994 resultados para KOI-55 planets


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The discovery of over a dozen low-mass companions to nearby stars has intensified scientific and public interest in a longer term search for habitable planets like our own. However, the nature of the detected companions, and in particular whether they resemble Jupiter in properties and origin, remains undetermined.

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Until the mid-1990s a person could not point to any celestial object and say with assurance that “here is a brown dwarf.” Now dozens are known, and the study of brown dwarfs has come of age, touching upon major issues in astrophysics, including the nature of dark matter, the properties of substellar objects, and the origin of binary stars and planetary systems.

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The first known extrasolar planet in orbit around a Sun-like star was discovered in 1995. This object, as well as over two dozen subsequently detected extrasolar planets, were all identified by observing periodic variations of the Doppler shift of light emitted by the stars to which they are bound. All of these extrasolar planets are more massive than Saturn is, and most are more massive than Jupiter. All orbit closer to their stars than do the giant planets in our Solar System, and most of those that do not orbit closer to their star than Mercury is to the Sun travel on highly elliptical paths. Prevailing theories of star and planet formation, which are based on observations of the Solar System and of young stars and their environments, predict that planets should form in orbit about most single stars. However, these models require some modifications to explain the properties of the observed extrasolar planetary systems.

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The role of the mitogen-activated protein kinase kinase (MKK)/extracellular-activated protein kinase (ERK) pathway in mitotic Golgi disassembly is controversial, in part because Golgi-localized targets have not been identified. We observed that Golgi reassembly stacking protein 55 (GRASP55) was phosphorylated in mitotic cells and extracts, generating a mitosis-specific phospho-epitope recognized by the MPM2 mAb. This phosphorylation was prevented by mutation of ERK consensus sites in GRASP55. GRASP55 mitotic phosphorylation was significantly reduced, both in vitro and in vivo, by treatment with U0126, a potent and specific inhibitor of MKK and thus ERK activation. Furthermore, ERK2 directly phosphorylated GRASP55 on the same residues that generated the MPM2 phospho-epitope. These results are the first demonstration of GRASP55 mitotic phosphorylation and indicate that the MKK/ERK pathway directly phosphorylates the Golgi during mitosis.