Restoration of SHIP-1 activity in human leukemic cells modifies NF-κB activation pathway and cellular survival upon oxidative stress

Gloire, Geoffrey; Charlier, Émilie; Rahmouni, Souad; Volanti, Cédric; Chariot, Alain; Erneux, Christophé; Piette, Jacques

doi:10.1038/sj.onc.1209542

Cited by 57 publications

(50 citation statements)

References 39 publications

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“…IB␣ Immunoprecipitation-Whole cell extraction and IB␣ immunoprecipitation were previously described by Gloire et al (27). The presence of unmodified IB␣ and IB␣ phosphorylated on tyrosine was determined by Western blotting.…”

Section: Methodsmentioning

confidence: 99%

Histone Deacetylase Inhibitor Trichostatin A Sustains Sodium Pervanadate-induced NF-κB Activation by Delaying IκBα mRNA Resynthesis

Horion

Gloire

Mjiyad

et al. 2007

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

Histone Deacetylase Inhibitor Trichostatin A Sustains Sodium Pervanadate-induced NF-κB Activation by Delaying IκBα mRNA Resynthesis

Horion

Gloire

Mjiyad

et al. 2007

Journal of Biological Chemistry

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“…In addition, SHIP interacts with Tec kinase and inhibits its function in T cells (31) as well as participates in a negative signaling complex by associating with the adaptor protein LAT (32). SHIP has also been shown to have a protective role in T lymphocytes exposed to oxidative stress (33). Despite this evidence, the impact of SHIP deletion on T cell biology was initially thought to be rather mild, although these mice exhibited defects in B cell development as well as excessive myeloid cell activation (34,35).…”

Section: Insights Into the Role Of Ship In T Lymphocytes From Gene Tamentioning

confidence: 99%

Phosphoinositide Lipid Phosphatases: Natural Regulators of Phosphoinositide 3-Kinase Signaling in T Lymphocytes

Harris

Parry

Westwick

et al. 2008

Journal of Biological Chemistry

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The phosphoinositide 3-kinase signaling pathway has been implicated in a range of T lymphocyte cellular functions, particularly growth, proliferation, cytokine secretion, and survival. Dysregulation of phosphoinositide 3-kinase-dependent signaling and function in leukocytes, including B and T lymphocytes, has been implicated in many inflammatory and autoimmune diseases. As befits a pivotal signaling cascade, several mechanisms exist to ensure that the pathway is tightly regulated. This minireview focuses on two lipid phosphatases, viz. the 3 -phosphatase PTEN (phosphatase and tensin homolog deleted on chromosome 10) and SHIP (Src homology 2 domain-containing inositol-5-phosphatase). We discuss their role in regulating T lymphocyte signaling as well their potential as future therapeutic targets.The PI3K 3 pathway plays a central role in regulating many biological processes, primarily via the generation of the potent second messenger PtdIns(3,4,5)P 3 , which acts as a docking site at the plasma membrane, recruiting and activating proteins containing pleckstrin homology (PH) domains (1). These downstream PI3K effectors include PDK-1 (3Ј-phosphoinositide-dependent kinase-1), which phosphorylates and activates the AGC protein kinases, including protein kinase B/Akt. Other kinases such as Tec family kinases can also interact directly with PtdIns(3,4,5)P 3 , as can GTPase-activating proteins and guanine nucleotide exchange factors as well as scaffolding proteins that nucleate the assembly of key signaling complexes (1, 2). PI3K and T LymphocytesT cells express all three class 1A PI3K isoforms (p110␣, p110␤, and p110␦), which are regulated by protein-tyrosine kinase-coupled receptors, as well as class 1B p110␥, which is activated by G protein-coupled receptors (GPCRs). The T cell antigen receptor (TCR), CD28 family co-stimulatory receptors, and cytokine receptors activate class 1A isoforms (3). Chemokines (by virtue of interacting with GPCRs), activate mainly class 1B PI3K (4). Use of pharmacological tools in leukemic human T cell lines first indicated a possible role for PI3K in T cell activation (5). Mice with a knock-in point mutation of p110␦ that abolishes kinase activity exhibit selective impairments in TCR signaling and reduced proliferation in vitro (6) and impaired function of CD4 ϩ CD25 ϩ Foxp3 ϩ T Reg cells (7). Interestingly, mice lacking both p110␥ and p110␦ show much more profound defects in thymocyte development and survival compared with mice lacking individual isoforms, indicating that these isoforms serve partially redundant functions in thymocytes (8, 9). Pathological consequences of combined p110␥␦ deficiency includes T cell lymphopenia, which leads to multiple-organ inflammation (10). Surprisingly, mice with T cellspecific loss of class 1A PI3K exhibit largely normal thymocyte development, and peripheral T cell numbers and subsets are unimpaired in young animals (11,12). In vitro proliferation of T cells from these mice in response to TCR ligation is abrogated, and there is complete loss of PI3K sig...

