Clone: | SMI 312 (See other available formats) |
Isotype: | Mouse IgG1, κ / Mouse IgM, κ |
Isotype Control: | Purified Mouse IgG1, κ Isotype Ctrl |
Isotype Control: | Purified Mouse IgM, κ Isotype Ctrl |
Reactivity: | Mammalian |
Immunogen: | Homogenized hypothalami recovered from Fischer 344 rats. |
Formulation: | Phosphate-buffered solution, pH 7.2, containing 0.09% sodium azide. |
Preparation: | The antibody was purified by affinity chromatography. |
Concentration: | 0.5 mg/ml |
Storage & Handling: | The antibody solution should be stored undiluted between 2°C and 8°C. |
Application: | IHC - Quality testedICC, IF, WB - Reported in the literature |
Recommended Usage: | Each lot of this antibody is quality control tested by immunohistochemistry. For immunohistochemistry, a concentration range of 0.5 - 5.0 µg per ml is suggested. It is recommended that the reagent be titrated for optimal performance for each application. |
ApplicationNotes: | Additional reported applications (for the relevant formats) include: immunocytochemistry1, 6, 12, 16, 19, immunofluorescent staining3, 8, 9, 18, and Western blotting5.SMI 312 is a mixture of monoclonal antibodies that react against complex networks of axons. It is directed against extensively phosphorylated axonal epitopes on neurofilaments M and H. SMI 312 has been selected to provide a specific marker for axons in tissue sections and cultures. In contrast to individual anti-phosphoneurofilament antibodies that identify different subsets of neurofilament phosphoepitopes, which are suitable for defining functional and regional differences in normal and pathologic axons, SMI 312 is a convenient marker for axons in general. SMI 312 visualizes axons in an area-specific maturation pattern in human fetal brain. The antibody cocktail defines nuclear borderlines and is useful in establishing early connectivity with SMI 311, anti-neurofilament (not phosphorylated) identified dendrites. SMI 312 visualizes aberrantly sprouting axons in neuritic plaques derived from cortico-cortical fibers in Alzheimer's disease and identifies loss of synaptic circuitry proposed to be the basis of memory. |
ApplicationReferences: | 1. Sternberger LA, et al. 1982. Proc. Natl. Acad. Sci. USA 79:1326. (IHC, ICC)2. Choi Y, et al. 2008. Genes & Dev. 22:2485. (IHC) PubMed 3. Bussière T, et al. 2004. Am. J. Pathol. 165:987. (IF)4. Chung RS, et al. 2003. J. Neurosci. 23:3336. (IHC)5. De Repentigny Y, et al. 2011. PLoS One 6:e21093. (IHC, WB)6. Wilkins A, et al. 2003. J. Neurosci. 23:4967. (ICC)7. Rudinskiy N, et al. 2012. Nat. Neurosci. 15:1422. (IHC)8. Wang JY, et al. 2014. Dev. Cell 28:670. (IF)9. Canetta SE, et al. 2011. PLoS One 6:e25108. (IF)10. Nicaise C, et al. 2012. J. Neurotrauma 29:2748. (IHC)11. Ma M, et al. 2013. Neurobiol. Dis. 56:34. (IHC)12. Zurashvili T, et al. 2013. Mol. Cell Biol. 33:1027. (ICC) |
Publication Library | |
RRID: | AB_2566782 (BioLegend Cat. No. 837904) |
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