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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 Antibodies) release and activating caspase-9 (show CASP9 Antibodies) and PARP (show COL11A2 Antibodies).
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.
Tat-DJ-1 protein (show PARK7 Antibodies) protects against dopaminergic neuronal cell death in 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP (show PTPN2 Antibodies))-induced PD mouse models.
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