PRMT4 Assay Kit_Luminescent
- Known as:
- PRMT4 Assay Kit_Luminescent
- Catalog number:
- 52041
- Product Quantity:
- 96 reactions
- Category:
- Peptides
- Supplier:
- Biotech support group
- Gene target:
- PRMT4 Assay Kit_Luminescent
Related genes to: PRMT4 Assay Kit_Luminescent
- Gene:
- CARM1 NIH gene
- Name:
- coactivator associated arginine methyltransferase 1
- Previous symbol:
- -
- Synonyms:
- PRMT4
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-14
- Date modifiied:
- 2016-11-11
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- CARM1 has attracted significant attention due to its role in carcinogenesis across a variety of cancers. Ferroptosis has emerged as a prospective target in anticancer therapy. - Source: PubMed
Publication date: 2026/06/12
Zhang YinGuan YinanYu HaoZhu TingtingWang ShengjiaCheng XiaohanMa Jingjing - Anaplastic large cell lymphoma (ALCL) is a subtype of T-cell non-Hodgkin lymphoma (NHL), classified into ALK(+) and ALK(-) subtypes, based on translocations of the ALK gene. ALK(+) ALCL have a favorable prognosis with polychemotherapy, yet some patients develop early chemoresistance, leading to treatment failure. The molecular mechanisms underlying this resistance remain poorly defined. Circular RNAs (circRNAs) have recently emerged as regulators of drug resistance in cancer, but their role in T-NHLs is largely unexplored. A comprehensive analysis of circRNA expression was performed here in primary ALK(+) ALCL biopsies. RNA-Seq identified 12 circRNAs associated with early relapse, including isoforms from the PTPN22 gene (circPTPN22), significantly upregulated in relapsed patients. Functional analyses showed that the ALK/STAT3 signaling pathway regulates circPTPN22 expression, linking oncogenic signaling to circRNA regulation. It was also found that circPTPN22 isoforms modulate responses to chemotherapy by regulating the arginine methyltransferase CARM1, a key enzyme involved in transcriptional regulation. Loss of CARM1 expression promoted drug tolerance in chemosensitive ALK(+) lymphoma cells. These findings identify the circPTPN22/CARM1 axis as a regulator of chemosensitivity and propose CARM1 inhibition as a potential strategy to overcome chemoresistance in patients with ALK(+) ALCL. - Source: PubMed
Publication date: 2026/06/04
Andraos ElissaFuchs SteffenBessière ChloéColras LolaDailhau SandraBousquet MarinaTouzart AuroreLhermitte LudovicGaspin ChristinePyronnet StéphaneLamant LaurenceMeggetto FabienneBabin Loelia - 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 - Tumor hypoxia in non-small cell lung cancer (NSCLC) promotes malignant progression and treatment resistance by enhancing abnormal vasculature, invasiveness, and metastasis. However, the molecular mechanisms underlying hypoxia-driven tumor progression remain incompletely understood. - Source: PubMed
Publication date: 2026/04/24
Qin XinyuZhang ChunlongWu SijiaLu JingWang GuohuaLi Yang - PRMT1 and PRMT4 (CARM1) are the epigenetic regulators concerned with the methylation of arginine residues, acting on both the histone and non-histone proteins, regulating chromatin dynamics, gene expression and signaling pathways. Impaired control and imbalanced regulation of this induces various types of cancers. This review provides a comprehensive assessment of the structure-activity relationship (SAR) of various small-molecule inhibitors targeting PRMT1 and PRMT4. A range of chemical frameworks like tetrazole, furan, thiazole, tetrahydroisoquinoline derivatives and many others were identified. These derivatives act through various mechanisms to inhibit the overexpressed PRMT1 and PRMT4. Significant SAR insights underscore the essential role within individual structural motifs, including the contribution of electron-withdrawing and electron-donating groups, which depict the activity, selectivity and potency for inhibition, electrostatic interactions and π-π stacking of structural units. Docking studies emphasize the key interaction of ligand molecules with the active site of the target. This review forms a solid foundation for the rational development of the next generation PRMT1 and PRMT4 inhibitors with better therapeutic potential by systematically correlating the chemical structure with biological activity across a number of classes through SAR and computational studies. - Source: PubMed
Publication date: 2026/05/08
Pal KanchanKasana ShivaniKurmi Balak DasPatel Preeti