Journal ArticleDOI
Protein tyrosine phosphatases: from genes, to function, to disease
TLDR
Recent breakthroughs in understanding of the role of the PTPs in the regulation of signal transduction and the aetiology of human disease are described.Abstract:
The protein tyrosine phosphatase (PTP) superfamily of enzymes functions in a coordinated manner with protein tyrosine kinases to control signalling pathways that underlie a broad spectrum of fundamental physiological processes. In this review, I describe recent breakthroughs in our understanding of the role of the PTPs in the regulation of signal transduction and the aetiology of human disease.read more
Citations
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Cell signaling by receptor-tyrosine kinases
TL;DR: Understanding of the complex signaling networks downstream from RTKs and how alterations in these networks are translated into cellular responses provides an important context for therapeutically countering the effects of pathogenic RTK mutations in cancer and other diseases.
Journal ArticleDOI
ROS Function in Redox Signaling and Oxidative Stress
TL;DR: It is argued that redox biology, rather than oxidative stress, underlies physiological and pathological conditions.
Journal ArticleDOI
Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling
TL;DR: This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival, ROS homeostasis and antioxidant gene regulation, mitochondrial oxidative stress, apoptosis, and aging.
Journal ArticleDOI
A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation
Jeffrey R. Erickson,Mei Ling A. Joiner,Xiaoqun Guan,William Kutschke,Jinying Yang,Carmine V. Oddis,Ryan K. Bartlett,John S. Lowe,Susan E. O'Donnell,Nukhet Aykin-Burns,Matthew C. Zimmerman,Kathy Zimmerman,Amy-Joan L. Ham,Robert M. Weiss,Douglas R. Spitz,Madeline A. Shea,Roger J. Colbran,Peter J. Mohler,Mark E. Anderson +18 more
TL;DR: It is shown that oxidation of paired regulatory domain methionine residues sustains CaMKII activity in the absence of Ca2+/CaM and highlights the critical importance of oxidation-dependent CaMK II activation to AngII and ischemic myocardial apoptosis.
Journal ArticleDOI
NRF2 and cancer: the good, the bad and the importance of context
Michael B. Sporn,Karen T. Liby +1 more
TL;DR: This Opinion article aims to rationalize conflicting perspectives by critiquing the context dependence of NRF2 functions and the experimental methods behind these conflicting data.
References
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Journal ArticleDOI
NOX enzymes and the biology of reactive oxygen
TL;DR: Professional phagocytes generate high levels of reactive oxygen species (ROS) using a superoxide-generating NADPH oxidase as part of their armoury of microbicidal mechanisms, leading to the concept that ROS are 'intentionally' generated in these cells with distinctive cellular functions related to innate immunity, signal transduction and modification of the extracellular matrix.
Journal ArticleDOI
Cellular signaling by fibroblast growth factor receptors.
TL;DR: The 22 members of the fibroblast growth factor (FGF) family of growth factors mediate their cellular responses by binding to and activating the different isoforms encoded by the four receptor tyrosine kinases (RTKs) designated FGFR1, FGFR2,FGFR3 and FGFR4.
Journal ArticleDOI
Protein Tyrosine Phosphatases in the Human Genome
Andres Alonso,Joanna Sasin,Nunzio Bottini,Ilan Friedberg,Iddo Friedberg,Andrei L. Osterman,Adam Godzik,Tony Hunter,Jack E. Dixon,Tomas Mustelin +9 more
TL;DR: The set of 107 genes in the human genome that encode members of the four protein tyrosine phosphatase (PTP) families are presented and the role of these enzymes in human disease will be discussed.
Journal ArticleDOI
Reactive Oxygen Species Promote TNFα-Induced Death and Sustained JNK Activation by Inhibiting MAP Kinase Phosphatases
TL;DR: It is shown that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid, which results in sustained JNK activation, which is required for cytochrome c release and caspase 3 cleavage.
Journal ArticleDOI
A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase (PTPN22) is associated with rheumatoid arthritis.
Ann B. Begovich,Victoria E.H. Carlton,Lee Honigberg,Steven J. Schrodi,Anand P. Chokkalingam,Heather C. Alexander,Kristin G. Ardlie,Qiqing Huang,Ashley M. Smith,Jill M. Spoerke,Marion T. Conn,Monica Chang,Sheng Yung P Chang,Randall K. Saiki,Joseph J. Catanese,Diane U. Leong,Veronica Garcia,Linda B. McAllister,Douglas A. Jeffery,Annette Lee,Franak Batliwalla,Elaine F. Remmers,Lindsey A. Criswell,Michael F. Seldin,Daniel L. Kastner,Christopher I. Amos,John J. Sninsky,Peter K. Gregersen +27 more
TL;DR: It is shown that the risk allele of a missense SNP in PTPN22 disrupts the P1 proline-rich motif that is important for interaction with Csk, potentially altering these proteins' normal function as negative regulators of T-cell activation.