p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) decreases a(GO:microtubule)

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PubMed:23487739

Overexpressed tau was hyperphosphorylated and resulted in decreased MT density and greater fragmentation. Using genetic screen, a histone deacetylase 6 (HDAC6) null mutation rescued tau-induced MT defects in both muscles and neurons. Genetic and pharmacological inhibition of the tubulin-specific deacetylase activity of HDAC6 indicates that the rescue effect may be mediated by increased MT acetylation.

Related Edges 4

• a(GO:microtubule) negativeCorrelation act(p(HGNC:HDAC6))
• a(HBP:Tubacin) directlyDecreases act(p(HGNC:HDAC6))
• act(p(HGNC:HDAC6)) negativeCorrelation a(GO:microtubule)
• act(p(HGNC:HDAC6)) decreases p(INTERPRO:"Tubulin/FtsZ, GTPase domain", pmod(Ac))

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