Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10636 (tau protein)
 5,110 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two different tubulin-assembly-promoting proteins were isolated from porcine brain microtubule protein. Following a heat step performed on microtubule protein, the thermal-stable proteins were fractionated by chromatography on phosphocellulose and Sepharose 4B. Two highly purified associated proteins were obtained. One resembles the previously described MAP2 protein (polypeptide molecular weight approximately 300,000), the other a mixture of four or five polypeptides previously described as tau protein (molecular weights between 55,000 and 70,000). Both proteins stimulate the polymerization of pure brain tubulin into microtubules with comparable activity. The resulting microtubules were characterized by electron microscopical analysis. Microtubules polymerized in the presence of MAP2 protein show typical side projections, which are conspicuously absent in microtubules assembled in the presence of tau protein. The latter microtubules show smooth surfaces. Some biochemical similarities and differences between the two different microtubule-associated proteins are discussed.
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PMID:Fractionation of brain microtubule-associated proteins. Isolation of two different proteins which stimulate tubulin polymerization in vitro. 72 84

Following experimental spinal cord injury (SCI), there is a delayed loss of neurofilament proteins but relatively little is known regarding the status of other cytoskeletal elements. The purpose of the present study was to compare the extent and time course of the MAP2 loss with that of neurofilament proteins, and to examine tau protein levels and distribution following SCI. Within 1 to 6 hours following SCI, there is rapid loss of MAP2, tau, and nonphosphorylated neurofilament proteins at the injury site. In contrast, the loss of phosphorylated neurofilament proteins was not significant until 1 week postinjury. In addition to the loss of MAP2 protein, there was extensive beading of MAP2-immunoreactive dendrites extending into the white matter. This was most pronounced 1 hour after injury and gradually resolved such that beading was no longer evident 2 weeks after SCI. The time course of beading resolution is similar to that of behavioral recovery following SCI, but the functional significance of the beading remains to be determined. Together, these results demonstrate that there are 2 phases of cytoskeletal disruption following SCI; a rapid loss of MAP2, tau, and nonphosphorylated neurofilament proteins, and a delayed loss of phosphorylated neurofilaments.
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PMID:Cytoskeletal disruption following contusion injury to the rat spinal cord. 1075 84