In Stock Cell Lines
Rattus norvegicus (Rat)
Heart
Adherent
The Ripk1 Knockout H9c2(2-1) Cell Line provides a genetically defined CRISPR/Cas9-edited rat cardiomyoblast model with loss of RIPK1, a master regulator of cell death and inflammation. Derived from the H9c2(2-1) subclone, this line enables precise investigation of TNF-alpha/TNFR1-mediated necroptosis and apoptosis involving RIPK3, MLKL, and Caspase-8. Applications include myocardial ischemia-reperfusion injury modeling, RIPK1 inhibitor screening, and mechanistic studies of necroptotic signaling. Compatible with Western blot, immunofluorescence, flow cytometry, and RNA-seq, it serves as a robust tool for cardiac cell death research. For inquiries, contact Ascent Research.
IFNAR2 Knockout K562 Polyclonal Cells
Cat. No. ARG20636
PCGF1 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG15920
NUB1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13800
IFRD1 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24610
CCL15 Knockout HAP1 Polyclonal Cells
Cat. No. ARG43162
FOCAD Knockout Raji Polyclonal Cells
Cat. No. ARG971
The Ripk1 Knockout H9c2(2-1) Cell Line is a CRISPR/Cas9-edited knockout model targeting the Ripk1 gene in the rat cardiomyoblast line H9c2(2-1). This cell line features stable disruption of the gene encoding receptor-interacting serine/threonine-protein kinase 1 (RIPK1). It provides a defined loss-of-function background for studying RIPK1-dependent signaling pathways in cardiac cells. As a validated knockout cell line, it supports reproducible functional analyses across diverse experimental contexts.
The H9c2(2-1) host line is a subclone of H9c2, derived from embryonic rat heart ventricle tissue. These cells exhibit characteristics of cardiac muscle progenitors and are extensively used as a cardiomyoblast model in vitro. The line retains the capacity to differentiate toward a cardiac phenotype, offering a relevant system for investigating myocardial cell death and inflammation mechanisms. Its genetic stability supports consistent CRISPR-engineered knockout cell generation for comparative studies.
RIPK1 acts as a kinase and adaptor protein that integrates signals from death receptors and Toll-like receptors. Its activation by TNF-alpha through TNFR1 leads to formation of a signaling complex containing TRADD, TRAF2, and cIAP1/2. Depending on ubiquitination status, RIPK1 promotes NF-??B survival signaling via the IKK complex and NEMO, or drives cell death. Deubiquitinated RIPK1 binds FADD and Caspase-8 to initiate apoptosis, or recruits RIPK3 to phosphorylate MLKL, executing necroptosis. Thus, RIPK1 orchestrates a critical decision point between pro-inflammatory, apoptotic, and necroptotic outcomes.
In the cardiac setting, RIPK1-mediated necroptosis and apoptosis are implicated in ischemia-reperfusion injury, where excessive cell death compromises myocardial function. The Ripk1 Knockout H9c2(2-1) line enables dissection of these pathways specifically in cardiomyoblast cells, allowing researchers to evaluate the role of RIPK1 in hypoxia-reoxygenation stress, inflammatory cytokine responses, and potential protective interventions. This model is thus directly relevant to translational studies aimed at mitigating cardiomyocyte loss in heart disease.
Researchers can employ the Ripk1 Knockout H9c2(2-1) Cell Line in a variety of experimental protocols to investigate necroptotic and apoptotic signaling. Typical assays include Western blotting for phosphorylated MLKL and cleaved Caspase-8, flow cytometry with PI/Annexin V to distinguish cell death modalities, and cell viability measurements using MTT or CCK-8 following treatment with necrostatin-1 or RIPK1 kinase inhibitors. Co-immunoprecipitation enables mapping of RIPK1 interaction networks, while RNA-seq facilitates global transcriptional profiling of RIPK1-dependent gene expression changes. This model is also well-suited for drug screening campaigns targeting the RIPK1 kinase domain. For additional information or technical inquiries, please contact Ascent Research.
