http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Ottmann, Oliver (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
-
Involvement of 14-3-3 in tubulin instability and impaired axon development is mediated by Tau
Joo, Yuyoung,Schumacher, Benjamin,Landrieu, Isabelle,Bartel, Maria,Smet-Nocca, Caroline,Jang, Ahram,Choi, Hee Soon,Jeon, Noo Li,Chang, Keun-A,Kim, Hye-Sun,Ottmann, Christian,Suh, Yoo-Hun The Federation of American Societies for Experimen 2015 The FASEB Journal Vol.29 No.10
<P>14-3-3 proteins act as adapters that exert their function by interacting with their various protein partners. 14-3-3 proteins have been implicated in a variety of human diseases including neurodegenerative diseases. 14-3-3 proteins have recently been reported to be abundant in the neurofibrillary tangles (NFTs) observed inside the neurons of brains affected by Alzheimer’s disease (AD). These NFTs are mainly constituted of phosphorylated Tau protein, a microtubule-associated protein known to bind 14-3-3. Despite this indication of 14-3-3 protein involvement in the AD pathogenesis, the role of 14-3-3 in the Tauopathy remains to be clarified. In the present study, we shed light on the role of 14-3-3 proteins in the molecular pathways leading to Tauopathies. Overexpression of the 14-3-3σ isoform resulted in a disruption of the tubulin cytoskeleton and prevented neuritic outgrowth in neurons. NMR studies validated the phosphorylated residues pSer214 and pSer324 in Tau as the 2 primary sites for 14-3-3 binding, with the crystal structure of 14-3-3σ in complex with Tau-pSer214 and Tau-pSer324 revealing the molecular details of the interaction. These data suggest a rationale for a possible pharmacologic intervention of the Tau/14-3-3 interaction.—Joo, Y., Schumacher, B., Landrieu, I., Bartel, M., Smet-Nocca, C., Jang, A., Choi, H. S., Jeon, N. L., Chang, K.-A., Kim, H.-S., Ottmann, C., Suh, Y.-H. Involvement of 14-3-3 in tubulin instability and impaired axon development is mediated by Tau.</P>
-
Cortes, Jorge,Rousselot, Philippe,Kim, Dong-Wook,Ritchie, Ellen,Hamerschlak, Nelson,Coutre, Steven,Hochhaus, Andreas,Guilhot, Francois,Saglio, Giuseppe,Apperley, Jane,Ottmann, Oliver,Shah, Neil,Erben, American Society of Hematology 2007 Blood Vol.109 No.8
<B>Abstract</B><P>The prognosis for patients with chronic myeloid leukemia (CML) in myeloid blast crisis (MBC) or lymphoid blast crisis (LBC) remains poor. Although imatinib can induce responses in a subset of these patients, resistance to the drug develops rapidly. Dasatinib is a novel, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases. After promising phase 1 results, we report the results of phase 2 clinical trials of dasatinib in patients with imatinib-resistant or -intolerant blast crisis CML (MBC, n = 74; LBC, n = 42). At the 8-month follow-up, dasatinib induced major hematologic responses (MaHRs) in 34% and 31% of MBC- and LBC-CML patients and major cytogenetic responses (MCyRs) in 31% and 50% of these patients, respectively. Most (86%) of these MCyRs were complete cytogenetic responses (CCyRs). Responses were rapid and durable: 88% and 46%, respectively, of MBC- and LBC-CML patients achieving MaHR had not experienced disease progression at the 8-month follow-up. Response rates were similar in patients with and without BCR-ABL mutations known to confer resistance to imatinib. Dasatinib was well tolerated. Nonhematologic adverse events were mild to moderate. Cytopenias were common and could be managed by dose modification. Dasatinib is highly active and produces hematologic and cytogenetic responses in a significant number of patients with imatinib-resistant or -intolerant MBC- and LBC-CML. These trials were registered at www.clinicaltrials.gov as #CA180006 and #CA180015.</P>
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
