Dutta, D.
Sharma, S.K.
Maheshwari, P.
Sudarshan, K.
Pujari, P.K.
Behavior of solids and liquids confined in nano domain has great relevance in fundamental research as well as applications in nanotribology, nanofabrication, membrane separation, interfacial adhesion and lubrication. In this work, we have studied phase transition behavior of different organic liquids confined in nanopores of ZSM-5 zeolite and silica using temperature dependent positron annihilation Doppler broadening and lifetime spectroscopy. It is observed that the freezing and melting properties of liquids confined in nanopores are different from their bulk behavior. The liquid molecules (isopropanol) that feel more attractive interaction with the pore wall show an increase in freezing temperature. Similarly, a liquid like benzene which is weakly attractive with pore wall as compared to its solid phase show a decrease in its freezing point under confinement. The confining pore diameters are in the range of 10-60 Aring. It was observed that the shift in phase transition temperature does not follow classical Gibbs-Thomson relation.
Berger, M.
Schwanda, C.
Suzuki, K.
Adachi, I.
Ahn, J. K.
Aihara, H.
Al Said, S.
Asner, D. M.
Atmacan, H.
Aulchenko, V.
Aushev, T.
Ayad, R.
Babu, V.
Badhrees, I.
Bakich, A. M.
Bansal, V.
Behera, P.
Bhardwaj, V.
Bhuyan, B.
Biswal, J.
Bonvicini, G.
Bozek, A.
Bračko, M.
Browder, T. E.
Červenkov, D.
Chen, A.
Cheon, B. G.
Chilikin, K.
Cho, K.
Choi, Y.
Cinabro, D.
Czank, T.
Dash, N.
Di Carlo, S.
Doležal, Z.
Dutta, D.
Eidelman, S.
Epifanov, D.
Fast, J. E.
Ferber, T.
Fulsom, B. G.
Garg, R.
Gaur, V.
Gabyshev, N.
Garmash, A.
Gelb, M.
Giri, A.
Goldenzweig, P.
Grzymkowska, O.
Guan, Y.
Guido, E.
Haba, J.
Hara, T.
Hayasaka, K.
Hayashii, H.
Hedges, M. T.
Hou, W.-S.
Iijima, T.
Inami, K.
Inguglia, G.
Ishikawa, A.
Itoh, R.
Iwasaki, M.
Iwasaki, Y.
Jacobs, W. W.
Jaegle, I.
Jia, S.
Jin, Y.
Joo, K. K.
Julius, T.
Kaliyar, A. B.
Kang, K. H.
Karyan, G.
Kawasaki, T.
Kichimi, H.
Kiesling, C.
Kim, D. Y.
Kim, H. J.
Kim, J. B.
Kim, K. T.
Kim, S. H.
Kinoshita, K.
Kodyš, P.
Korpar, S.
Kotchetkov, D.
Križan, P.
Kroeger, R.
Krokovny, P.
Kuhr, T.
Kulasiri, R.
Kuzmin, A.
Kwon, Y.-J.
Lange, J. S.
Lee, I. S.
Lee, S. C.
Li, L. K.
Li, Y.
Li Gioi, L.
Libby, J.
Liventsev, D.
Lubej, M.
Luo, T.
Masuda, M.
Matsuda, T.
Matvienko, D.
Merola, M.
Miyabayashi, K.
Miyata, H.
Mizuk, R.
Mohanty, G. B.
Moon, H. K.
Mori, T.
Mussa, R.
Nakano, T.
Nakao, M.
Nanut, T.
Nath, K. J.
Natkaniec, Z.
Nayak, M.
Niiyama, M.
Nisar, N. K.
Nishida, S.
Okuno, S.
Ono, H.
Onuki, Y.
Pakhlov, P.
Pakhlova, G.
Pal, B.
Park, H.
Paul, S.
Pavelkin, I.
Pedlar, T. K.
Pestotnik, R.
Piilonen, L. E.
Popov, V.
Ritter, M.
Rostomyan, A.
Russo, G.
Sakai, Y.
Salehi, M.
Sandilya, S.
Santelj, L.
Sanuki, T.
Savinov, V.
Schneider, O.
Schnell, G.
Schwartz, A. J.
Seino, Y.
Senyo, K.
Seon, O.
Sevior, M. E.
Shebalin, V.
Shen, C. P.
Shibata, T.-A.
Shimizu, N.
Shiu, J.-G.
Shwartz, B.
Simon, F.
Sokolov, A.
Sol
Dutta, D.
Xiong, F.
Zhu, L. Y.
Arrington, J.
Averett, T.
Beise, E.
Calarco, J.
Chang, T.
Chen, J. P.
Chudakov, E.
