Disease relevance of tyrosine

• Plasma phenylalanine (Phe) and tyrosine (Tyr) concentrations were measured by high-performance liquid chromatography in arteriolar blood obtained by finger prick from 78 normal volunteers and 36 heterozygote carriers of phenylketonuria (PKU) [1].
• In this study, we show that thirty-five of thirty-seven tested Bacillus thuringiensis strains possess the potential to produce melanin in the presence of L-tyrosin at elevated temperature (42 degrees C) [2].
• Infusion of Epi (500 nM) to the hindquarters of fed rats led to a sharp decrease in the Tyr release to 50% within 5 min, accompanied by an increase in perfusion pressure and edema around the perfused tissues [3].

High impact information on tyrosine

• A marked difference in inhibition of site-specific phosphorylation of EGFR was observed at Tyr1068 compared to other tyrosine residues (Tyr845, 992 and 1045) [4].
• STAT1 Ser phosphorylation is induced by the TCR in the absence of STAT1 Tyr phosphorylation, indicating that in T cells STAT1 Ser and Tyr phosphorylation are independent events [5].
• Benzimidazole (BZ) resistance in Haemonchus contortus is linked primarily with the mutation in the beta-tubulin isotype 1 gene that substitute phenylalanine (Phe) to tyrosine (Tyr) at 200 codon of the gene [6].
• This mutation appears to be recessive, since only homozygous mutant (Tyr/Tyr) individuals survived after BZ treatment of two resistant populations in which the three genotypes (rr, rs, ss) were initially present [7].
• Phe was at a maximum in guinea-pig brain after 30 min, while Tyr levels reached a peak at 120 min [8].

Anatomical context of tyrosine

• Whether the above results are affected by changes in Tyr transport at the plasma membrane was tested by measuring Tyr efflux from the perfused muscle [3].
• These results suggested that the suppression of Tyr release by alpha-adrenergic activity was mainly due to the effect on Tyr efflux, whereas that by beta-adrenergic activity was not at the Tyr transport level but at the proteolysis level, demonstrating that Epi directly inhibits proteolysis of skeletal muscle via the beta-adrenoceptor [3].
• Results indicated that the levels of tyrosine (Tyr) and dopamine (DA) were lowered, the levels of 5-hydroxytryptamine (5-HT) and 5-hydoxyindole acetic acid (5-HIAA) increased, and the frequency of the spontaneous discharge of nerve cells in VMH lowered in the obese rat group as compared with the normal group [9].

Associations of tyrosine with other chemical compounds

• Phe, Phe/Tyr and Phe2/Tyr values were higher in heterozygotes, whereas Tyr was higher in controls in both situations investigated [10].
• 0. The presence of sulfotyrosine is indicated by the detection of free tyrosine after tandem mass spectrometry (MS/MS) analysis under conditions in which the sulfuryl group of sulfotyrosine is labile [11].
• While tyrosine phosphorylation is frequently correlated to enzyme activation, thiol oxidation leads to inactivation of PTPs and to superactivation of PTKs [12].
• These results provide experimental evidence that this conserved histidine functions as a general acid/base catalyst in tyrosine recombinases [13].
• Colchicine, an effective drug for the treatment of gout, inhibited the MSU crystal-induced tyrosine phosphorylation of Tec, thus modulating its kinase activity [14].
• The novel DFG-out conformation with two diarylurea inhibitors (BIRB796, PF-4618433) reveals a distinct subclass of non-receptor tyrosine kinases identifiable by the gatekeeper Met-502 and the unique hinge loop conformation of Leu-504 [15].
• The most interesting finding though, is that mutating His-217 relieved the inhibitory effect of tyrosine on A. aeolicus prephenate dehydrogenase [16].

Gene context of tyrosine

• Treatment of tumor-bearing nude mice with the tyrosine kinase inhibitor ZD6474, which specifically inhibits RET, epidermal growth factor receptor (EGFR), and vascular endothelium growth factor receptor (VEGFR) tyrosine kinases, resulted in a dose-dependent inhibition of tumor growth [17].
• Activation of PLCgamma2 via GPVI is dependent on 2 complementary events: its interaction with the tyrosine 136 of LAT and its membrane location, which itself requires events mediated by the 3 C-terminal tyrosines of LAT [18].
• Yeast two-hybrid and coimmunoprecipitation analyses demonstrated that AnkA could bind to Abl-interactor 1 (Abi-1), an adaptor protein that interacts with Abl-1 tyrosine kinase, thus mediating AnkA phosphorylation [19].
• Tyrosine phosphorylation of PECAM-1 was associated with delayed opening of interendothelial junctions [20].
• Synapses are structurally simplified and the organization of postjunctional folds is aberrant in mice lacking tyrosine phosphorylation of the AChR beta-subunit [21].
• Efficient tyrosine phosphorylation of Mtss1 in response to PDGF also involves a coiled-coil domain, which is essential for a proper distribution to the cell leading edge and dorsal ruffles [22].
• BK channel regulation was not dependent upon direct phosphorylation of the BK alpha-subunit, rather channel function was controlled by the tyrosine phosphorylation status of the adapter protein cortactin that assembles directly with the BK channel [23].
• We demonstrate that siRNA screening can identify tyrosine kinase targets containing activating mutations in Janus kinase (JAK) 3 (A572V) in CMK cells and c-KIT (V560G) in HMC1.1 cells [24].
• ECP and EDN crystal structures revealed and EPO structure modeling suggested that the nitrated tyrosine residues in the toxins are surface exposed [25].
• These data indicate that LPS recognition by TLR4 activates the SFKs, c-SRC, FYN, and YES, which, in turn, contribute to tyrosine phosphorylation of zonula adherens proteins to open the endothelial paracellular pathway [26].

Analytical, diagnostic and therapeutic context of tyrosine

• In guinea-pigs peak plasma levels of Phe and Tyr occurred 30 min after treatment [8].

References