RFX5 antibody - N-terminal region (ARP37992_T100)
- Known as:
- RFX5 (anti-) - N-terminal region (ARP37992_T100)
- Catalog number:
- arp37992_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RFX5 antibody - N-terminal region (ARP37992_T100)
Related genes to: RFX5 antibody - N-terminal region (ARP37992_T100)
- 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 antibody - N-terminal region (ARP37992_T100)
Related articles to: RFX5 antibody - N-terminal region (ARP37992_T100)
- 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 - The three-dimensional chromatin architecture is critical for gene regulation, yet factors beyond CCCTC-binding factor (CTCF) and cohesin remain poorly characterized. Here, we identify RFX5 as a novel regulator of chromatin organization. Using CRISPR-mediated RFX5 knockout A375 cells, together with RNA-seq, ChIP-seq, ATAC-seq, QHR-4C, and Hi-C, we demonstrate that RFX5 binds to promoters and enhancers, co-localizes with CTCF, RAD21, and H3K27ac, maintains chromatin accessibility, and preserves chromatin loop strength. RFX5 deletion alters the expression of ~2,000 genes, with strong suppression of cancer-associated genes and oncogenic pathways. Loss of RFX5 reduces CTCF/RAD21 occupancy and promoter accessibility at downregulated genes. Notably, RFX5 acts as an insulator to balance chromatin looping: its absence weakens enhancer-promoter contacts at oncogenic loci while enabling inappropriate long-range enhancer interactions at upregulated genes. Hi-C analysis reveals globally diminished loop strength, with only mild effects on TAD insulation and compartmentalization. These findings establish RFX5 as a key architectural factor that links 3D genome structure to transcriptional programs in cancer and immunity. - Source: PubMed
Publication date: 2026/05/23
Ge XiaoZhang YijunHan YiruLiu XuanJia ZhilianLiang YongjunWang Yongming - Major histocompatibility complex (MHC) class II deficiency is a rare, life-threatening primary immunodeficiency that presents in early infancy with a SCID phenotype. However, emerging data indicate substantial clinical and immunological heterogeneity, including atypical presentations and neurological involvement. - Source: PubMed
Publication date: 2026/04/22
Haskologlu SuleAytekin CanerIslamoglu CandanKostel Bal SevgiBaskın KubraErman BaranKendirli TanılCeylaner SerdarDogu FigenIkinciogullari Aydan - Casein Kinase 2 (CK2) is a constitutively active kinase regulating proliferation and immune signaling and is frequently dysregulated in cancer, including acute myeloid leukemia (AML), making it a therapeutic target. CK2 comprises two catalytic subunits, CK2α or CK2α', with two regulatory β subunits. The role of CK2α, the predominant catalytic subunit and principal mediator of CK2 kinase activity in hematopoietic cells, in steady-state hematopoiesis remains undefined. To define how CK2α shapes hematopoietic cells, we used bone marrow and spleen tissue samples of wild type control and conditional knock out (KO) of CK2α () in the hematopoietic compartment of transgenic mice. Using single-cell RNA sequencing, we profiled the transcriptomic changes associated with CK2α loss. Although HSC abundance was comparable between the control and CK2α-deficient samples, HSCs experienced the largest transcriptional response to CK2α loss among all cell types. CK2α-deficient HSCs displayed transcriptional remodeling for inflammatory and immune-associated programs, interferon signaling, and antigen presentation. Expression of inflammatory genes such as and , changed in opposite directions in bone marrow and spleen HSCs, demonstrating the transcriptional consequences of CK2α loss shaped by tissue context. Using a network-based approach, we identified immune-associated transcription factors , , , and AP-1 family members as regulatory hubs driving these inflammatory transcriptional states in CK2α-deficient HSCs. Cell-cell communication profiling revealed multiple gains and losses in ligand-receptor communication between the HSCs and their immune microenvironment in KO. Our findings identify CK2α as a regulator of immune transcriptional programs in HSCs and suggest that disruption of CK2 signaling influences stem cell behavior and immune activation in contexts relevant to hematologic malignancies and CK2-targeted cancer therapies. - Source: PubMed
Publication date: 2026/04/15
Valensi HannahRajaiah RajeshShanmugam MarudhuMuhammad DaniyalGolla UpendarMercer KatherineKarampuri AnushDovat SinisaBehura ChandrikaUzun Yasin