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|Tested species reactivity||Mouse|
|Published species reactivity||Not Applicable|
|Host / Isotype||Goat / IgG|
|Immunogen||Mouse Mu immunonglobin|
|Conjugate||Alexa Fluor® 555|
|Storage buffer||PBS, pH 7.5|
|Contains||5mM sodium azide|
|Storage Conditions||4° C, store in dark|
|Cross Adsorption||Against human IgGl, IgG2a, IgG2b, IgG3, IgA, human serum and purified human paraproteins prior to conjugation|
|Antibody Form||Whole Antibody|
|Tested Applications||Dilution *|
|Immunocytochemistry (ICC)||1-10 µg/ml|
|Immunofluorescence (IF)||1-10 µg/mL|
|Immunohistochemistry (IHC)||1-10 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Miscellaneous PubMed (MISC)||See 4 publications below|
Anti-Mouse secondary antibodies are affinity-purified antibodies with well-characterized specificity for mouse immunoglobulins and are useful in the detection, sorting or purification of its specified target. Secondary antibodies offer increased versatility enabling users to use many detection systems (e.g. HRP, AP, fluorescence). They can also provide greater sensitivity through signal amplification as multiple secondary antibodies can bind to a single primary antibody. Most commonly, secondary antibodies are generated by immunizing the host animal with a pooled population of immunoglobulins from the target species and can be further purified and modified (i.e. immunoaffinity chromatography, antibody fragmentation, label conjugation, etc.) to generate highly specific reagents.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
|Not Applicable||Not Cited||NF-κB activation and polyubiquitin conjugation are required for pulmonary inflammation-induced diaphragm atrophy.||Haegens A,Schols AM,Gorissen SH,van Essen AL,Snepvangers F,Gray DA,Shoelson SE,Langen RC||American journal of physiology. Lung cellular and molecular physiology (302:L103)||2012|
|Not Applicable||Not Cited||Deficiency of α-actinin-3 is associated with increased susceptibility to contraction-induced damage and skeletal muscle remodeling.||Seto JT,Lek M,Quinlan KG,Houweling PJ,Zheng XF,Garton F,MacArthur DG,Raftery JM,Garvey SM,Hauser MA,Yang N,Head SI,North KN||Human molecular genetics (20:2914)||2011|
|Not Applicable||Not Cited||An Actn3 knockout mouse provides mechanistic insights into the association between alpha-actinin-3 deficiency and human athletic performance.||MacArthur DG,Seto JT,Chan S,Quinlan KG,Raftery JM,Turner N,Nicholson MD,Kee AJ,Hardeman EC,Gunning PW,Cooney GJ,Head SI,Yang N,North KN||Human molecular genetics (17:1076)||2008|
|Not Applicable||Not Cited||Elimination of plasma membrane phosphatidylinositol (4,5)-bisphosphate is required for exocytosis from mast cells.||Hammond GR,Dove SK,Nicol A,Pinxteren JA,Zicha D,Schiavo G||Journal of cell science (119:2084)||2006|