Tau (Phospho-Thr231) Antibody Blocking Peptide

For

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.

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.

The tau/MAP repeat binds to tubulin. Type I isoforms contain 3 repeats while type II isoforms contain 4 repeats.

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.

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 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 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.

Contains 4 Tau/MAP repeats.