TY - JOUR
T1 - Oxidative stress-associated protein tyrosine kinases and phosphatases in fanconi anemia
AU - Li, Jie
AU - Pang, Qishen
PY - 2014/5/10
Y1 - 2014/5/10
N2 - Significance: Fanconi anemia (FA) is a genetic disorder featuring chromosomal instability, developmental defects, progressive bone marrow failure, and predisposition to cancer. Besides the predominant role in DNA damage response and/or repair, many studies have linked FA proteins to oxidative stress. Oxidative stress, defined as imbalance in pro-oxidant and antioxidant homeostasis, has been considered to contribute to disease development, including FA. Recent Advances: A variety of signaling pathways may be influenced by oxidative stress, particularly the equilibrium between protein kinases and phosphatases, consequently leading to an aberrant phosphorylation state of cellular proteins. Dysfunction of kinases/phosphatases has been implicated in the pathophysiology of human diseases. In FA, evidence is emerging that links abnormal phosphorylation/de-phosphorylation of signaling molecules to clinical complications and malformations. Critical Issues: In this study, we review the recent findings on the oxidative stress-related kinases and phosphatases, particularly tyrosine phosphatases in FA. Future Directions: Understanding the role of oxidative stress-related kinases and phosphatases in FA may provide unique and generic possibilities for the future development of therapeutic strategies by targeting the dysregulated protein kinases and phosphatases in a clinical setting. Antioxid. Redox Signal. 20, 2290-2301.
AB - Significance: Fanconi anemia (FA) is a genetic disorder featuring chromosomal instability, developmental defects, progressive bone marrow failure, and predisposition to cancer. Besides the predominant role in DNA damage response and/or repair, many studies have linked FA proteins to oxidative stress. Oxidative stress, defined as imbalance in pro-oxidant and antioxidant homeostasis, has been considered to contribute to disease development, including FA. Recent Advances: A variety of signaling pathways may be influenced by oxidative stress, particularly the equilibrium between protein kinases and phosphatases, consequently leading to an aberrant phosphorylation state of cellular proteins. Dysfunction of kinases/phosphatases has been implicated in the pathophysiology of human diseases. In FA, evidence is emerging that links abnormal phosphorylation/de-phosphorylation of signaling molecules to clinical complications and malformations. Critical Issues: In this study, we review the recent findings on the oxidative stress-related kinases and phosphatases, particularly tyrosine phosphatases in FA. Future Directions: Understanding the role of oxidative stress-related kinases and phosphatases in FA may provide unique and generic possibilities for the future development of therapeutic strategies by targeting the dysregulated protein kinases and phosphatases in a clinical setting. Antioxid. Redox Signal. 20, 2290-2301.
UR - http://www.scopus.com/inward/record.url?scp=84898606392&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84898606392&partnerID=8YFLogxK
U2 - 10.1089/ars.2013.5715
DO - 10.1089/ars.2013.5715
M3 - Review article
C2 - 24206276
AN - SCOPUS:84898606392
SN - 1523-0864
VL - 20
SP - 2290
EP - 2301
JO - Antioxidants and Redox Signaling
JF - Antioxidants and Redox Signaling
IS - 14
ER -