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AB136407

Anti-Neurofibrillary tangles antibody

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(4 Publications)

Rabbit Polyclonal Neurofilament heavy polypeptide antibody. Suitable for IHC-P and reacts with Human samples. Cited in 4 publications.

View Alternative Names

KIAA0845, NFH, NEFH, Neurofilament heavy polypeptide, NF-H, 200 kDa neurofilament protein, Neurofilament triplet H protein

1 Images
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Neurofibrillary tangles antibody (AB136407)
  • IHC-P

Unknown

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Neurofibrillary tangles antibody (AB136407)

Immunohistochemical analysis of tangles and senile plaques in Human Alzheimer's brain tissue using ab136407 at a dilution of 1/200.

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

IHC-P

applications

Specificity

ab136407 specifically stains neurofibrillary tangles and degenerating plaque neurites in cases of Alzheimer's disease, Down's Syndrome and normal aged individuals.

Reactivity data

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Properties and storage information

Form
Liquid
Purity
Whole antiserum
Storage buffer
Preservative: 0.01% Thimerosal (merthiolate)
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Neurofibrillary tangles also known as neuro tangles result from abnormal accumulations of the tau protein. Tau a microtubule-associated protein with a mass of about 60 kDa typically stabilizes microtubules in neuronal axons. Normally neurons express tau in the central nervous system (CNS) where it supports axonal transport by binding to and stabilizing microtubules. However misfolded tau proteins form aggregates leading to the development of neurofibrillary tangles.
Biological function summary

Tau proteins in neurons become hyperphosphorylated triggering their detachment from microtubules. This hyperphosphorylation causes tau proteins to misfold and aggregate into paired helical filaments and straight filaments. These aggregates are not part of a complex but compromise neuronal function by disrupting intracellular transport. The accumulation of such aggregates interferes with cell health and synaptic function contributing to neurodegeneration.

Pathways

Tau pathology involves several important cellular processes. The tau protein participates in signal transduction pathways such as the MAPK/ERK pathway and the microtubule assembly pathway. Misregulated tau phosphorylation impacts microtubule stability linking it to neuronal signaling alterations. Other proteins like glycogen synthase kinase 3-beta (GSK3β) and cyclin-dependent kinase 5 (CDK5) modulate tau hyperphosphorylation within these pathways affecting tau's normal function and leading to its aggregation.

Neurofibrillary tangles primarily relate to Alzheimer's disease and frontotemporal dementia. These tau aggregates are associated with neuronal death and cognitive decline. In Alzheimer's disease beta-amyloid accumulation can further influence tau pathology by promoting tau phosphorylation through pathways involving GSK3β. In frontotemporal dementia mutations in the MAPT gene encoding tau lead to neurofibrillary tangle formation contributing to the disease's progression. These tangles and accompanying neuronal loss characterize tauopathies underlining their significance in neurodegenerative disease research.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Neurofilaments usually contain three intermediate filament proteins : NEFL, NEFM, and NEFH which are involved in the maintenance of neuronal caliber. NEFH has an important function in mature axons that is not subserved by the two smaller NF proteins. May additionally cooperate with the neuronal intermediate filament proteins PRPH and INA to form neuronal filamentous networks (By similarity).
See full target information NEFH

Publications (4)

Recent publications for all applications. Explore the full list and refine your search

Frontiers in pharmacology 16:1596469 PubMed40444050

2025

Chronic administration of prebiotics and probiotics prevent pathophysiological hallmarks of Alzheimer's disease in the cortex of APP/PS1 mice.

Applications

Unspecified application

Species

Unspecified reactive species

Giorgia Sarti,Chiara Traini,Giada Magni,Selene Attorre,Giorgio Tognozzi,Edoardo Calussi,Maria Grazia Giovannini,Maria Giuliana Vannucchi,Daniele Lana

Frontiers in immunology 15:1421455 PubMed39434878

2024

Erlotinib regulates short-term memory, tau/Aβ pathology, and astrogliosis in mouse models of AD.

Applications

Unspecified application

Species

Unspecified reactive species

Hyun-Ju Lee,Jeong-Woo Hwang,Jieun Kim,A-Ran Jo,Jin-Hee Park,Yoo Joo Jeong,Ji-Yeong Jang,Su-Jeong Kim,Jeong-Heon Song,Hyang-Sook Hoe

Signal transduction and targeted therapy 8:358 PubMed37735155

2023

Tauopathy promotes spinal cord-dependent production of toxic amyloid-beta in transgenic monkeys.

Applications

Unspecified application

Species

Unspecified reactive species

Zhuchi Tu,Sen Yan,Bofeng Han,Caijuan Li,Weien Liang,Yingqi Lin,Yongyan Ding,Huiyi Wei,Lu Wang,Hao Xu,Jianmeng Ye,Bang Li,Shihua Li,Xiao-Jiang Li

Molecular medicine reports 12:3862-3868 PubMed26016457

2015

Rg1 exhibits neuroprotective effects by inhibiting the endoplasmic reticulum stress-mediated c-Jun N-terminal protein kinase apoptotic pathway in a rat model of Alzheimer's disease.

Applications

Unspecified application

Species

Unspecified reactive species

Jun-Shan Mu,Hang Lin,Jian-Xin Ye,Min Lin,Xiao-Ping Cui
View all publications

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