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19. Internal cleavage and synergy with twisted gastrulation enhance BMP inhibition by BMPER

Author

Lockhart-Cairns, M.P., Lim, K.T.W., Zuk, A., Godwin, A.R.F., Cain, S.A., Sengle, G., and Baldock, C.

Abstract

Bone morphogenetic proteins (BMPs) are essential signalling molecules involved in developmental and pathological processes and are regulated in the matrix by secreted glycoproteins. One such regulator is BMP-binding endothelial cell precursor-derived regulator (BMPER) which can both inhibit and enhance BMP signalling in a context and concentration-dependent manner. Twisted gastrulation (Tsg) can also promote or ablate BMP activity but it is unclear whether Tsg and BMPER directly interact and thereby exert a synergistic function on BMP signalling. Here, we show that human BMPER binds to Tsg through the N-terminal BMP-binding region which alone more potently inhibits BMP-4 signalling than full-length BMPER. Additionally, BMPER and Tsg cooperatively inhibit BMP-4 signalling suggesting a synergistic function to dampen BMP activity. Furthermore, full-length BMPER is targeted to the plasma membrane via binding of its C-terminal region to cell surface heparan sulphate proteoglycans but the active cleavage fragment is diffusible. Small-angle X-ray scattering and electron microscopy show that BMPER has an elongated conformation allowing the N-terminal BMP-binding and C-terminal cell-interactive regions to be spatially separated. To gain insight into the regulation of BMPER bioavailability by internal cleavage, a disease-causing BMPER point mutation, P370L, previously identified in the acid-catalysed cleavage site, was introduced. The mutated protein was secreted but the mutation prevented intracellular cleavage resulting in a lack of bioactive cleavage fragment. Furthermore, mutant BMPER was extracellularly cleaved at a downstream site presumably becoming available due to the mutation. This susceptibility to extracellular proteases and loss of bioactive N-terminal cleavage fragment may result in loss of BMPER function in disease.

Published
2019

20. Absolute Activity Determination of [sup.198]Au solid source using 4[pi][beta]--[gamma] coincidence counting corrected by Monte-Carlo calculation

Author

Mo, L., Wu, H.Y., and Baldock, C.

Subjects
Nuclear reactors -- Analysis, Nuclear reactors -- Models, Nuclear reactors -- Design and construction, Monte Carlo method -- Usage, Compton effect -- Usage, Business, Electronics, Electronics and electrical industries
Abstract

For the commissioning process of the OPAL nuclear reactor of the Australian Nuclear Science and Technology Organization (ANSTO), the thermal neutron flux is measured through the activity measurement of an activated Au wire, Au-A1 (0.112 % of Au) alloy wire and Au foil. The absolute activities of [sup.198]Au in the form of Au wire, Al-Au wire and Au foil were determined using the conventional 4[pi][beta]--[gamma] coincidence-counting method. Monte Carlo simulation technique was employed to simulate the complicated absorption and attenuation processes of electrons and gamma photon interactions with the surrounding materials. The Monte Carlo calculated probabilities of escape beta particles, internal conversion electrons and photon-interaction generated photoelectrons and Compton electrons were used to determine the correction term of the coincidence equation. The corrections for the Au wire (length: 8.000 mm, radius: 0.064 mm), Al-Au wire (length: 7.690 mm, radius: 0.255 mm) and Au foil (thickness: 0.025 mm, radius: 3.000 mm) were found to be 5.2% [+ or -] 0.1%,2.6% [+ or -] 0.1% and 4.2% [+ or -] 0.2% respectively. The study demonstrates that the Monte Carlo calculation for the correction term of the coincidence equation can be applied to the absolute activity determination of radionuclides with well-defined source geometries with an uncertainty of better than 1%. Index Terms--[sup.198]Au, 4[pi][beta]--[gamma] coincidence-counting, activity, Monte Carlo simulation.

Published
2007

48. The molecular genetics of Marfan syndrome and related disorders

Author

Robinson, P N, Arteaga-Solis, E, Baldock, C, Collod-Béroud, G, Booms, P, De Paepe, A, Dietz, H C, Guo, G, Handford, P A, Judge, D P, Kielty, C M, Loeys, B, Milewicz, D M, Ney, A, Ramirez, F, Reinhardt, D P, Tiedemann, K, Whiteman, P, and Godfrey, M

Published
2006

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