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RISS 인기검색어
- 검색키워드
- 저자 : Paola Ferri (검색결과 2 건)
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Ghidinelli, Monica,Poitelon, Yannick,Shin, Yoon Kyoung,Ameroso, Dominique,Williamson, Courtney,Ferri, Cinzia,Pellegatta, Marta,Espino, Kevin,Mogha, Amit,Monk, Kelly,Podini, Paola,Taveggia, Carla,Nave, Public Library of Science 2017 PLoS biology Vol.15 No.6
<▼1><P>Myelin is required for proper nervous system function. Schwann cells in developing nerves depend on extrinsic signals from the axon and from the extracellular matrix to first sort and ensheathe a single axon and then myelinate it. Neuregulin 1 type III (Nrg1III) and laminin α2β1γ1 (Lm211) are the key axonal and matrix signals, respectively, but how their signaling is integrated and if each molecule controls both axonal sorting and myelination is unclear. Here, we use a series of epistasis experiments to show that Lm211 modulates neuregulin signaling to ensure the correct timing and amount of myelination. Lm211 can inhibit Nrg1III by limiting protein kinase A (PKA) activation, which is required to initiate myelination. We provide evidence that excessive PKA activation amplifies promyelinating signals downstream of neuregulin, including direct activation of the neuregulin receptor ErbB2 and its effector Grb2-Associated Binder-1 (Gab1), thereby elevating the expression of the key transcription factors Oct6 and early growth response protein 2 (Egr2). The inhibitory effect of Lm211 is seen only in fibers of small caliber. These data may explain why hereditary neuropathies associated with decreased laminin function are characterized by focally thick and redundant myelin.</P></▼1><▼2><P><B>Author summary</B></P><P>Myelin is formed by the wrapping of glial cell membranes around axons and is required for the fast conduction of nerve impulses and to support axons. In the peripheral nervous system, myelin is produced by Schwann cells. Peripheral myelin defects cause debilitating diseases, whose molecular pathogeneses are only partially understood. Here, we reveal for the first time how 2 crucial extracellular modulators of myelin formation, neuregulin 1 type III (Nrg1III) and laminin α2β1γ1 (Lm211), work together in the peripheral nervous system. Although Lm211 was believed to promote myelination, we show that it can also inhibit myelin formation by suppressing the activity of Nrg1III, limiting the activation of its downstream signaling cascade. These results help to explain why certain inherited neuropathies are characterized by hypermyelination and redundant myelin sheaths.</P></▼2>
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Raffaella Marcheselli,Luigi Marcheselli,Laura Cortesi,Alessia Bari,Claudia Cirilli,Samantha Pozzi,Paola Ferri,Martina Napolitano,Massimo Federico,Stefano Sacchi 한국유방암학회 2015 Journal of breast cancer Vol.18 No.4
Purpose: Evolving therapies have improved the prognoses of patients with breast cancer; and currently, the number of longterm survivors is continuously increasing. However, these patients are at increased risk of developing a second cancer. Thus, late side effects are becoming an important issue. In this study, we aimed to investigate whether patient and tumor characteristics, and treatment type correlate with secondary tumor risk. Methods: This case-control study included 305 patients with a diagnosed second malignancy after almost 6 months after the diagnosis of primary breast cancer and 1,525 controls (ratio 1:5 of cases to controls) from a population-based cohort of 6,325 women. The control patients were randomly selected from the cohort and matched to the cases according to age at diagnosis, calendar period of diagnosis, disease stage, and time of followup. Results: BRCA1 or BRCA2 mutation, human epidermal growth factor receptor 2 (HER2)+ status, chemotherapy, and radiotherapy were related to increased risk of developing a second cancer, whereas hormonotherapy showed a protective effect. Chemotherapy, radiotherapy, and estrogenic receptor level <10% increased the risk of controlateral breast cancer. HER2+ status increased the risk of digestive system and thyroid tumors, while BRCA1 or BRCA2 mutation increased the risk of cancer in the genital system. Conclusion: Breast cancer survivors are exposed to an excess of risk of developing a second primary cancer. The development of excess of malignancies may be related either to patient and tumor characteristics, such as BRCA1 or BRCA2 mutation and HER2+ status, or to treatments factors.
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