ASK Family Proteins in Stress Response and Disease

Fujisawa, Takao; Takeda, Kohsuke; Ichijo, Hidenori

doi:10.1007/s12033-007-0053-x

Cited by 55 publications

(46 citation statements)

References 27 publications

(28 reference statements)

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“…This is in good agreement with the known fact that ASK1 is a member of the MAPKKK family preferentially activated by various cytotoxic stresses (19,27) and plays a causal role in cell death induced by a number of stimuli (18). Activation of ASK1 has been shown to be often mediated by ROS (19,27,54,55). The present study also demonstrated that ASK1 phosphorylation induced by STS, TNF␣, and FasL was dependent on ROS.…”

Section: Discussionsupporting

confidence: 92%

“…*, p Ͻ 0.05 versus isotonic. natively termed protein kinase B, and apoptosis signal-regulating kinase 1 (ASK1), a Ser/Thr-protein kinase that belongs to the MAPKKK family because of the following previous observations: Modulation of Akt by a hypertonic stimulation (16) was opposite to that by an apoptotic stimulation (17) in renal epithelial Madin-Darby canine kidney cells, and ASK1 was inhibited by Akt in L929 cells (18) and activated by a variety of apoptotic stimuli in a number of cell types (18,19). The present study demonstrates that in human epithelial HeLa cells shrinkage-induced activation of Akt1 is involved in the RVI process and that ASK1-induced inhibition of Akt1 activation causes inhibition of RVI in apoptotic HeLa cells.…”

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confidence: 99%

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Inhibition of Protein Kinase Akt1 by Apoptosis Signal-regulating Kinase-1 (ASK1) Is Involved in Apoptotic Inhibition of Regulatory Volume Increase

Subramanyam¹,

Takahashi²,

Hasegawa

et al. 2010

Journal of Biological Chemistry

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Most animal cell types regulate their cell volume after an osmotic volume change. The regulatory volume increase (RVI) occurs through uptake of NaCl and osmotically obliged water after osmotic shrinkage. However, apoptotic cells undergo persistent cell shrinkage without showing signs of RVI. Persistence of the apoptotic volume decrease is a prerequisite to apoptosis induction. We previously demonstrated that volume regulation is inhibited in human epithelial HeLa cells stimulated with the apoptosis inducer. Here, we studied signaling mechanisms underlying the apoptotic inhibition of RVI in HeLa cells. Hypertonic stimulation was found to induce phosphorylation of a Ser/ Thr protein kinase Akt (protein kinase B). Shrinkage-induced Akt activation was essential for RVI induction because RVI was suppressed by an Akt inhibitor, expression of a dominant negative form of Akt, or small interfering RNA-mediated knockdown of Akt1 (but not Akt2). Staurosporine, tumor necrosis factor-␣, or a Fas ligand inhibited both RVI and hypertonicityinduced Akt activation in a manner sensitive to a scavenger for reactive oxygen species (ROS). Any of apoptosis inducers also induced phosphorylation of apoptosis signal-regulating kinase 1 (ASK1) in a ROS-dependent manner. Suppression of (ASK1) expression blocked the effects of apoptosis, in hypertonic conditions, on both RVI induction and Akt activation. Thus, it is concluded that in human epithelial cells, shrinkage-induced activation of Akt1 is involved in the RVI process and that apoptotic inhibition of RVI is caused by inhibition of Akt activation, which results from ROS-mediated activation of ASK1.

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Inhibition of Protein Kinase Akt1 by Apoptosis Signal-regulating Kinase-1 (ASK1) Is Involved in Apoptotic Inhibition of Regulatory Volume Increase

Subramanyam¹,

Takahashi²,

Hasegawa

et al. 2010

Journal of Biological Chemistry

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“…We tested the expression of apoptosis-regulating genes Traf2, Traf6, Parp1, Atf6, Ask1, Ask2, Dapk1, and Apaf1 in siBrg1 NCCs (21)(22)(23)(24)(25)(26)(27)(28). Of these genes, only Ask1 (apoptosis signal-regulating kinase 1) exhibited increased expression (a 1.65-fold increase; P < 0.03) in siBrg1NCCs; the other genes showed no significant changes (Fig.…”

