Key Specifications Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|M||WB, ICC||Rb||Affinity Purified||Polyclonal Antibody|
|Description||Anti-Nitric Oxide Synthase II Antibody|
|Presentation||Affinity purified immunoglobulin. Liquid in 0.02M Phosphate buffer, 0.25 M NaCl, pH 7.6 with 0.1% Sodium azide as a preservative.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Store at 2-8°C in undiluted aliquots for up to 6 months.|
|Material Size||100 µg|
Anti-Nitric Oxide Synthase II Antibody SDS
|Reference overview||Application||Species||Pub Med ID|
|LPS induces KH-type splicing regulatory protein-dependent processing of microRNA-155 precursors in macrophages.|
Tina Ruggiero, Michele Trabucchi, Francesca De Santa, Simona Zupo, Brian D Harfe, Michael T McManus, M Geoff Rosenfeld, Paola Briata, Roberto Gherzi
The FASEB journal : official publication of the Federation of American Societies for Experimental Biology 23 2898-908 2009
The importance of post-transcriptional mechanisms for the regulation of the homoeostasis of the immune system and the response to challenge by microorganisms is becoming increasingly appreciated. We investigated the contribution of microRNAs (miRNAs) to macrophage activation induced by lipopolysaccharide (LPS). We first observed that Dicer knockout in bone marrow-derived macrophages (BMDMs) increases the LPS-induced expression of some inflammation mediators. miRNA microarray analysis in BMDMs revealed that LPS significantly induces the expression of a single miRNA, miR-155, and this induction depends on enhanced miR-155 maturation from its precursors. The single-strand RNA-binding protein KH-type splicing regulatory protein (KSRP) binds to the terminal loop of miR-155 precursors and promotes their maturation. Both inhibition of miR-155 and KSRP knockdown enhance the LPS-induced expression of select inflammation mediators, and the effect of KSRP knockdown is reverted by mature miR-155. Our studies unveil the existence of an LPS-dependent post-transcriptional regulation of miR-155 biogenesis. Once induced, miR-155 finely tunes the expression of select inflammation mediators in response to LPS.
|Transient axonal injury in the absence of demyelination: a correlate of clinical disease in acute experimental autoimmune encephalomyelitis.|
Aboul-Enein, Fahmy, et al.
Acta Neuropathol., 111: 539-47 (2006) 2006
Axonal degeneration contributes to the transient and permanent neurological deficits seen in multiple sclerosis, an inflammatory disease of the central nervous system. To study the immunological mechanisms causing axonal degeneration, we induced experimental autoimmune encephalomyelitis (EAE) in wildtype Lewis rats and Lewis rats with a slowly progressive myelin degeneration due to proteolipid protein (PLP) overexpression. EAE was triggered either by the transfer of encephalitogenic T-cells alone or by the co-transfer of T-cells with demyelinating antibodies. Inducible nitric oxide synthase (iNOS) expression in perivascular macrophages was associated with a transient functional disturbance of axons, reflected by the focal and reversible accumulation of amyloid precursor protein. Clinical disease correlated with the numbers of APP positive axon spheroids. Demyelination was associated with a further increase of iNOS expression in macrophages and with a higher degree of axonal injury. Our studies suggest that nitric oxide and its metabolites contribute to axonal pathology and possibly also to subsequent neurological dysfunction in EAE.
|Adenosine A2A receptor stimulation potentiates nitric oxide release by activated microglia.|
Josep Saura, Ester Angulo, Aroa Ejarque, Vicent Casadó, Josep M Tusell, Rosario Moratalla, Jiang-Fan Chen, Michael A Schwarzschild, Carme Lluis, Rafael Franco, Joan Serratosa
Journal of neurochemistry 95 919-29 2005
The absence of adenosine A2A receptors, or its pharmacological inhibition, has neuroprotective effects. Experimental data suggest that glial A2A receptors participate in neurodegeneration induced by A2A receptor stimulation. In this study we have investigated the effects of A2A receptor stimulation on control and activated glial cells. Mouse cortical mixed glial cultures (75% astrocytes, 25% microglia) were treated with the A2A receptor agonist CGS21680 alone or in combination with lipopolysaccharide (LPS). CGS21680 potentiated lipopolysaccharide-induced NO release and NO synthase-II expression in a time- and concentration-dependent manner. CGS21680 potentiation of lipopolysaccharide-induced NO release was suppressed by the A2A receptor antagonist ZM-241385 and did not occur on mixed glial cultures from A2A receptor-deficient mice. In mixed glial cultures treated with LPS + CGS21680, the NO synthase-II inhibitor 1400W abolished NO production, and NO synthase-II immunoreactivity was observed only in microglia. Binding experiments demonstrated the presence of A2A receptors on microglial but not on astroglial cultures. However, the presence of astrocytes was necessary for CGS21680 potentiating effect. In light of the reported neurotoxicity of microglial NO synthase-II and the neuroprotection of A2A receptor inhibition, these data suggest that attenuation of microglial NO production could contribute to the neuroprotection afforded by A2A receptor antagonists.
|Selective and antigen-dependent effects of myelin degeneration on central nervous system inflammation.|
Aboul-Enein, Fahmy, et al.
J. Neuropathol. Exp. Neurol., 63: 1284-96 (2004) 2004
|Pathways and Biomarkers of Oxidative Stress (EMD)|
|White Paper- Modern Methods in Oxidative Stress Research (EMD)|
|Anti-Nitric Oxide Synthase II - Data Sheet|