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“…phosphorylation and degradation of IjB via the proteasome with only minor or absent phosphorylation at Tyr42 (149).…”

Section: Brigelius-flohé and Flohémentioning

confidence: 99%

“…The atypical pathway is triggered by growth factors like EGF, ciliary neurotrophic factor (CNTF), or nerve growth factor (NGF) binding to RTKs, but receptor occupation can be mimicked by H 2 O 2 and PP inhibitors (147). Activation of the atypical pathway is mainly T cell-specific and depends on the presence of the phosphatase SHIP-1 (149 10). IKKb phosphorylates IjB at serines (Ser) 32 and 36 leading to the ubiquitination and degradation of IjB.…”

Section: Basics Of Nf-kb Activationmentioning

confidence: 99%

“…The DSP family not only de-phosphorylates tyrosine, Ser, and Thr residues, but also further comprises phosphatases acting on nonprotein substrates, such as phosphoinositol phospholipids (PIPs). Examples for the latter specificity are the Src homology-2 (SH2)-domain-containing inositide phosphatases (SHIPs) (149), which de-phosphorylate the membrane-bound PI3K-generated key signaling lipid PI(3,4,5)P 3 at position 5 to PI(3,4)P 2 , and the phosphatase and tensin homologue (PTEN), which dephosphorylates the 3 position of both PI(3,4,5)P 3 and PI(3,4)P 2 (304). Sharing the active site motif with the PTP/DSP family, PTEN is a typical example of a redox-sensitive phosphatase (280).…”

Section: Brigelius-flohé and Flohémentioning

confidence: 99%

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Basic Principles and Emerging Concepts in the Redox Control of Transcription Factors

Brigelius‐Flohé

Flohé

2011

Antioxidants & Redox Signaling

522

442

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Convincing concepts of redox control of gene transcription have been worked out for prokaryotes and lower eukaryotes, whereas the knowledge on complex mammalian systems still resembles a patchwork of poorly connected findings. The article, therefore, reviews principles of redox regulation with special emphasis on chemical feasibility, kinetic requirements, specificity, and physiological context, taking well investigated mammalian transcription factor systems, nuclear transcription factor of bone marrow-derived lymphocytes (NFjB), and kelch-like ECH-associated protein-1 (Keap1)/Nrf2, as paradigms. Major conclusions are that (i) direct signaling by free radicals is restricted to O 2 -and NO and can be excluded for fast reacting radicals such as OH, OR, or Cl ; (ii) oxidant signals are H 2 O 2 , enzymatically generated lipid hydroperoxides, and peroxynitrite; (iii) free radical damage is sensed via generation of Michael acceptors; (iv) protein thiol oxidation/alkylation is the prominent mechanism to modulate function; (v) redox sensors must be thiol peroxidases by themselves or proteins with similarly reactive cysteine or selenocysteine (Sec) residues to kinetically compete with glutathione peroxidase (GPx)-and peroxiredoxin (Prx)-type peroxidases or glutathione-S-transferases, respectively, a postulate that still has to be verified for putative mammalian sensors. S-transferases and Prxs are considered for system complementation. The impact of NF-jB and Nrf2 on hormesis, management of inflammatory diseases, and cancer prevention is critically discussed. Antioxid. Redox Signal. 15, 2335-2381.

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Restoration of SHIP-1 activity in human leukemic cells modifies NF-κB activation pathway and cellular survival upon oxidative stress

Cited by 57 publications

References 39 publications

Histone Deacetylase Inhibitor Trichostatin A Sustains Sodium Pervanadate-induced NF-κB Activation by Delaying IκBα mRNA Resynthesis

Histone Deacetylase Inhibitor Trichostatin A Sustains Sodium Pervanadate-induced NF-κB Activation by Delaying IκBα mRNA Resynthesis

Phosphoinositide Lipid Phosphatases: Natural Regulators of Phosphoinositide 3-Kinase Signaling in T Lymphocytes

Basic Principles and Emerging Concepts in the Redox Control of Transcription Factors

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