In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The DNMT3B Knockout THP-1 Cell Line is a CRISPR/Cas9-edited loss-of-function model targeting the de novo DNA methyltransferase DNMT3B in THP-1 human monocytic leukemia cells. This cell line enables investigation into DNA methylation-dependent gene silencing, with DNMT3B acting downstream of regulators such as OCT4 and SOX2 and interacting with epigenetic partners like DNMT1 and MeCP2. Applications include epigenetic research, cancer epigenetics, and screening of DNA methylation inhibitors, utilizing techniques such as bisulfite sequencing, ATAC-seq, and drug sensitivity assays. The model is particularly suited for studying monocyte/macrophage function and leukemia-associated methylation aberrations.
CNDP2 Knockout K562 Polyclonal Cells
Cat. No. ARG19403
CHEK2 Knockout CAL27 Polyclonal Cells
Cat. No. ARG11501
ACTR1B Knockout DLD-1 Polyclonal Cells
Cat. No. ARG35500
AR Knockout CaSki Polyclonal Cells
Cat. No. ARG35427
CBR4 Knockout jurkat Polyclonal Cells
Cat. No. ARG42736
CHD2 Knockout Hela Polyclonal Cells
Cat. No. ARG7838
The DNMT3B Knockout THP-1 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring targeted disruption of the DNMT3B gene. This cell line provides a stable loss-of-function model for investigating de novo DNA methylation in a human monocytic leukemia background. DNMT3B, a key methyltransferase, establishes DNA methylation patterns genome-wide, and its ablation allows dissection of epigenetic silencing mechanisms. The knockout was generated using CRISPR/Cas9 to introduce a disrupting mutation, yielding a cell line devoid of functional DNMT3B protein.
THP-1 is a well-established monocytic leukemia cell line derived from an acute monocytic leukemia patient. It serves as a widely used model for monocyte and macrophage functions, being capable of differentiation into macrophage-like cells upon stimulation. THP-1 cells exhibit characteristics such as phagocytosis and cytokine secretion, making them ideal for studying innate immunity and leukemogenesis. This host background enables detailed exploration of how DNMT3B loss influences monocyte/macrophage biology and epigenetic regulation in leukemia.
DNMT3B catalyzes the transfer of methyl groups from SAM to CpG dinucleotides, leading to transcriptional silencing and chromatin condensation. It is regulated by upstream factors including OCT4, SOX2, and ERK signaling, and interacts with epigenetic partners such as DNMT1, UHRF1, PCNA, histone deacetylases, and MeCP2. These complexes coordinate methylation maintenance and chromatin modification. Downstream targets include p16 and MLH1, which are repressed by DNMT3B-mediated methylation, thereby controlling cell cycle and differentiation. Through these interactions, DNMT3B shapes the epigenome in response to developmental and oncogenic cues.
In the THP-1 leukemia model, DNMT3B knockout provides insights into aberrant DNA methylation in myeloid malignancies. This cell line is valuable for probing how de novo methylation affects monocyte differentiation, macrophage polarization, and drug responses. It also serves as a tool to study epigenetic mechanisms underlying ICF syndrome and cancer, where DNMT3B dysfunction is implicated. By comparing knockout and wild-type cells, researchers can delineate methylation-dependent pathways critical for leukemic growth and immune function.
The DNMT3B Knockout THP-1 Cell Line supports diverse assays including bisulfite sequencing for methylation profiling, RT-qPCR and western blotting for expression analysis, and ATAC-seq for chromatin accessibility. Functional studies like colony formation and drug sensitivity tests can assess epigenetic drug effects. This model is suitable for high-throughput screens and studies of tumor microenvironment interactions. For further information, please contact Ascent Research.