Section: Resultsmentioning

confidence: 99%

Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development

Xiong²,

Shang³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Development of the cerebral vessels, pharyngeal arch arteries (PAAs). and cardiac outflow tract (OFT) requires multipotent neural crest cells (NCCs) that migrate from the neural tube to target tissue destinations. Little is known about how mammalian NCC development is orchestrated by gene programming at the chromatin level, however. Here we show that Brahma-related gene 1 (Brg1), an ATPase subunit of the Brg1/Brahma-associated factor (BAF) chromatin-remodeling complex, is required in NCCs to direct cardiovascular development. Mouse embryos lacking Brg1 in NCCs display immature cerebral vessels, aberrant PAA patterning, and shortened OFT. Brg1 suppresses an apoptosis factor, Apoptosis signal-regulating kinase 1 (Ask1), and a cell cycle inhibitor, p21 cip1 , to inhibit apoptosis and promote proliferation of NCCs, thereby maintaining a multipotent cell reservoir at the neural crest. Brg1 also supports Myosin heavy chain 11 (Myh11) expression to allow NCCs to develop into mature vascular smooth muscle cells of cerebral vessels. Within NCCs, Brg1 partners with chromatin remodeler Chromodomain-helicase-DNAbinding protein 7 (Chd7) on the PlexinA2 promoter to activate PlexinA2, which encodes a receptor for semaphorin to guide NCCs into the OFT. Our findings reveal an important role for Brg1 and its downstream pathways in the survival, differentiation, and migration of the multipotent NCCs critical for mammalian cardiovascular development.N eural crest cells (NCCs) originate from the neural crest of the dorsal neural tube and migrate to many regions of the embryo, where they differentiate into a variety of local cells, including cardiovascular tissues (1). NCCs that emigrate from the neural crest of rhombomere 6-8 to pharyngeal arches and the heart are essential for the patterning of pharyngeal arch arteries (PAAs) and the cardiac outflow tract (OFT) (2, 3). These NCCs also differentiate into vascular smooth muscle cells (SMCs) of PAAs and the muscular septum of the aorta and pulmonary trunk (4, 5). In contrast, NCCs from the cephalic neural tube migrate to the face and forebrain to form craniofacial bones, as well as SMCs of facial and forebrain vessels (6). Thus, NCCs are critical for the formation of cardiac OFT and vascular supplies of large areas of the body.Disruption of NCC development, either directly or indirectly, results in many forms of human birth defects with cardiovascular malformations, including Alagille, Carpenter, Ivemark, Leopard, Williams, DiGeorge, and CHARGE syndromes (7). These syndromes involve defects in PAAs or cardiac OFT, such as coarctation of the aorta, interrupted aortic arch, pulmonary artery stenosis, double-outlet right ventricle, tetralogy of Fallot, or persistent truncus arteriosus. During PAA and OFT development, NCCs are regulated by numerous transcription factors, including Pax3, Pbx1/2/3, Tbx1/2/3/20, Msx1/2, Hand2, AP2a, Cited2, Pitx2, Sox4, Foxc1/c2/d3/h1, Fog2, Gata3/4/6, and Notch/NICD (8). Such extensive involvement of transcription factors indicates the importance of gene pr...

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“…22 In nonerythroid cell models, ROS have been reported to induce apoptosis by activating apoptosis signal regulating kinase 1 and jun-kinase; this mechanism may contribute to erythroid cell apoptosis in thalassemia. 36 In addition, there is evidence that apoptosis in thalassemic red blood cells is mediated by the Fas cell surface death receptor (FAS) and FAS-ligand pathway, which is triggered by high levels of ROS. 37 A recent study has demonstrated that heat shock protein 70 interacts directly with free a-globin chains, and thereby becomes sequestered in the cytoplasm.…”

Section: 21mentioning

confidence: 99%

α-Globin as a molecular target in the treatment of β-thalassemia

Mettananda

Gibbons

Higgs

2015

Blood

122

120

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The thalassemias, together with sickle cell anemia and its variants, are the world’s most common form of inherited anemia, and in economically undeveloped countries, they still account for tens of thousands of premature deaths every year. In developed countries, treatment of thalassemia is also still far from ideal, requiring lifelong transfusion or allogeneic bone marrow transplantation. Clinical and molecular genetic studies over the course of the last 50 years have demonstrated how coinheritance of modifier genes, which alter the balance of α-like and β-like globin gene expression, may transform severe, transfusion-dependent thalassemia into relatively mild forms of anemia. Most attention has been paid to pathways that increase γ-globin expression, and hence the production of fetal hemoglobin. Here we review the evidence that reduction of α-globin expression may provide an equally plausible approach to ameliorating clinically severe forms of β-thalassemia, and in particular, the very common subgroup of patients with hemoglobin E β-thalassemia that makes up approximately half of all patients born each year with severe β-thalassemia.

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ASK Family Proteins in Stress Response and Disease

Cited by 55 publications

References 27 publications

Inhibition of Protein Kinase Akt1 by Apoptosis Signal-regulating Kinase-1 (ASK1) Is Involved in Apoptotic Inhibition of Regulatory Volume Increase

Inhibition of Protein Kinase Akt1 by Apoptosis Signal-regulating Kinase-1 (ASK1) Is Involved in Apoptotic Inhibition of Regulatory Volume Increase

Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development

α-Globin as a molecular target in the treatment of β-thalassemia

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