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Mouse Macrophages (with TNFR knockout), Bone Marrow (MTS-0922-JF59)

Overview

Description
With tumor necrosis factor receptor (TNFR) knockout, this product is isolated from the bone marrow of pathogen-free laboratory mice after immortalization with a recombinant retrovirus, which contains the v-raf and myc oncogenes. This product is negative in the tests of mycoplasma, bacteria, fungi and yeast. The expression of CD11b is positive by flow cytometry. It is guaranteed to further culture in the conditions provided by Creative Biolabs. Repeated freezing and thawing of cells is not recommended.
Applications
Numerous types of experimental manipulations, including morphological, gene expression, and physiological studies.
Species
Mouse
Product Type
Mouse Macrophages

Specification

Cell Source
Bone marrow
Marker expression
Expressed on macrophages, CD11b plays a critical role in regulating pathogen recognition, phagocytosis, and cell survival. The expression of CD11b is positive by flow cytometry.
Status
Frozen
Formulation
Cryopreservation medium
Quality Control
Cells are negative for mycoplasma, bacteria, fungi and yeast.
Medium
Recommended medium
Shipping Info
Dry ice
Size
1 vial
Handling Notes
Upon receiving, transfer this product directly from dry ice to liquid nitrogen(-150°C~-190°C) and store it in a liquid nitrogen tank.
We cannot guarantee the cell viability if the cells are not treated appropriately according to handling procedure.
Notes
Avoid repeated freezing & thawing.

Product Disclaimer

Product Disclaimer
This product is provided for research only, not suitable for human or animal use.
We ensure the safety of our products, but we still recommend handling any biological materials with standard precautions as if able to spread infectious disease.
FAQs Customer Reviews Related Products

What TNF receptor subtype is knocked out, and how do you verify the loss of TNF-α responsiveness?

These macrophages lack TNFR1, the primary receptor responsible for mediating inflammatory TNF-α signaling. We validate the knockout through sequencing and Western blot, confirming the absence of TNFR1 protein. Functional assays show a loss of classical TNF-α-induced NF-κB activation and diminished downstream cytokine production, ensuring a clean TNFR1-null phenotype.

Are TNFR KO macrophages stable after thawing, and what viability rates should I expect?

When thawed according to our protocol, the cells typically achieve>85-90% viability. They adhere well to tissue culture plates and exhibit typical macrophage morphology within 24 hours. Avoiding unnecessary mechanical stress and using the recommended medium will maximize recovery. Our support team can also help troubleshoot any thawing inconsistencies.

Can these cells be used in transcriptomic or proteomic experiments to analyze TNF signaling pathways?

Yes, they are excellent tools for multiomics studies, particularly those analyzing the transcriptional or proteomic impact of TNF-α signaling. By comparing KO and wild-type macrophages, you can clearly map TNFR1-specific regulatory nodes. These cells are compatible with RNA-seq, proteomics, phospho-protein analysis, and cytokine profiling.

  • We used these TNFR1 KO macrophages for inflammatory signaling studies
    The cells were healthy and easy to maintain. The lack of response to TNF-α was clear and easy to quantify. We ordered multiple lots for a long-term project.
  • Strong performance and high viability
    The cells revived with high viability and exhibited consistent morphology. They responded normally to LPS, which was critical for our comparative experiments.
  • The supplier provided very detailed documentation on validation and viability
    This made it easy to integrate the cells into our regulated workflow. Our lab struggled to separate TNF-dependent vs TLR4-dependent effects. Using these KO cells made the distinction crystal clear. This improved the overall interpretation of our project.

For Research Use Only. Do Not Use in Food Manufacturing or Medical Procedures (Diagnostics or Therapeutics). Do Not Use in Humans.

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