In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The NOD2 Knockout HL-60 Cell Line is a CRISPR/Cas9-edited knockout model derived from the human promyelocytic leukemia HL-60 line. It provides loss of NOD2 function, enabling investigation of intracellular pattern recognition receptor signaling in myeloid cell contexts. The gene encodes a muramyl dipeptide sensor that activates NF-??B and MAPK pathways via RIPK2, leading to pro-inflammatory cytokine and defensin production. This cell line is ideal for studying innate immune mechanisms, inflammatory bowel disease, and evaluating RIPK2 inhibitors using assays such as ELISA, western blotting, and NF-??B reporter systems.
Sucla2 Knockout NIH 3T3 Cell Line
Cat. No. ARG44146
P4HB Knockout 769-P Polyclonal Cells
Cat. No. ARG18177
FXR1 Knockout HT29 Polyclonal Cells
Cat. No. ARG14700
ARHGAP12 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24204
DLAT Knockout MES-OV Polyclonal Cells
Cat. No. ARG38861
CSNK1G3 Knockout 786-O Polyclonal Cells
Cat. No. ARG5070
The NOD2 Knockout HL-60 Cell Line is a CRISPR/Cas9-edited knockout cell line originating from the human HL-60 promyelocytic leukemia line. This model provides a loss-of-function system in which NOD2 expression is disrupted, enabling precise studies of intracellular pattern recognition receptor signaling and innate immune processes. The cell line is well-suited for assays investigating NOD2-dependent pathways.
HL-60 cells are a classical model for myeloid differentiation and leukemia, established from a 36-year-old female with acute promyelocytic leukemia. These cells can be induced to differentiate along granulocytic or monocytic/macrophage-like lineages using chemical agents such as DMSO or phorbol esters. This property renders HL-60 useful for investigating myeloid cell functions in both undifferentiated and mature states.
NOD2 functions as a cytosolic receptor for bacterial muramyl dipeptide (MDP). Ligand binding triggers NOD2 self-oligomerization and recruitment of RIPK2 via CARD interactions, which in turn activates the IKK complex and TAK1. Downstream, NF-??B and MAP kinase cascades??including p38, JNK, and ERK??are engaged, leading to transcription of pro-inflammatory cytokines (e.g., TNF, IL-6, IL-8) and antimicrobial peptides such as defensins. NOD2 also interfaces with autophagy through interactions with ATG16L1 and CARD9. Upstream regulators include TNF-?? and TLR agonists, which modulate NOD2 expression, while the receptor itself serves as a critical sensor of microbial wall components.
In the HL-60 background, NOD2 knockout eliminates the primary MDP-sensing pathway, enabling dissection of innate immune signaling in a myeloid progenitor context. Because HL-60 can be driven toward macrophage-like cells??a lineage where NOD2 is highly relevant??this model allows evaluation of receptor-dependent cytokine secretion, NF-??B transcriptional responses, and autophagy induction upon MDP challenge. It is particularly useful for characterizing how NOD2 loss influences differentiation-linked immune functions and for modeling aspects of Crohn??s disease and Blau syndrome.
This knockout cell line supports a wide range of experimental approaches, including western blotting, RT-qPCR, ELISA, NF-??B reporter assays, and MDP stimulation studies to quantify pathway activation. It is also applicable in co-immunoprecipitation of NOD2?CRIPK2 complexes, phospho-signaling analysis of MAPK members, and autophagy flux monitoring. The model facilitates pharmacological testing of RIPK2 inhibitors and functional rescue with disease-associated NOD2 variants. For further inquiries, please contact Ascent Research.
