1. Adelaide Research & Scholarship

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Results 1-10 of 13 (Search time: 0.004 seconds).
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PreviewIssue DateTitleAuthor(s)
1996bcl-w, a novel member of the bcl-2 family, promotes cell survivalGibson, L.; Holmgreen, S.; Huang, D.; Bernand, O.; Copeland, N.; Jenkins, N.; Sutherland, G.; Baker, E.; Adams, J.; Cory, S.
1996Expression of functional decay-accelerating factor (Cd55) in transgenic mice protects against human complement-mediated attack1van Denderen, B.; Pearse, M.; Katerelos, M.; Nottle, M.; Du, Z.T.; Aminian, A.; Adam, W.; Shenoy-Scaria, A.; Lublin, D.; Shinkel, T.; d'Apice, A.
1996Physiological Levels of Calcitonin Regulate the Mouse Osteoclast Calcitonin Receptor by a Protein Kinase A-Mediated MechanismWada, S.; Udagawa, N.; Nagata, N.; Martin, T.; Findlay, D.
1996Calcitonin Receptor Down-Regulation Relates to Calcitonin Resistance in Mature Mouse OsteoclastsWada, S.; Udagawa, N.; Nagata, N.; Martin, T.; Findlay, D.
1996Effects of Continuous Calcitonin Treatment on Osteoclast-like Cell Development and Clacitonin Receptor Expression in Mouse Bone Marrow CulturesIkegame, M.; Rakopoulos, M.; Martin, T.; Moseley, J.; Findlay, D.
2008PU.1 and NFATc1 mediate osteoclastic induction of the mouse β₃ integrin promoterCrotti, T.; Sharma, S.; Fleming, J.; Flannery, M.; Ostrowski, M.; Goldring, S.; McHugh, K.
2001A novel missense mutation in lysosomal sulfamidase is the basis of MPS III A in a spontaneous mouse mutantBhattacharyya, R.; Gliddon, B.; Beccari, T.; Hopwood, J.; Stanley, P.
2010Prox1 expression is negatively regulated by miR-181 in endothelial cellsKazenwadel, J.; Michael, M.; Harvey, N.
1999GPR56, a novel secretin-like human G-protein-coupled receptor geneLiu, M.; Parker, R.; Darby, K.; Eyre, H.; Copeland, N.; Crawford, J.; Gilbert, D.; Sutherland, G.; Jenkins, N.; Herzog, H.
1997Structural organization of the mouse and human GALR1 Galanin receptor genes (Galnr and GALNR) and chromosomal localization of the mouse geneJacoby, A.; Webb, G.; Liu, M.; Kofler, B.; Hort, Y.; Fathi, Z.; Bottema, C.; Shine, J.; Iismaa, T.

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