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Here the authors demonstrate that mice lacking the alpha-tubulin (show TUBA4A Proteins) acetyltransferase Atat1 (show C6orf134 Proteins) in sensory neurons display profound deficits in their ability to detect mechanical stimuli.
alphaTAT1 has a conserved function as the major alpha-tubulin acetyltransferase in ciliated organisms and has an important role in regulating subcellular specialization of subsets of microtubules.
Data indicate that alpha-tubulin acetyltransferase 1 Atat1 (show C6orf134 Proteins) is not required for survival and development but may regulate more advanced functions.
Acetylation of alpha-tubulin (show TUBA4A Proteins) is under the control of the acetyltransferase MEC-17 (show C6orf134 Proteins) and deacetylases SIRT2 (Sirtuin 2 (show SIRT2 Proteins)) and HDAC6 (histone deacetylase 6 (show HDAC6 Proteins)). Adipocyte development is inhibited in MEC-17 (show C6orf134 Proteins)-knockdown cells, but enhanced in MEC-17 (show C6orf134 Proteins)-overexpressing cells.
Tat-DJ-1 protein (show PARK7 Proteins) protects against dopaminergic neuronal cell death in 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP (show PTPN2 Proteins))-induced PD mouse models.
Sequencing of TAT indicated two new homozygous mutations p.L312P (c.935T>C) and p.T408M (c.1223C>T) for the proband and his asymptomatic sister.
Two known mutations and one novel mutation was found in the TAT gene of Tunesian Richner-Hanhart syndrome patients. The geographical distribution of RHS mutations shows regional specificities.
The high potential application of Tat and its entrapment in elastic cationic niosomes for development of a transdermal gene delivery system are described.
A paternal inherited frameshift mutation c.1213delCinsAG at codon 405 causing a premature stop codon, and a maternally inherited deletion of 193kb encompassing the complete TAT gene yield the first complete TAT deletion in tyrosinaemia type II described.
tumor suppressive mechanism of TAT was associated with its proapoptotic role in a mitochondrial-dependent manner by promoting cytochrome-c (show CYCS Proteins) release and activating caspase-9 (show CASP9 Proteins) and PARP.
a silent exonic transversion in TAT causes complete missplicing by exon 11 skipping in oculocutaneous tyrosinaemia type II
Genetically modified adenoviral vector with the protein transduction domain of Tat improves gene transfer to CAR-deficient cells.
This nuclear gene encodes a mitochondrial protein tyrosine aminotransferase which is present in the liver and catalyzes the conversion of L-tyrosine into p-hydroxyphenylpyruvate. Mutations in this gene cause tyrosinemia (type II, Richner-Hanhart syndrome), a disorder accompanied by major skin and corneal lesions, with possible mental retardation. A regulator gene for tyrosine aminotransferase is X-linked.
, tyrosine aminotransferase, cytosolic
, tyrosine transaminase
, tyrosine aminotransferase
, tyrosine aminotransferase-like