MAB5430 | Anti-Tau Antibody, Caspase Cleaved (truncated at Asp421)

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      Tableau de caractéristiques principal

      Espèces réactives Principales applications Hôte Format Type d'anticorps
      HumainImmunohistochimie, ELISA, WBSourisPurifié(e) Anticorps monoclonal
      Référence MAB5430
      Famille de marques Chemicon®
      Nom de marque
      • Chemicon
      Description Anti-Tau Antibody, Caspase Cleaved (truncated at Asp421)
      Références bibliographiques
      Informations produit
      Format Purifié(e)
      Présentation Purified immunoglobulin. Liquid in PBS. Contains no preservative.
      Application Anti-Tau Antibody, Caspase Cleaved (truncated at Asp421) is an antibody against Tau for use in ELISA, WB, IH.
      Principales applications
      • Immunohistochimie
      • ELISA
      • Western Blotting
      Notes opératoires Western blot



      Optimal working dilutions must be determined by end user.
      Informations biologiques
      Espèces d'immunogène Peptide corresponding to the C-terminus of tau truncated as aspartic acid 421.
      Épitope Caspase Cleaved (truncated at Asp421)
      Clone tau-C3
      Concentration Please refer to the Certificate of Analysis for the lot-specific concentration.
      Hôte Souris
      Spécificité Reacts with Tau, caspase cleaved (truncated at Asp421). The antibody shows no reactivity with full length tau nor other tau C-terminal truncations. The antibody stains amyloid beta treated neurons and brain tissue in Alzheimer's disease, more specifically it stains a subset of neurofibrillary tangles, tau-containing neuritic plaques and neuropil threads.
      Isotype IgG1
      Espèces réactives Humain
      Type d'anticorps Anticorps monoclonal
      Code Entrez Gene
      Résumé Entrez Gene This gene encodes the microtubule-associated protein tau (MAPT) whose transcript undergoes complex, regulated alternative splicing, giving rise to several mRNA species. MAPT transcripts are differentially expressed in the nervous system, depending on stage of neuronal maturation and neuron type. MAPT gene mutations have been associated with several neurodegenerative disorders such as Alzheimer's disease, Pick's disease, frontotemporal dementia, cortico-basal degeneration and progressive supranuclear palsy.
      Symbole du gène
      • PPND
      • MAPT
      • MTBT2
      • MAPTL
      • tau
      • FTDP-17
      • MSTD
      • TAU
      • FLJ31424
      • MTBT1
      • PHF-tau
      • DDPAC
      • MGC138549
      Code UniProt
      Résumé UniProt FUNCTION: SwissProt: P10636 # Promotes microtubule assembly and stability, and might be involved in the establishment and maintenance of neuronal polarity. The C-terminus binds axonal microtubules while the N- terminus binds neural plasma membrane components, suggesting that tau functions as a linker protein between both. Axonal polarity is predetermined by tau localization (in the neuronal cell) in the domain of the cell body defined by the centrosome. The short isoforms allow plasticity of the cytoskeleton whereas the longer isoforms may preferentially play a role in its stabilization.
      SIZE: 758 amino acids; 78878 Da
      SUBUNIT: Interacts with PSMC2 through SQSTM1 (By similarity). Interacts with SQSTM1 when polyubiquitinated.
      SUBCELLULAR LOCATION: Cytoplasm, cytosol. Cell membrane. Note=Mostly found in the axons of neurons, in the cytosol and in association with plasma membrane components.
      TISSUE SPECIFICITY: Expressed in neurons. Isoform PNS-tau is expressed in the peripheral nervous system while the others are expressed in the central nervous system.DEVELOPMENTAL STAGE: Four-repeat (type II) tau is expressed in an adult-specific manner and is not found in fetal brain, whereas three-repeat (type I) tau is found in both adult and fetal brain.
      DOMAIN: SwissProt: P10636 The tau/MAP repeat binds to tubulin. Type I isoforms contain 3 repeats while type II isoforms contain 4 repeats.
      PTM: Phosphorylation at serine and threonine residues in S-P or T- P motifs by proline-directed protein kinases (PDPK: CDC2, CDK5, GSK-3, MAPK) (only 2-3 sites per protein in interphase, seven-fold increase in mitosis, and in PHF-tau), and at serine residues in K- X-G-S motifs by MAP/microtubule affinity-regulating kinase (MARK) in Alzheimer diseased brains. Phosphorylation decreases with age. Phosphorylation within tau's repeat domain or in flanking regions seems to reduce tau's interaction with, respectively, microtubules or plasma membrane components. Phosphorylation on Ser-610, Ser- 622, Ser-641 and Ser-673 in several isoforms during mitosis. & Polyubiquitinated. Requires functional TRAF6 and may provoke SQSTM1-dependent degradation by the proteasome (By similarity). PHF-tau can be modified by three different forms of polyubiquitination. 'Lys-48'-linked polyubiquitination is the major form, 'Lys-6'-linked and 'Lys-11'-linked polyubiquitination also occur. & Glycation of PHF-tau, but not normal brain tau. Glycation is a non-enzymatic post-translational modification that involves a covalent linkage between a sugar and an amino group of a protein molecule forming ketoamine. Subsequent oxidation, fragmentation and/or cross-linking of ketoamine leads to the production of advanced glycation endproducts (AGES). Glycation may play a role in stabilizing PHF aggregation leading to tangle formation in AD.
      DISEASE: SwissProt: P10636 # In Alzheimer disease, the neuronal cytoskeleton in the brain is progressively disrupted and replaced by tangles of paired helical filaments (PHF) and straight filaments, mainly composed of hyperphosphorylated forms of TAU (PHF-TAU or AD P-TAU). & Defects in MAPT are a cause of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP17) [MIM:600274, 172700]; also called frontotemporal dementia (FTD) or historically termed Pick complex. This form of frontotemporal dementia is characterized by presenile dementia with behavioral changes, deterioration of cognitive capacities and loss of memory. In some cases, parkinsonian symptoms are prominent. Neuropathological changes include frontotemporal atrophy often associated with atrophy of the basal ganglia, substantia nigra, amygdala. In most cases, protein tau deposits are found in glial cells and/or neurons. & Defects in MAPT are a cause of pallido-ponto-nigral degeneration (PPND) [MIM:168610]. The clinical features include ocular motility abnormalities, dystonia and urinary incontinence, besides progressive parkinsonism and dementia. & Defects in MAPT are a cause of corticobasal degeneration (CBD). It is marked by extrapyramidal signs and apraxia and can be associated with memory loss. Neuropathologic features may overlap Alzheimer disease, progressive supranuclear palsy, and Parkinson disease. & Defects in MAPT are a cause of progressive supranuclear palsy (PSP) [MIM:601104, 260540]; also known as Steele-Richardson- Olszewski syndrome. PSP is characterized by akinetic-rigid syndrome, supranuclear gaze palsy, pyramidal tract dysfunction, pseudobulbar signs and cognitive capacities deterioration. Neurofibrillary tangles and gliosis but no amyloid plaques are found in diseased brains. Most cases appear to be sporadic, with a significant association with a common haplotype including the MAPT gene and the flanking regions. Familial cases show an autosomal dominant pattern of transmission with incomplete penetrance; genetic analysis of a few cases showed the occurrence of tau mutations, including a deletion of Asn-613. & Defects in MAPT may be a cause of hereditary dysphasic disinhibition dementia (HDDD) [MIM:607485]. HDDD is a frontotemporal dementia characterized by progressive cognitive deficits with memory loss and personality changes, severe dysphasic disturbances leading to mutism, and hyperphagia.
      SIMILARITY: Contains 4 Tau/MAP repeats.
      Informations physico-chimiques
      Informations sur les matériaux
      Informations toxicologiques
      Informations de sécurité selon le SGH
      Informations sur la sécurité
      Notifications sur l'utilisation du produit
      Notification sur l'utilisation
      • 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.
      Informations relatives au stockage et à l'expédition
      Conditions de stockage Maintain at 2-8°C in undiluted aliquots for up to 6 months after date of receipt.
      Informations sur l'emballage
      Quantité 100 µg
      Informations sur le transport
      Information complémentaire




