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Milosavljevic, Tanja; Petrović, M.; Cvetković, Ivana; Grigorov, Ilijana

doi:10.1023/a:1019922805828

Cited by 13 publications

(5 citation statements)

References 34 publications

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“…The binding of C/EBP␤ to the promoter has been reported to be stimulated by phosphorylation at several amino acid residues, including Ser-105, Ser-299, and Thr-235 (Nakajima et al, 1993;Trautwein et al, 1993;Chinery et al, 1997). The DNA-binding of C/EBP␦ has also been found to be regulated by phosphorylation (Ray and Ray, 1994;Milosavljevic et al, 2002); however, which kinase mediates this effect is not understood. We found the increases in the phosphorylation of nuclear C/EBP␤ at Thr-235 and the nuclear translocation and DNA-binding of C/EBP␤ and C/EBP␦ after stimulation with MG132.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Regulation of Cyclooxygenase-2 in Response to Proteasome Inhibitors Involves Reactive Oxygen Species-mediated Signaling Pathway and Recruitment of CCAAT/Enhancer-binding Protein δ and CREB-binding Protein

Chen

Huang

Chen

2005

MBoC

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Inhibition of ubiquitin-proteasome pathway has been shown to be a promising strategy for the treatment of inflammation and cancer. Here, we show that proteasome inhibitors MG132, PSI-1, and lactacystin induce COX-2 expression via enhancing gene transcription rather than preventing protein degradation in the human alveolar NCI-H292 and A549, and gastric AGS epithelial cells. NF-IL6 and CRE, but not NF-κB elements on the COX-2 promoter were involved in the gene transcription event. The binding of CCAAT/enhancer binding protein (C/EBP)β and C/EBPδ to the CRE and NF-IL6 elements, as well as the recruitment of CBP and the enhancement of histone H3 and H4 acetylation on the COX-2 promoter was enhanced by MG132. However, it did not affect the total protein levels of C/EBPβ and C/EBPδ. MG132-induced DNA-binding activity of C/EBPδ, but not C/EBPβ was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPδ suppressed COX-2 expression, further strengthening the role of C/EBPδ in COX-2 gene transcription. In addition, the generation of intracellular reactive oxygen species (ROS) in response to MG132 contributed to the activation of MAPKs and Akt. These findings reveal that the induction of COX-2 transcription induced by proteasome inhibitors requires ROS-dependent protein kinases activation and the subsequent recruitments of C/EBPδ and CBP.

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Section: Discussionmentioning

confidence: 99%

Transcriptional Regulation of Cyclooxygenase-2 in Response to Proteasome Inhibitors Involves Reactive Oxygen Species-mediated Signaling Pathway and Recruitment of CCAAT/Enhancer-binding Protein δ and CREB-binding Protein

Chen

Huang

Chen

2005

MBoC

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“…For example, CAAT/enhancer-binding protein (C/EBP) ␤, originally identified and named nuclear factor IL-6 (10), and STAT3 are capable of cooperative activation of the haptoglobin promoter (11). The synthesis of ␣2-macroglobulin (␣2M), an APP protein, is also enhanced in response to IL-6 during acute phase reaction and may require C/EBP␤ (12). Acute phase reaction induces a specific interaction of c-Jun and STAT3 to result in the transcriptional activation of the ␣2 M gene (13) and that of diverse genes (14).…”

Section: Interleukin (Il)mentioning

confidence: 99%

Pyrrolidine Dithiocarbamate Inhibits Interleukin-6 Signaling through Impaired STAT3 Activation and Association with Transcriptional Coactivators in Hepatocytes

Zhu

Xie

et al. 2006

J. Biol. Chem.

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“…Simulated mergers of the halo models were carried out using a new, general-purpose N -body algorithm [38] that combines the elements of a hashed tree code with a quadrupolar expansion of force moments for the bulk dynamics, and the highly accurate Hermite predictorcorrector scheme for near-neighbor and massive-particle interactions. The code implements individual block time steps, individual stepping and softening criteria, and full functional parallelization.…”

Section: • = 3 × 10mentioning

confidence: 99%

Dark Matter Spikes and Annihilation Radiation from the Galactic Center

et al. 2002

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The annihilation rate of weakly interacting cold dark matter particles at the galactic center could be greatly enhanced by the growth of a density spike around the central supermassive black hole (SBH). Here we discuss the effects of hierarchical mergers on the central spike. Mergers between halos containing SBHs lead to the formation of SBH binaries which transfer energy to the dark matter particles, lowering their density. The predicted flux of annihiliation photons from the galactic center is several orders of magnitude smaller than in models that ignore the effects of SBHs and mergers. Measurement of the annihilation radiation could in principle be used to constrain the merger history of the galaxy.The dark matter puzzle is one of the central challenges facing particle physics and cosmology [1]. A popular candidate for non-baryonic cold dark matter (CDM) is the lightest supersymmetric particle, plausibly the neutralino χ [2,3]. The mass of the neutralino is constrained by accelerator searches and theoretical considerations of thermal freeze-out to lie in the range 30GeV < ∼ M χ < ∼ 10TeV [4,5]. Neutralinos are generically found to decouple at a temperature that is roughly M χ /20, which means that they are nonrelativistic already at decoupling and hence behave like CDM.Dark matter particles may be detected directly, via laboratory experiments [6], or indirectly, via their annihilation products [7]. Indirect schemes are typically based on searches for gamma rays from neutralino annihilations in the dark matter halo of the Milky Way (MW) galaxy [8,9,10]. Since the photon flux depends on the squared density of neutralinos integrated along the line of sight, the signal is greatly enhanced in directions where the dark matter is clumped. This includes the galactic center, where the density in a smooth halo would be maximum, as well as any lines of sight intersecting the centers of relic halos that orbit as subclumps in the MW halo [11,12]. The signal from the galactic center is further enhanced if there is a CDM "spike" associated with the central supermassive black hole (SBH). Adiabatic growth of a SBH at the center of a pre-existing halo produces a power-law distribution of matter around the SBH, a "spike," with density; M • is the SBH mass and σ is the 1D velocity dispersion of the dark matter particles. 14,15,16] and r h ∼ 1 pc. These spikes lead to predictions of higherthan-observed rates of γ-ray annihilation products [17].One element missing from earlier discussions of dark matter spikes is the destructive effect of hierarchical mergers. A dark matter halo as massive as that of the MW, M ∼ 10 12 M ⊙ , has almost certainly experienced a significant merger event since a redshift of z ∼ 2. Furthermore, SBHs with masses of ∼ 10 9 M ⊙ were present in at least some halos already at redshifts of 5 − 6 [18,19], and SBHs probably acquired most of their mass by a redshift of 2 − 3, the epoch of peak quasar activity [20]. In the CDM paradigm, big halos grow through the buildup of smaller ones [21]; if more than one of...

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Untitled

Cited by 13 publications

References 34 publications

Transcriptional Regulation of Cyclooxygenase-2 in Response to Proteasome Inhibitors Involves Reactive Oxygen Species-mediated Signaling Pathway and Recruitment of CCAAT/Enhancer-binding Protein δ and CREB-binding Protein

Transcriptional Regulation of Cyclooxygenase-2 in Response to Proteasome Inhibitors Involves Reactive Oxygen Species-mediated Signaling Pathway and Recruitment of CCAAT/Enhancer-binding Protein δ and CREB-binding Protein

Pyrrolidine Dithiocarbamate Inhibits Interleukin-6 Signaling through Impaired STAT3 Activation and Association with Transcriptional Coactivators in Hepatocytes

Dark Matter Spikes and Annihilation Radiation from the Galactic Center

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