| Code | CSB-RA878853MA1HU |
| Size | US$210 |
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| Application | Recommended Dilution |
|---|---|
| FC | 1:50-1:200 |
Reticulon 4, commonly known as Nogo, represents a fascinating target in neuroscience research due to its critical role in inhibiting neurite outgrowth and axonal regeneration in the central nervous system. This membrane protein, particularly its Nogo-A isoform, acts as a major myelin-associated inhibitor that restricts neuronal plasticity and recovery following injury. Understanding RTN4 signaling pathways has become essential for researchers investigating spinal cord injury, stroke recovery, and neurodegenerative conditions where promoting axonal regeneration could offer therapeutic benefits.
This recombinant monoclonal antibody, clone 11D11, provides researchers with the consistency and reliability that modern experimental workflows demand. Developed using recombinant technology and expressed as a human IgG4 isotype, this antibody offers sequence-defined specificity against human RTN4, ensuring reproducible results across experiments and eliminating the lot-to-lot variability that can complicate long-term studies. The antibody was generated using recombinant human RTN4 protein as the immunogen, supporting precise epitope targeting.
Validation through flow cytometry demonstrates robust detection of RTN4 in A549 cells, with recommended dilutions ranging from 1:50 to 1:200. The validation protocol employed fixed and permeabilized cells, confirming the antibody's suitability for detecting intracellular RTN4 populations. Clear separation between test and control conditions was observed when acquiring over 10,000 events, indicating strong signal-to-noise performance. The antibody is also validated for ELISA applications, offering flexibility across different experimental platforms.
Supplied in a stabilized liquid format containing glycerol and PBS with Proclin 300 preservative, this affinity-purified antibody is well-suited for neuroscience laboratories investigating axonal regeneration, neural plasticity, and the molecular mechanisms underlying CNS repair.
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