesis, but their role in the pathogenesis of CAC remains unclear. This study reveals that SGs exhibit a stage-specific function during CAC progression, being protective in acute colitis but transitioning to a tumor-promoting role in the dysplasia-carcinoma sequence. We first demonstrate that, during acute colitis, fluctuating oxidative stress drives dynamic SGs assembly. However, despite persistently elevated oxidative stress from chronic colitis to dysplasia, SGs levels paradoxically decline. This decline is attributed to the upregulation of TOM1, a novel negative regulator that binds the NTF2L domain of the core SGs scaffold protein G3BP1 to promote SGs disassembly, thereby counteracting the oxidative stress-driven assembly. The consequent disassembly facilitates the nuclear translocation of the oncogenic transcription factor FUBP1, which in turn promotes c-Myc expression and thereby contributes to tumorigenesis. Our findings establish the regulation of SGs dynamics, particularly via TOM1 and G3BP1, as a promising therapeutic strategy for CAC. - Source: PubMed
Publication date: 2026/05/07
Wan ZiyuQian MeiruiYu JiawenShu TaiyuWang DanLiang XueChen RuoShi BoCui HongyongChen ZhinanJiang Jianli - Current first-line drugs rarely achieve functional curesfor chronic hepatitis B patients, which urges us to explore novel anti-HBV therapeutic strategies. In this study, we found that the novel chemical compound 0411, a derivative of the FUBP1 inhibitor, FUBPI-IN-1, significantly suppressed HBV transcription both in vitro and in vivo. Transcriptome sequencing demonstrated that 0411 treatment markedly upregulated the expression of the dual-specificity phosphatase 5 (DUSP5) gene, a crucial regulator of the MAPK pathway. Further functional studies illustrated that the antiviral activity of compound 0411 was dependent on DUSP5. Mechanismly, 0411 treatment in HepG2-NTCP cells enhances the deposition of active histone modifications on the promoter of DUSP5 significantly. In conclusion, our findings demonstrate the potential of 0411 as an effective agent against HBV transcription. - Source: PubMed
Publication date: 2026/04/16
Zhao ShuangWei HaishaLiang YiFan Hui - - Source: PubMed
Publication date: 2026/02/16
Wang XiaosongXing LeiYang RuiChen HangWang MinJiang RongZhang LuyuChen Junxia - Disease-specific diversity in RNA transcripts stems from RNA splicing, ribosomal abnormalities, and other factors. However, the mechanisms underlying the regulation of rRNA expression in the nucleolus and mRNA expression in the cytoplasm during cancer and neuronal differentiation remain largely unknown. In this article, we review current knowledge and discuss the regulatory mechanisms of rRNA and mRNA expression in human diseases using the splicing model of PUF60 (poly(U) binding splicing factor 60)-also known as (), , , and (Gene ID: 22827). Noncoding RNAs, much like coding RNAs, have been found to be translated into proteins with significant physiological functions. Splicing is also involved in dominant ORF RNAs implicated in the expression of both noncoding and coding RNAs. Here, we analyze recent findings regarding gene splicing, ribosome formation, and the determination of selected ORFs (dominant ORFs) in a system modeled on FIR splicing in two databases (RefSeq and ENSEMBL). rRNA transcription affects ribosomes, whereas mRNA expression and splicing affect the intracellular proteome. Our objective is to develop efficient methods for identifying biomarkers for disease diagnosis and therapeutic targets. In the field of cancer treatment, therapeutic drugs targeting intracellular signaling have proven effective. - Source: PubMed
Publication date: 2026/01/08
Matsushita KazuyukiKitamura KouichiTanaka NobukoKobayashi SoheiSuenaga YusukeHoshino Tyuji