AB1518
Anti-Neurofibrillary Tangles Antibody
serum, Chemicon®
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100 μL
€583.00
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
serum
antibody product type
primary antibodies
clone
polyclonal
species reactivity
human
manufacturer/tradename
Chemicon®
technique(s)
ELISA: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
western blot: suitable
shipped in
dry ice
target post-translational modification
unmodified
Specificity
Specifically stains neurofibrillary tangles and degenerating plaque neurites in cases of Alzheimer′s disease, Down′s Syndrome and normal aged individuals.
Immunogen
Neurofibrillary tangles which were extracted in boiling SDS and purified by sucrose gradient centrifugation.
Application
Anti-Neurofibrillary Tangles Antibody is an antibody against Neurofibrillary Tangles for use in ELISA, WB, IH, IH(P).
Immunohistochemistry on paraffin, vibratome and frozen sections: ≥1:200, ≥1:2,000, respectively.
Western blotting: ≥1:500.
ELISA using immunogen peptide: ≥1:4,000.
Optimal working dilutions must be determined by end user.
Western blotting: ≥1:500.
ELISA using immunogen peptide: ≥1:4,000.
Optimal working dilutions must be determined by end user.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Neurodegenerative Diseases
Physical form
Rabbit antisera with 0.01% thimerosal.
Storage and Stability
Store at -20°C in undiluted aliquots for up to 12 months. Avoid repeated freeze/thaw cycles.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Milena Penkowa et al.
Journal of neuroscience research, 77(1), 35-53 (2004-06-16)
Transgenic expression of interleukin-6 (IL-6) in the CNS under the control of the glial fibrillary acidic protein (GFAP) gene promoter (GFAP-IL6 mice) induces significant inflammation and neurodegeneration but also affords neuroprotection against acute traumatic brain injury. This neuroprotection is likely
Reducing amyloid-related Alzheimer's disease pathogenesis by a small molecule targeting filamin A.
Wang, HY; Bakshi, K; Frankfurt, M; Stucky, A; Goberdhan, M; Shah, SM; Burns, LH
The Journal of Neuroscience null
Focal expression of mutated tau in entorhinal cortex neurons of rats impairs spatial working memory.
Julio J Ramirez et al.
Behavioural brain research, 216(1), 332-340 (2010-08-24)
Entorhinal cortex neuropathology begins very early in Alzheimer's disease (AD), a disorder characterized by severe memory disruption. Indeed, loss of entorhinal volume is predictive of AD and two of the hallmark neuroanatomical markers of AD, amyloid plaques and neurofibrillary tangles
Martina L Mustroph et al.
Behavioural brain research, 233(1), 141-148 (2012-05-09)
Tauopathy in the hippocampus is one of the earliest cardinal features of Alzheimer's disease (AD), a condition characterized by progressive memory impairments. In fact, density of tau neurofibrillary tangles (NFTs) in the hippocampus strongly correlates with severity of cognitive impairments
Milena Penkowa et al.
Journal of neuroscience research, 79(4), 522-534 (2004-12-23)
We examined metallothionein (MT)-induced neuroprotection during kainic acid (KA)-induced excitotoxicity by studying transgenic mice with MT-I overexpression (TgMT mice). KA induces epileptic seizures and hippocampal excitotoxicity, followed by inflammation and delayed brain damage. We show for the first time that
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