Coman, M.
Clasie, B.
Crawford, C.
Dieterich, S.
Dohrmann, F.
Fissum, K.
Frullani, S.
Gao, H.
Gilman, R.
Glashausser, C.
Gomez, J.
Hafidi, K.
Hansen, J.-O.
Higinbotham, D. W.
Holt, R. J.
de Jager, C. W.
Jiang, X.
Kinney, E.
Kramer, K.
Kumbartzki, G.
LeRose, J.
Liyanage, N.
Mack, D.
Markowitz, P.
McCormick, K.
Meziani, Z.-E.
Michaels, R.
Mitchell, J.
Nanda, S.
Potterveld, D.
Ransome, R.
Reimer, P. E.
Reitz, B.
Saha, A.
Schulte, E. C.
Seely, J.
?irca, S.
Strauch, S.
Sulkosky, V.
Vlahovic, B.
Weinstein, L. B.
Wijesooriya, K.
Williamson, C. F.
Wojtsekhowski, B.
Xiang, H.
Xu, W.
Zeng, J.
Zheng, X.
Dutta, D.
van Westrum, D.
Abbott, D.
Ahmidouch, A.
Amatuni, Ts. A.
Armstrong, C.
Arrington, J.
Assamagan, K. A.
Bailey, K.
Baker, O. K.
Barrow, S.
Beard, K.
Beatty, D.
Beedoe, S.
Beise, E.
Belz, E.
Bochna, C.
Bosted, P. E.
Breuer, H.
Bruins, E. E. W.
Carlini, R.
Cha, J.
Chant, N.
Chrien, R. E.
Cothran, C.
Cummings, W. J.
Danagoulian, S.
Day, D.
DeSchepper, D.
Ducret, J.-E.
Duncan, F.
Dunne, J.
Eden, T.
Ent, R.
Fortune, H. T.
Frolov, V.
Geesaman, D. F.
Gao, H.
Gilman, R.
Guèye, P.
Hansen, J. O.
Hinton, W.
Holt, R. J.
Jackson, C.
Jackson, H. E.
Jones, C.
Kaufman, S.
Kelly, J. J.
Keppel, C.
Khandaker, M.
Kim, W.
Kinney, E.
Klein, A.
Koltenuk, D.
Kramer, L.
Lorenzon, W.
McFarlane, K.
Mack, D. J.
Madey, R.
Markowitz, P.
Martin, J.
Mateos, A.
Meekins, D.
Meier, E.
Miller, M. A.
Milner, R.
Mitchell, J.
Mohring, R.
Mkrtchyan, H.
Nathan, A. M.
Niculescu, G.
Niculescu, I.
O’Neill, T. G.
Potterveld, D.
Price, J. W.
Reinhold, J.
Salgado, C.
Schiffer, J. P.
Segel, R. E.
Stoler, P.
Suleiman, R.
Sawafta, R.
Sutter, R. J.
Tadevosyan, V.
Tang, L.
Terburg, B.
Welch, T. P.
Williamson, C.
Wood, S.
Yan, C.
Yang, Jae-Choon
Yu, J.
Zeidman, B.
Zhao, W.
Zihlmann, B.
Dutta, D.
Ray, S.
Home, P.
Saha, B.
Wang, S.
Sheibani, N.
Tawfik, O.
Cheng, N.
Paul, S.
Angiogenesis is critically dependent on endothelial cell-specific transcriptional mechanisms. However, the molecular processes that regulate chromatin domains and thereby dictate transcription of key endothelial genes are poorly understood. Here, we report that, in endothelial cells, angiogenic signal-mediated transcriptional induction of Vegfr1 (vascular endothelial growth factor receptor 1) is dependent on the histone chaperone, HIRA (histone cell cycle regulation-defective homolog A). Our molecular analyses revealed that, in response to angiogenic signals, HIRA is induced in endothelial cells and mediates incorporation of lysine 56 acetylated histone H3.3 (H3acK56) at the chromatin domain of Vegfr1. HIRA-mediated incorporation of H3acK56 is a general mechanism associated with transcriptional induction of several angiogenic genes in endothelial cells. Depletion of HIRA inhibits H3acK56 incorporation and transcriptional induction of Vegfr1 and other angiogenic genes. Our functional analyses revealed that depletion of HIRA abrogates endothelial network formation on Matrigel and inhibits angiogenesis in an in vivo Matrigel plug assay. Furthermore, analysis in a laser-induced choroidal neovascularization model showed that depletion of HIRA significantly inhibits neovascularization. Our results for the first time decipher a histone chaperone (HIRA)-dependent molecular mechanism in endothelial gene regulation and indicate that histone chaperones could be new targets for angiogenesis therapy.