UcallM® One-Step ATAC-seq Kit

Chromatin accessibility describes loosely-packed genomic regions permissive for transcription-factor binding; ATAC-seq interrogates these open chromatin landscapes to dissect gene-regulatory circuitry. Conventional ATAC-seq requires laborious nuclei-isolation steps with variable yields. UcallM® One-Step ATAC-seq Kit uses proprietary one-step ATAC buffer: after brief PBS washing, intact cells are directly subjected to Tn5 transposition, drastically simplifying protocols. Cells processed with this buffer remain stable at 4 °C for up to 72 h, facilitating clinical-sample logistics.

Experimental Workflow

Key Advantages 1.Low-cell-input requirement: as few as 50 000 cells per sample 2.Proprietary one-step reagent simplifies workflow, improves experimental reproducibility and success rate 3.Simultaneously reveals open-chromatin positions and DNA-binding-protein / transcription-factor interaction footprints Applications 1.Epigenetic-gene-regulation studies; identify promoters, super-enhancers and other cis-regulatory elements 2.Pinpoint transcription-factor drivers of cell-fate decisions and disease phenotypes 3.Multi-omics integration: combine with CUT&Tag, Hi-C etc. to build multi-dimensional regulatory networks Measured Data

UcallM® One-Step ATAC-seq kit Measured Results

V Company Measured Results Figure 1-44. Fragment Length Distribution Plot

Row 1: Measured results of UcallM® One-Step ATAC-seq kit; Row 2: Measured results of V Company Figure 1-45. IGV Peak Track

Left: Measured results of UcallM® One-Step ATAC-seq kit; Right: Measured results of V Company Figure 1-46. TSS Signal Enrichment Heatmap Customer Publications 1.Nat Cell Biol. Targeting DNA G-quadruplexes with dCas9-fusion effectors (DOI:10.1038/s41556-024-01448-1). This study combines CRISPR technology and G4-binding protein/ligand to develop a new strategy for selectively targeting genomic G4 structures. ATAC-seq was applied in this article to analyze the effect of the dCas9-nucleolin system targeting G4 on chromatin structure. The results revealed that G4 stabilization markedly reduces chromatin accessibility at target gene promoter regions and inhibits transcription factor binding. Meanwhile, RNA-seq data showed downregulated expression of these genes, while only minor fluctuations were observed in a small number of off-target genes across the whole transcriptome, verifying the high specificity of this system. Integrative analysis indicated that G4 structures directly modulate transcriptional activity by altering chromatin conformation.

Figure 1-47. Detection of the effect of dCas9-nucleolin/sgR-5 transfection on chromatin accessibility 2.Adv Sci. Super-enhancer vulnerabilities in pancreatic-ductal-adenocarcinoma therapy (DOI:10.1002/advs.202308637). This article systematically investigated the function of super-enhancers (SEs) in pancreatic ductal adenocarcinoma therapy using multi-omics approaches. The research team performed H3K27ac ChIP-seq and ATAC-seq on activated pancreatic stellate cells (a-PSCs). Combined with the ROSE algorithm, SE regions associated with pro-fibrogenic genes (e.g. FAP-α, IL6) were identified. CRISPR/Cas9 knockout of enhancer loci was used to validate their regulatory functions. In parallel, RNA-seq analysis of samples treated with JQ1 (BRD4 inhibitor) demonstrated that SE depletion significantly suppresses pro-fibrogenic pathways and remodels the tumor microenvironment. This study uncovered the regulation of gene expression associated with a-PSCs activation by SEs.

Figure 1-48. Multi-omics Integrative Analysis of SEs