Reversible oxidation and inactivation of protein tyrosine phosphatases in vivo.

By T. Meng, T. Fukada, N. Tonks. Molecules and Cells, 2002

1,072 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0c0da11c5f04f68010ab24f6b0e7db9a23703d89

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In Immunology

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Citations in the corpus

Hydrogen Peroxide: A Signaling Messenger (2006, neutral): “The slow rate of reaction of TDPs with H2O2 explains why the application of physiologic levels (< 10 μM) of H2O2 to cells neither inhibits these enzymes nor enhances tyrosine phosphorylation (51, 123, 141, 164).”
The 'ins' and 'outs' of podosomes and invadopodia: characteristics, formation and function (2011, neutral): “Furthermore, ROS can transiently oxidize and inhibit protein Tyr phosphatases and some lipid phosphatase”
ROS Function in Redox Signaling and Oxidative Stress (2014, background): “Intracellular MAP kinase signaling following PDGF stimulation is also reinforced through oxidation and inactivation of the PDGFR-associated phosphatase SHP-2 [25].”
Hydrogen peroxide sensing, signaling and regulation of transcription factors (2014, background): “If these enzymes had only an antioxidant function, why is there such a variety? For all these reasons, it was concluded that a signaling protein like PTP1B that is redox regulated by H2O2 [16][17][18] but has a low reactivity towards H2O2 [19], could not be a direct sensor of H2O2 [20][21][22][13].”
NOX enzymes and the biology of reactive oxygen (2004, background): “For example, a recently described cysteine oxidation product in the active site of protein tyrosine phosphatase 1B (a cyclic sulphenyl-amide”
Reactive oxygen species in cancer (2010, background): “For example, irreversible oxidation of phosphatases within the catalytic sites hinders their enzymatic activity [233].”
Reactive oxygen species in vascular biology: implications in hypertension (2004, neutral): “The best-established direct targets of ROS signaling are protein tyrosine phosphatases (Lee et al. 1998; Meng et al. 2002) and transcription factors (Haddad 2002; Turpaev 2002).”
The signaling mechanism of ROS in tumor progression (2007, background): “SHP2, one of the SH2-containing PTP, can be inactivated by ROS in PDGF-treated Rat-1 cell, which is associated with autophosphorylation of PDGFR leading to MAPK activation [107].”