成对螺旋细丝蛋白抗体

我公司是国内最权威的抗体代理商，成对螺旋细丝蛋白抗体价格优惠，成对螺旋细丝蛋白抗体质量保证，欢迎来电订购或咨询在线客服！

英文名称  Anti-PHF/Paired Helical Filaments

中文名称  成对螺旋细丝蛋白抗体

别    名  Microtubule-associated protein tau; Neurofibrillary tangle protein; Paired helical filament-tau; PHF-tau; TAU_HUMAN.

浓    度  1mg/1ml

规 格  0.2ml/200μg

抗体来源  Rabbit  

克隆类型  polyclonal

交叉反应  Human, Mouse, Rat, Cow, Horse

产品类型  一抗    

研究领域  神经生物学 信号转导 Alzheimer's  

蛋白分子量  predicted molecular weight: 79kDa

性    状  Lyophilized or Liquid

成对螺旋细丝蛋白抗体随着国内抗体行业的崛起，我国自主品牌的抗体，都蛮多了，质量也不错，技术在逐渐成熟，价格也比国外的廉价的多，受到国内顾客的热捧，我们公司为了方便客户，特推出阴离子转运蛋白-1抗体规格15ug、30ug、50ug、100ug，15ug和30ug等，我们全国包邮，大中城市免费快递。抗体分子是生物学和医学领域用途最为广泛的蛋白分子。抗体作为疾病预防、诊断和治疗的制剂已有上百年的发展历史。随着生命科学研究的迅猛发展，抗体工程在生物技术领域越来越占有非常重要的地位。我公司可为您提供快速的、高质量的和经济的多克隆抗体制备服务，并将成为您在科研及生产中的得力助手。

免 疫 原  KLH conjugated synthetic peptide derived from human Paired Helical Filaments

亚    型  IgG

纯化方法  affinity purified by Protein A

储 存 液  Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4

产品应用   WB=1:100-500  ELISA=1:500-1000  IHC-P=1:100-500  IHC-F=1:100-500  ICC=1:100-500  IF=1:100-500

（石蜡切片需做抗原修复）

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存条件  Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.

Important Note  This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

产品介绍 Neuropathology Paired structures that are core constituents of the neurofibrillary tangles of Alzheimer's disease and occur in Down syndrome, Hallervorden-Spatz disease, lead encephalopathy, lipofuscinosis, subacute sclerosing panencephalitis, and tuberous sclerosis.

Function : 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/MAPT 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.

Subunit : Interacts with PSMC2 through SQSTM1 (By similarity). Interacts with SQSTM1 when polyubiquitinated. Interacts with FKBP4 (By similarity). Binds to CSNK1D. Interacts with SGK1.

Subcellular Location : Cytoplasm, cytosol. Cell membrane; Peripheral membrane protein; Cytoplasmic side. Cytoplasm, cytoskeleton. Cell projection, axon. 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.

Post-translational modifications : Phosphorylation at serine and threonine residues in S-P or T-P motifs by proline-directed protein kinases (PDPK1: CDK1, CDK5, GSK3, MAPK) (only 2-3 sites per protein in interphase, seven-fold increase in mitosis, and in the form associated with paired helical filaments (PHF-tau)), and at serine residues in K-X-G-S motifs by MAP/microtubule affinity-regulating kinase (MARK1 or MARK2), causing detachment from microtubules, and their disassembly. Phosphorylation decreases with age. Phosphorylation within tau/MAP's repeat domain or in flanking regions seems to reduce tAU/MAP'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. Phosphorylation at Ser-548 by GSK3B reduces ability to bind and stabilize microtubules. Phosphorylation at Ser-579 by BRSK1 and BRSK2 in neurons affects ability to bind microtubules and plays a role in neuron polarization. Phosphorylated at Ser-554, Ser-579, Ser-602, Ser-606 and Ser-669 by PHK. Phosphorylation at Ser-214 by SGK1 mediates microtubule depolymerization and neurite formation in hippocampal neurons. There is a reciprocal down-regulation of phosphorylation and O-GlcNAcylation. Phosphorylation on Ser-717 completely abolishes the O-GlcNAcylation on this site, while phosphorylation on Ser-713 and Ser-721 reduces glycosylation by a factor of 2 and 4 respectively. Phosphorylation on Ser-721 is reduced by about 41.5% by GlcNAcylation on Ser-717.

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.

O-glycosylated. O-GlcNAcylation content is around 8.2%. There is reciprocal down-regulation of phosphorylation and O-GlcNAcylation. Phosphorylation on Ser-717 completely abolishes the O-GlcNAcylation on this site, while phosphorylation on Ser-713 and Ser-721 reduces O-GlcNAcylation by a factor of 2 and 4 respectively. O-GlcNAcylation on Ser-717 decreases the phosphorylation on Ser-721 by about 41.5%.

Glycation of PHF-tau, but not normal brain TAU/MAPT. 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 : Note=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). O-GlcNAcylation is greatly reduced in Alzheimer disease brain cerebral cortex leading to an increase in TAU/MAPT phosphorylations.

Defects in MAPT are a cause of frontotemporal dementia (FTD) [MIM:600274]; also called frontotemporal dementia (FTD), pallido-ponto-nigral degeneration (PPND) 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 Pick disease of the brain (PIDB) [MIM:172700]. It is a rare form of dementia pathologically defined by severe atrophy, neuronal loss and gliosis. It is characterized by the occurrence of tau-positive inclusions, swollen neurons (Pick cells) and argentophilic neuronal inclusions known as Pick bodies that disproportionally affect the frontal and temporal cortical regions. Clinical features include aphasia, apraxia, confusion, anomia, memory loss and personality deterioration.

Note=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. [DISEASE] Defects in MAPT are a cause of progressive supranuclear palsy type 1 (PSNP1) [MIM:601104]; also abbreviated as PSP and also known as Steele-Richardson-Olszewski syndrome. PSNP1 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 are a cause of Parkinson-dementia syndrome (PARDE) [MIM:260540]. A syndrome characterized by parkinsonism tremor, rigidity, dementia, ophthalmoparesis and pyramidal signs. Neurofibrillary degeneration occurs in the hippocampus, basal ganglia and brainstem nuclei.

成对螺旋细丝蛋白抗体Similarity : Contains 4 Tau/MAP repeats.

Database links : UniProtKB/Swiss-Prot: P10636.5

PHF以神经原纤维缠结(neurofibrillary tangles, NFT)存在于神经元的胞体;以神经毯和神经炎性斑存在于受累神经元的退化树突.微管相关蛋白tau是PHF的主要组成成分.在AD脑中,特别是在PHF结构中的tau被异常过度磷酸化.用磷酸化依赖的特异抗tau抗体检测,已证明PHF中的tau蛋白至少有21个异常磷酸化位点.