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TPPP/p25 is co-enriched and co-localized with alpha-synuclein in brain inclusions of Parkinson's disease patients. Interaction of alpha-synuclein with various deletion mutants and fragments of TPPP/p25 were characterized.
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The objective of this paper is to highlight a critical point of a recently published Skoufias's paper in which the crucial role of the microtubules in TPPP/p25 dimerization leading to microtubule bundling was suggested.
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This study demonstrated that the AAV9-mediated p25 overexpression mouse model, which is a practical model exhibiting neurodegeneration-like pathological and behavioral changes.
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The knowledge accumulated so far underlines the key roles of the multifunctional TPPP/p25 in both physiological and diverse pathological processes, consequently its validation as drug target sorely needs a new innovative strategy that is briefly reviewed here.
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TPPP may have a role in poor prognosis in hepatocellular carcinoma
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the central folded domain of TPPP/p25 following binding to microtubules can drive s homotypic protein-protein interactions leading to bundled microtubules.
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Results reveal a link between p25 and BACE1 in Alzheimer disease (AD) brains and suggest that upregulated Cdk5 activation by p25 accelerates AD pathogenesis by enhancing BACE1 activity via phosphorylation.
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Epigenetic changes in TPPP, in combination with experiences of maltreatment, may confer risk for depression in children.
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suggest that the zinc as a specific divalent cation could be involved in the fine-tuning of the physiological TPPP/p25 level counteracting both the enrichment and the lack of this protein leading to distinct central nervous system diseases
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results suggest that ROCK regulates beta-catenin stability in cells via preventing TPPP1-mediated inhibition of HDAC6 activity, to reduce its acetylation and degradation via phosphorylation by CK1 and GSK3beta
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GSK3 promotes the mitochondrial translocation of p53, enabling its interaction with Bcl2 to allow Bax oligomerization and the subsequent release of cytochrome C.
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dual Rock and Cdk phosphorylation of Tppp1 inhibits its regulation of the cell cycle to increase cell proliferation
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The RhoA-ROCK-LIMK2-TPPP pathway controls metaphase spindle-orientation; TPPP colocalizes with LIMK2 at the mitotic spindle.
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Although serine-129 phosphorylation of alpha-synuclein facilitates TPPP-mediated alpha-SYN oligomerization, this modification does not seem to play an inevitable role in the early step of alpha-SYN oligomer formation in a cellular model of multiple system atrophy.
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The authors conclude that the modest structural changes that p25alpha undergoes can promote weak intermolecular contacts and that polyanions such as heparin play a central role in stabilizing these aggregates.
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Wnt induces the phosphorylation of LRP6 which consequently access the catalytic pocket of GSK3 as pseudo-substrates, thus directly blocking its activity against beta-catenin.
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GSK3 has a significant role in maintaining repression of growth factor-inducible genes during quiescence. CREB, NFkB and AP-1 mediate this regulation of gene expression by GSK-3.
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Data show that TPPP may work as a protective factor for cells against the damage effects of the accumulation of abnormal forms of PrPs, besides its function as an agent for dynamic stabilization of microtubular ultrastructures.
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Binding of Zn(2) bivalent cation to structurally disordered TPPP/p25 influences TPPP/p25-promoted tubulin polymerization and GTPase activity.
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Interactions of pathological hallmark proteins: tubulin polymerization promoting protein/p25, beta-amyloid, and alpha-synuclein.
