RFX5 (Human) Recombinant Protein (Q01)
- Known as:
- RFX5 (Human) Recombinant Protein (Q01)
- Catalog number:
- H00005993-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- RFX5 (Human) Recombinant Protein (Q01)
Related genes to: RFX5 (Human) Recombinant Protein (Q01)
- Gene:
- RFX5 NIH gene
- Name:
- regulatory factor X5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2019-04-23
Related products to: RFX5 (Human) Recombinant Protein (Q01)
Related articles to: RFX5 (Human) Recombinant Protein (Q01)
- Transcription factors (TFs) are key players in eukaryotic gene regulation, but the DNA binding specificity of many TFs remains unknown. Here, we assay 284 mostly uncharacterized putative human TFs using selective microfluidics-based ligand enrichment followed by sequencing (SMiLE-seq), revealing 74 new DNA binding motifs. To investigate whether TFs lacking detectable motifs preferably bind epigenetically modified DNA, we develop methylation-sensitive SMiLE-seq (meSMiLE-seq), a microfluidic assay that simultaneously probes binding to methylated and unmethylated DNA. Using meSMiLE-seq, we assay 114 TFs and identify DNA-binding models for 48 proteins, including known methylation-sensitive binding modes for POU5F1 and RFX5. 11 TFs prefer methylated DNA or display alternative methylation-dependent motifs (e.g. PRDM13), while 13 show aversion to methylated sequences (e.g. USF3). Finally, we identify ZHX2 as a putative Z-DNA binder. Altogether, our study significantly expands the human TF codebook, while providing a versatile platform to quantitatively assay the impact of DNA modifications on TF binding. - Source: PubMed
Publication date: 2026/08/05
Gralak Antoni JFaltejskova KaterinaYang Ally W HSteiner ClemenceRusseil JulieGrenningloh NadiaInukai SachiDemir MustafaDainese RiccardoOwen CooperPankevich Eugenia V Hughes Timothy RKulakovskiy Ivan VKribelbauer-Swietek Judith Fvan Mierlo GuidoDeplancke Bart - This study aimed to identify and characterize macrophage-associated inflammatory regulatory signatures in ulcerative colitis (UC) by integrating bulk and single-cell transcriptomic data, and to explore their potential regulatory and pharmacological relevance. - Source: PubMed
Publication date: 2026/07/22
Meng HaoyangChen YongliangChai YongchunYu SikeMa PeiyaoLei RuibinZhou ShuhanLv Wenliang - Regulatory factor X5 (RFX5) is a context-dependent transcriptional integrator with key implications for cancer immunotherapy and targeted therapy. In hepatocellular carcinoma (HCC), RFX5 is amplified to drive proliferation and apoptosis resistance via the tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein theta (YWHAQ)-phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) axis. In immune-inflamed tumours, RFX5 regulates antigen presentation, major histocompatibility complex (MHC) class I expression, and CD8 T-cell infiltration, which correlates with enhanced immune surveillance and favourable clinical outcomes. These divergent observations lead us to propose a hypothesis-generating lineage-signal dual-switch framework, which posits that RFX5 functions are dynamically shaped by tumour lineage and microenvironmental immune cues rather than representing fixed oncogenic or tumour-suppressive behaviour. Clinically, altered RFX5 expression correlates with clinical prognosis and immune checkpoint blockade (ICB) response in specific tumour types based on retrospective analyses. Current evidence does not support RFX5 as an independent predictive biomarker, and it may only have reference value when integrated into composite antigen-presentation or MHC signatures. No incremental predictive value beyond established immune biomarkers has been verified. Key translational challenges include defining cell-type-specific targets, distinguishing tumour-intrinsic effects from immune-related alterations, and linking RFX5 activity to therapeutic vulnerabilities. - Source: PubMed
Publication date: 2026/07/01
Zhang LiDu ShanmeiLiu Kui - Post-translational modifications (PTMs) of chromatin remodelers are abundant but functionally understudied. Here we investigate the role of asymmetric dimethylation of arginine 1064 (BAF155me2a) on the SWI/SNF core subunit BAF155, a mark deposited by CARM1/PRMT4 that has been linked to tumor progression but whose molecular function remains unclear. Using immunoprecipitation-mass spectrometry with a dimethyl-specific antibody, we found that R1064me2 selectively enhances BAF155 interactions with RNA processing factors, including the anti-termination protein SCAF4, splicing factors, and the transcription factor RFX5. CUT&RUN profiling showed that BAF155me2a, SCAF4, and RFX5 co-occupy promoter regions, and reciprocal immunoprecipitations confirmed that the SCAF4-BAF155 interaction depends on R1064 methylation. To test the functional consequences of this modification, we generated cells expressing either wild-type BAF155 or a methylation-deficient BAF155-R1064K mutant. Loss of methylation did not alter chromatin accessibility, BAF155 genomic occupancy, or SCAF4 recruitment. However, nascent transcription measured by TT-seq revealed a coordinated reduction in 5' sense transcripts and upstream antisense transcripts (PROMPTs) at BAF155-bound promoters, with a quantitatively larger decrease in PROMPTs at SCAF4 co-bound sites. The effect was restricted to the promoter-proximal region and resolved toward the gene end, consistent with a defect in productive elongation downstream of RNA polymerase II recruitment. These data support a model in which BAF155 dimethylation provides a co-transcriptional interface coupling SWI/SNF to RNA processing machinery, and identify regulation of nascent transcription as a non-canonical function of SWI/SNF PTMs. - Source: PubMed
Publication date: 2026/05/19
Sokolowski MalloryScoville DeenaKuhlers Peyton CRaab Jesse R - Hepatocellular carcinoma (HCC) exhibits profound molecular heterogeneity, which complicates prognosis and therapy. Identifying key molecular subtypes and their driving oncogenes is crucial for developing targeted strategies. This study aimed to delineate chemokine-based HCC subtypes and investigate the functional role and mechanism of a critical identified driver, Immediate Early Response 3 (IER3). - Source: PubMed
Publication date: 2026/05/28
Chen XinZhang QingZhang Nuobei