Search

Your search keyword '"Bothmer, Anne H."' showing total 3 results
Start Over Author "Bothmer, Anne H."
3 results on '"Bothmer, Anne H."'

1. Germline NPM1 mutations lead to altered rRNA 2′-O-methylation and cause dyskeratosis congenita

Author

Nachmani, Daphna, Bothmer, Anne H., Grisendi, Silvia, Mele, Aldo, Bothmer, Dietmar, Lee, Jonathan D., Monteleone, Emanuele, Cheng, Ke, Zhang, Yang, Bester, Assaf C., Guzzetti, Alison, Mitchell, Caitlin A., Mendez, Lourdes M., Pozdnyakova, Olga, Sportoletti, Paolo, Martelli, Maria-Paola, Vulliamy, Tom J., Safra, Modi, Schwartz, Schraga, Luzzatto, Lucio, Bluteau, Olivier, Soulier, Jean, Darnell, Robert B., Falini, Brunangelo, Dokal, Inderjeet, Ito, Keisuke, Clohessy, John G., and Pandolfi, Pier Paolo

Published
2019
Full Text
View/download PDF

2. Domain structure during magnetization reversal of PtMn/CoFe exchange bias micropatterned lines.

Author

Liedke, Maciej Oskar, Potzger, Kay, Bothmer, Anne H., Fassbender, Juergen, Hillebrands, Burkard, Rickart, Marc, and Freitas, Paulo P.

Subjects
FERROMAGNETIC materials, MAGNETIC domain, MAGNETIZATION, ANISOTROPY, HYSTERESIS loop, ADIABATIC demagnetization
Abstract

The magnetic domain configuration and the magnetization reversal behavior of micropatterned exchange bias elements were investigated by means of magnetic force microscopy. In addition to the unidirectional anisotropy the shape anisotropy determines the overall magnetization reversal behavior. In order to modify the ratio between both anisotropy contributions, the exchange bias field strength was reduced by means of 5 keV He+ ion irradiation. For the as-prepared samples, a monodomain magnetization state with the magnetization direction aligned along the exchange bias field direction was found regardless of the element shape. After irradiation the unidirectional anisotropy contribution is reduced and hence the previously homogeneous magnetization state breaks up into small domains with 360° domain walls in between. The appearance of these domain walls, which was mainly observed for the descending branch of the magnetization reversal, is found to depend strongly on the structure width and orientation. [ABSTRACT FROM AUTHOR]

Published
2006
Full Text
View/download PDF

3. Germline NPM1mutations lead to altered rRNA 2'-O-methylation and cause dyskeratosis congenita

Author

Nachmani, Daphna, Bothmer, Anne H., Grisendi, Silvia, Mele, Aldo, Bothmer, Dietmar, Lee, Jonathan D., Monteleone, Emanuele, Cheng, Ke, Zhang, Yang, Bester, Assaf C., Guzzetti, Alison, Mitchell, Caitlin A., Mendez, Lourdes M., Pozdnyakova, Olga, Sportoletti, Paolo, Martelli, Maria-Paola, Vulliamy, Tom J., Safra, Modi, Schwartz, Schraga, Luzzatto, Lucio, Bluteau, Olivier, Soulier, Jean, Darnell, Robert B., Falini, Brunangelo, Dokal, Inderjeet, Ito, Keisuke, Clohessy, John G., and Pandolfi, Pier Paolo

Abstract

RNA modifications are emerging as key determinants of gene expression. However, compelling genetic demonstrations of their relevance to human disease are lacking. Here, we link ribosomal RNA 2'-O-methylation (2'-O-Me) to the etiology of dyskeratosis congenita. We identify nucleophosmin (NPM1) as an essential regulator of 2'-O-Me on rRNA by directly binding C/D box small nucleolar RNAs, thereby modulating translation. We demonstrate the importance of 2'-O-Me-regulated translation for cellular growth, differentiation and hematopoietic stem cell maintenance, and show that Npm1inactivation in adult hematopoietic stem cells results in bone marrow failure. We identify NPM1germline mutations in patients with dyskeratosis congenita presenting with bone marrow failure and demonstrate that they are deficient in small nucleolar RNA binding. Mice harboring a dyskeratosis congenita germline Npm1mutation recapitulate both hematological and nonhematological features of dyskeratosis congenita. Thus, our findings indicate that impaired 2'-O-Me can be etiological to human disease.

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results