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Ejaz Syeda Rabia,Khan Muhammad Azhar,Gulbadan Shagufta,Akhtar Majid Niaz,Ahmad Mukhtar,Hussain Altaf,Islam Misbah ul 한국세라믹학회 2022 한국세라믹학회지 Vol.59 No.4
Co 2+ and Cr 3+ -substituted SrBaCu Fe 28- y O 46 X-type hexaferrite with x = y = 0, 0.1 to 0.5 (step = 0.1) were prepared Co Cr 2- x x y through auto-combustion sol–gel method and sintered at 1250 °C for 5 h which was found from thermal analysis. The thermal investigation, phase detection, spectral, magnetic, and dielectric characteristics of the prepared composition were investigated by TGA, XRD, FTIR, VSM, and dielectric measurement. XRD patterns of the entire composition confi rmed the development of a single phase of X-type structure. The enhancement in the lattice parameters and cell volume was observed by varying the Co–Cr concentration, attributed to the larger ionic radii substitution. FTIR\spectra of all samples exhibit two absorption peaks in the wavenumber range of 500–550 cm −1 and 418–425 cm −1 that confi rm the formation of hexaferrite. The dielectric properties have been inspected based on frequency and substitution variation in the sample. The dielectric constant exhibits the increasing trend with the Co–Cr ratio. The enhancement in Ac conductivity was also found by increased substitution ions. Single semi-circles were examined in Nyquist plots, attributed to the contribution of the grain boundaries. Detailed magnetic parameters such as saturation magnetization, remanence, squareness ratio, coercivity, and magneto-crystalline anisotropy constant were measured. By the increase in Co–Cr substitution the increased of saturation magnetization ( Ms ) from 61.12 emu/g to 64.89 emu/g, the remanence ( Mr ) from 27.43 emu/g to 30.71 emu/g, and coercivity ( H c ) from 1654.56 Oe to 1863.54 Oe was found. Therefore, the synthesized SrBaCu 2 X-type hexagonal ferrites with the appropriate amount of Co–Cr substitution are suitable candidates for microwave devices and valuable in longitudinal recording media.
Shin, Hye-Rim,Islam, Rabia,Yoon, Won-Joon,Lee, Taegyung,Cho, Young-Dan,Bae, Han-sol,Kim, Bong-Su,Woo, Kyung-Mi,Baek, Jeong-Hwa,Ryoo, Hyun-Mo American Society for Biochemistry and Molecular Bi 2016 The Journal of biological chemistry Vol.291 No.11
<P>The canonical Wnt signaling pathway, in which -catenin nuclear localization is a crucial step, plays an important role in osteoblast differentiation. Pin1, a prolyl isomerase, is also known as a key enzyme in osteogenesis. However, the role of Pin1 in canonical Wnt signal-induced osteoblast differentiation is poorly understood. We found that Pin1 deficiency caused osteopenia and reduction of -catenin in bone lining cells. Similarly, Pin1 knockdown or treatment with Pin1 inhibitors strongly decreased the nuclear -catenin level, TOP flash activity, and expression of bone marker genes induced by canonical Wnt activation and vice versa in Pin1 overexpression. Pin1 interacts directly with and isomerizes -catenin in the nucleus. The isomerized -catenin could not bind to nuclear adenomatous polyposis coli, which drives -catenin out of the nucleus for proteasomal degradation, which consequently increases the retention of -catenin in the nucleus and might explain the decrease of -catenin ubiquitination. These results indicate that Pin1 could be a critical target to modulate -catenin-mediated osteogenesis.</P>
Bae, Han-Sol,Yoon, Won-Joon,Cho, Young-Dan,Islam, Rabia,Shin, Hye-Rim,Kim, Bong-Soo,Lim, Jin-Muk,Seo, Min-Seok,Cho, Seo-Ae,Choi, Kang-Young,Baek, Seung-Hak,Kim, Hong-Gee,Woo, Kyung-Mi,Baek, Jeong-Hwa Wiley (John WileySons) 2017 Journal of Bone and Mineral Research Vol. No.
<P>Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal disorder caused by mutations in RUNX2, coding a key transcription factor of early osteogenesis. CCD patients suffer from developmental defects in cranial bones. Despite numerous investigations and clinical approaches, no therapeutic strategy has been suggested to prevent CCD. Here, we show that fetal administration of Entinostat/MS-275, a class I histone deacetylase (HDAC)-specific inhibitor, partially prevents delayed closure of cranial sutures in Runx2(+/-) mice strain of C57BL/6J by two mechanisms: 1) posttranslational acetylation of Runx2 protein, which stabilized the protein and activated its transcriptional activity; and 2) epigenetic regulation of Runx2 and other bone marker genes. Moreover, we show that MS-275 stimulates osteoblast proliferation effectively both in vivo and in vitro, suggesting that delayed skeletal development in CCD is closely related to the decreased number of progenitor cells as well as the delayed osteogenic differentiation. These findings provide the potential benefits of the therapeutic strategy using MS-275 to prevent CCD. (c) 2017 American Society for Bone and Mineral Research.</P>
Yoon, Won-Joon,Cho, Young-Dan,Kim, Woo-Jin,Bae, Han-Sol,Islam, Rabia,Woo, Kyung-Mi,Baek, Jeong-Hwa,Bae, Suk-Chul,Ryoo, Hyun-Mo American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.13
<P>Fibroblast growth factor 2 (FGF2) signaling plays a pivotal role in bone growth/differentiation through the activation of osteogenic master transcription factor Runx2, which is mediated by the ERK/MAPK-dependent phosphorylation and the p300-dependent acetylation of Runx2. In this study, we found that Pin1-dependent isomerization of Runx2 is the critical step for FGF2-induced Runx2 transactivation function. We identified four serine or threonine residues in the C-terminal domain of Runx2 that are responsible for Pin1 binding and structural modification. Confocal imaging studies indicated that FGF2 treatment strongly stimulated the focal accumulation of Pin1 in the subnuclear area, which recruited Runx2. In addition, active forms of RNA polymerase-II also colocalized in the same subnuclear compartment. Dipentamethylene thiuram monosulfide, a Pin1 inhibitor, strongly attenuated their focal accumulation as well as Runx2 transactivation activity. The Pin1-mediated structural modification of Runx2 is an indispensable step connecting phosphorylation and acetylation and, consequently, transcriptional activation of Runx2 by FGF signaling. Thus, the modulation of Pin1 activity may be a target for the regulation of bone formation.</P>