• Current Applied Physics
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• v.18 no.11
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• pp.1458-1464
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• 2018

An improved method for the preparation of g-$C_3N_4$ is described. Currently, heating (> $400^{\circ}C$) of urea is the common method used for preparing the g-$C_3N_4$. We have found that sonication of melamine in $HNO_3$ solution, followed by washing with anhydrous ethanol, not only reduce the crystallite size of g-$C_3N_4$ but also facilitate intriguing electronic structure and photoluminescence (PL) properties. Moreover, loading of metal (Pt and Ag) nanoparticles, by applying the borohydride reduction method, has resulted in multicolor-emission from g-$C_3N_4$. With the help of PL spectra and local electronic structure study, at C K-edge, N K-edge, Pt L-edge and Ag K-edge by X-ray absorption spectroscopy (XAS), a precise mechanism of tunable luminescence is established. The PL mechanism ascribes the amendments in the transitions, via defect and/or metal states assimilation, between the ${\pi}^*$ states of tris-triazine ring of g-$C_3N_4$ and lone pair states of nitride. It is evidenced that interaction between the C/N 2p and metal 4d/5d orbitals of Ag/Pt has manifested a net detraction in the ${\delta}^*{\rightarrow}LP$ transitions and enhancement in the ${\pi}^*{\rightarrow}LP$ and ${\pi}^*{\rightarrow}{\pi}$ transitions, leading to broad PL spectra from g-$C_3N_4$ organic semiconductor compound.

• BMB Reports
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• v.44 no.2
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• pp.123-128
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• 2011

Leucine-rich repeat containing protein 10 (LRRC10) is characterized as a cardiac-specific gene, suggesting a role in heart development and disease. A severe cardiac morphogenic defect in zebrafish morphants was recently reported but a contradictory result was found in mice, suggesting a more complicated molecular mechanism exists during mouse embryonic development. To elucidate how LRRC10 is regulated, we analyzed the 5'enhancer region approximately 3 kilo bases (kb) upstream of the Lrrc10 start site using luciferase reporter gene assays. Our characterization of the Lrrc10 promoter indicates it possesses complicated cis-and trans-acting elements. We show that GATA4 and MEF2C could both increase transcriptional activity of Lrrc10 promoter individually but that they do not act synergistically, suggesting that there exists a more complex regulation pattern. Surprisingly, knockout of Gata4 and Mef2c binding sites in the 5’enhancer region (-2,894/-2,889) didn't change the transcriptional activity of the Lrrc10 promoter and the likely GATA4 binding site identified was located in a region only 100 base pair (bp) upstream of the promoter. Our data provides insight into the molecular regulation of Lrrc10 expression, which probably also contributes to its tissue-specific expression.