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Merck

AB16311

Anti-Nitric Oxide Synthase II Antibody

Chemicon®, from rabbit

Synonym(e):

NOS II, iNOS

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Über diesen Artikel

UNSPSC-Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

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Biologische Quelle

rabbit

Qualitätsniveau

100

Konjugat

unconjugated

Antikörperform

affinity purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Aufgereinigt durch

affinity chromatography

Speziesreaktivität

mouse

Hersteller/Markenname

Chemicon®

Methode(n)

immunocytochemistry: suitable
western blot: suitable

NCBI-Hinterlegungsnummer

NM_000625.3
NM_153292.1

UniProt-Hinterlegungsnummer

P35228

Versandbedingung

wet ice

Posttranslationale Modifikation Target

unmodified

Immunogen

Synthetic peptide corresponding to amino acids 1131-1144 of mouse macrophage NOS, coupled to KLH.

Anwendung

This Anti-Nitric Oxide Synthase II Antibody is validated for use in WB, IC for the detection of Nitric Oxide Synthase II.
Western Blot: 5 μg/mL using chemiluminescent detection. Higher concentrations of the antibody may be required if colorimetric detection is used. Antibody dilution will also vary with the concentration of the antigen. Immunocytochemistry: Use at 2-5 μg/mL

Optimal working dilutions must be determined by end user.

Biochem./physiol. Wirkung

Reactive with mouse NOS-II (iNOS).

Sonstige Hinweise

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Replaces: AB1631

Rechtliche Hinweise

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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Lagerklassenschlüssel

12 - Non Combustible Liquids

WGK

WGK 2

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Die Dokumentenbibliothek aufrufen

Bleranda Zeka et al.
Acta neuropathologica communications, 4(1), 82-82 (2016-08-10)
Neuromyelitis optica/spectrum disorder (NMO/SD) is a severe, inflammatory disease of the central nervous system (CNS). In the majority of patients, it is associated with the presence of pathogenic serum autoantibodies (the so-called NMO-IgGs) directed against the water channel aquaporin 4
Beatriz Linillos-Pradillo et al.
International journal of molecular sciences, 24(18) (2023-09-28)
The liver is the organ responsible for the metabolism and detoxification of BPF, the BPA analogue that is replacing it in plastic-based products. It is not known whether BPF can trigger inflammatory responses via the NLRP3 inflammasome, which plays a
Jordon Dunham et al.
Journal of neuropathology and experimental neurology, 76(6), 467-478 (2017-05-16)
Oxidative damage and iron redistribution are associated with the pathogenesis and progression of multiple sclerosis (MS), but these aspects are not entirely replicated in rodent experimental autoimmune encephalomyelitis (EAE) models. Here, we report that oxidative burst and injury as well
Isabella Wimmer et al.
Acta neuropathologica communications, 7(1), 14-14 (2019-02-02)
Human inflammatory or neurodegenerative diseases, such as progressive multiple sclerosis (MS), occur on a background of age-related microglia activation and iron accumulation as well as pre-existing neurodegeneration. Most experimental models for CNS diseases, however, are induced in rodents, which are

Verwandter Inhalt

White Paper- Modern Methods in Oxidative Stress Research

"Redox reactions are powerful chemical processes that involve the reduction and oxidation of proteins and metabolites found in living things. The mechanisms that regulate them are key to maintaining homeostasis and the balance between good health and disease pathology. Oxidative stress is the state where the delicate balance of redox biology is upset, and the pathology of oxidative stress are the cellular consequences to such an imbalance."

Anti-Nitric Oxide Synthase II - Data Sheet

RABBIT ANTI-NITRIC OXIDE SYNTHASE II (NOS-II; iNOS)

Pathways and Biomarkers of Oxidative Stress

"Aging: getting older, exhibiting the signs of age, the decline in the physical (and mental) well-being over time, leading to death. Since the beginning of time, man has been obsessed with trying to slow down, stop, or even reverse the signs of aging. Many have gone as far as experimenting with nutritional regimens, eccentric exercises, fantastic rituals, and naturally occurring or synthetic wonder-elements to evade the signs of normal aging. Biologically speaking, what is aging? And what does the latest research tell us about the possibility of discovering the elusive “fountain of youth”? Many advances in our understanding of aging have come from systematic scientific research, and perhaps it holds the key to immortality. Scientifically, aging can be defined as a systems-wide decline in organismal function that occurs over time. This decline occurs as a result of numerous events in the organism, and these events can be classified into nine “hallmarks” of aging, as proposed by López-Otin et al. (2013). Several of the pathologies associated with aging are a direct result of these events going to extremes and may also involve aberrant activation of proliferation signals or hyperactivity. The hallmarks of aging have been defined based on their fulfillment of specific aging related criteria, such as manifestation during normal aging, acceleration of aging if experimentally induced or aggravated, and retardation of aging if prevented or blocked, resulting in increased lifespan. The nine hallmarks of aging are genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. The biological processes underlying aging are complex. By understanding the hallmarks in greater detail, we can get closer to developing intervention strategies that can make the aging process less of a decline, and more of a recline."

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