      Certificats d'analyse

      TitreNuméro de lot
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 21155732115573
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 21236582123658
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 21384562138456
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 19874681987468
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 20059292005929
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 20371932037193
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 20513822051382
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 20552952055295
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 21535582153558
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 23243942324394
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - 24940632494063
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - LV1833247LV1833247
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - NG1742781NG1742781
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - NG1896096NG1896096
      Anti-Tau, Caspase Cleaved (truncated at Asp421) - NG1914808NG1914808

      Références bibliographiques

      Aperçu de la référence bibliographiqueEspèceNº PubMed
      Apoptosis in transgenic mice expressing the P301L mutated form of human tau.
      Rita M Ramalho, Ricardo J S Viana, Rui E Castro, Clifford J Steer, Walter C Low, Cecília M P Rodrigues
      Molecular medicine (Cambridge, Mass.) 14 309-17 2008

      Afficher le résumé Article en texte intégral
      Tau truncation during neurofibrillary tangle evolution in Alzheimer's disease.
      Guillozet-Bongaarts, Angela L, et al.
      Neurobiol. Aging, 26: 1015-22 (2005) 2005

      Afficher le résumé
      The generation of a 17 kDa neurotoxic fragment: an alternative mechanism by which tau mediates beta-amyloid-induced neurodegeneration.
      Park, So-Young and Ferreira, Adriana
      J. Neurosci., 25: 5365-75 (2005) 2005

      Afficher le résumé
      Early N-terminal changes and caspase-6 cleavage of tau in Alzheimer's disease.
      Horowitz, Peleg M, et al.
      J. Neurosci., 24: 7895-902 (2004) 2004

      Afficher le résumé
      Caspase cleavage of tau: linking amyloid and neurofibrillary tangles in Alzheimer's disease.
      Gamblin, T Chris, et al.
      Proc. Natl. Acad. Sci. U.S.A., 100: 10032-7 (2003) 2003

      Afficher le résumé


      Research Focus - Volume 2, 2013

      Fiche technique

      Anti-Tau, Caspase Cleaved (truncated at Asp421) - Data Sheet

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      Life Science Research > Antibodies and Assays > Primary Antibodies