FUBP1 antibody - middle region (ARP35704_P050)
- Known as:
- FUBP1 (anti-) - middle region (ARP35704_P050)
- Catalog number:
- arp35704_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FUBP1 antibody - middle region (ARP35704_P050)
Related genes to: FUBP1 antibody - middle region (ARP35704_P050)
- 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 - middle region (ARP35704_P050)
Related articles to: FUBP1 antibody - middle region (ARP35704_P050)
- Mitochondrial stress activates nuclear transcriptional programs to restore homeostasis and promote longevity; yet, the nuclear effector that directly reshapes chromatin during stress remains unclear. Through a forward genetic screen in , we identify FUBL-3, the homolog of human far-upstream elements binding protein 1 (FUBP1), as a conserved regulator that couples mitochondrial stress to chromatin remodeling. FUBL-3 translocates to intestinal nuclei upon stress, where it drives nucleosome remodeling and deacetylase-dependent chromatin condensation and activates mitochondrial unfolded protein response (UPR). Loss of disrupts chromatin compaction and abolishes stress-induced lifespan extension, while its overexpression is sufficient to restructure chromatin, trigger UPR, and extend lifespan. Notably, human FUBP1 rescues mutants in worms and mediates chromatin remodeling in mammalian cells under mitochondrial stress. FUBP1 binds promoters of proteostasis and mitochondrial quality control genes, supporting its role in nuclear adaptation. Our study identifies FUBL-3/FUBP1 as a conserved mitochondrial-to-nuclear communicator that reprograms chromatin architecture to promote stress resilience and healthy aging. - Source: PubMed
Publication date: 2026/06/24
Zhang QianDong HangyuJiang YayunWang ZihaoLi JiashengTian Ye - Oligodendroglioma is a primary central nervous system tumor classified by the presence of isocitrate dehydrogenase (IDH) mutations and codeletion of 1p/19q. Here we describe the generation of an IDH-mutant 1p/19q-codeleted oligodendroglioma mouse model using in utero electroporation. We identified IDH1, PIK3CA, , and as the optimal combination (termed Oligo) to drive fully penetrant tumors that histologically resemble human grade II/III IDH-mutant, 1p/19q-codeleted oligodendroglioma. Replacing with loss in this mouse model shifted tumor histology towards high grade astrocytoma. Oligo tumors displayed metabolic and transcriptional changes associated with and mutations, and single cell sequencing identified a bias towards oligodendrocyte differentiation compared to an IDH wild-type glioblastoma mouse model. Oligo tumors represent the first mouse model system to recapitulate the genetic, histological and transcriptional features of human IDH-mutant 1p/19q-codeleted oligodendrogliomas, offering a platform to further dissect tumor biology and test new therapeutic strategies. - Source: PubMed
Publication date: 2026/05/19
Kundu Ipsita GToro NicolasMochizuki Aaron YLanghnoja JaldeepAyyagari Rithvik VCronk James CReel Sarah MArounleut PhonepasongEsqueda Luis TronFuller Christine EViswanath PavithraHeimberger Amy BHorbinski Craig MPhoenix Timothy N - Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide. Aberrant expression of RNA binding fox-1 homolog 2 (RBFOX2) has been implicated in tumorigenesis and progression; however, its biological functions and clinical significance in CRC remain poorly understood. This study aimed to elucidate the role of RBFOX2 in CRC. - Source: PubMed
Publication date: 2026/05/31
Liu WenDongDai GuangMingLiao GuoLongOuyang PengHuang JinTuanXu Meng - 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