AB16311

Anti-Nitric Oxide Synthase II Antibody

Name: Anti-Nitric Oxide Synthase II Antibody
Brand: MM

Chemicon^®, from rabbit

Sinónimos:

NOS II, iNOS

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Código UNSPSC:

12352203

eCl@ss:

32160702

NACRES:

NA.41

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origen biológico

rabbit

Nivel de calidad

100

conjugado

unconjugated

forma del anticuerpo

affinity purified immunoglobulin

tipo de anticuerpo

primary antibodies

clon

polyclonal

purificado por

affinity chromatography

reactividad de especies

mouse

fabricante / nombre comercial

Chemicon^®

técnicas

immunocytochemistry: suitable
western blot: suitable

Nº de acceso NCBI

NM_000625.3
NM_153292.1

Nº de acceso UniProt

P35228

Condiciones de envío

wet ice

modificación del objetivo postraduccional

unmodified

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Este artículo	AB1632	AB1529	AB16301
Sigma-Aldrich AB16311 Anti-Nitric Oxide Synthase II Antibody	Sigma-Aldrich AB1632 Anti-Nitric Oxide Synthase I Antibody	Sigma-Aldrich AB1529 Anticuerpo anti-óxido nítrico sintasa I	Sigma-Aldrich AB16301 Anti-Nitric Oxide Synthase III Antibody
Quality Level 100	Quality Level 100	Quality Level 100	Quality Level 100
antibody form affinity purified immunoglobulin	antibody form affinity purified immunoglobulin	antibody form serum	antibody form affinity purified immunoglobulin
biological source rabbit	biological source rabbit	biological source sheep	biological source rabbit
technique(s) immunocytochemistry: suitable, western blot: suitable	technique(s) ELISA: suitable, immunohistochemistry: suitable, western blot: suitable	technique(s) immunohistochemistry: suitable, western blot: suitable	technique(s) immunocytochemistry: suitable, western blot: suitable
clone polyclonal	clone polyclonal	clone polyclonal	clone polyclonal
UniProt accession no. P35228	UniProt accession no. P29475	UniProt accession no. P29475	UniProt accession no. P29474

Inmunógeno

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

Aplicación

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.

Acciones bioquímicas o fisiológicas

Reactive with mouse NOS-II (iNOS).

Otras notas

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

Replaces: AB1631

Información legal

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

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Código de clase de almacenamiento

12 - Non Combustible Liquids

Clase de riesgo para el agua (WGK)

WGK 2

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Aquaporin 4-specific T cells and NMO-IgG cause primary retinal damage in experimental NMO/SD.

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

Activation of NLRP3 Inflammasome in Liver of Long Evans Lactating Rats and Its Perinatal Effects in the Offspring after Bisphenol F Exposure.

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

Microglia pre-activation and neurodegeneration precipitate neuroinflammation without exacerbating tissue injury in experimental autoimmune encephalomyelitis.

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

Oxidative Injury and Iron Redistribution Are Pathological Hallmarks of Marmoset Experimental Autoimmune Encephalomyelitis.

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

Contenido relacionado

Anti-Nitric Oxide Synthase II - Data Sheet

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

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."

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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