veoexrmpzt
Dołączył: 21 Lut 2011
Posty: 371
Przeczytał: 0 tematów
Ostrzeżeń: 0/5
Skąd: England
|
 Wysłany: Pon 7:27, 14 Mar 2011 Temat postu: tory burch lwn tmd oenl rpq |
 |
|
c-Jun regulates cell microtubule inhibitors on the sensitivity of vinblastine
High concentration of vinblastine (30mnol · L a ') sensitive to DNA re-replication was no significant mitotic block and apoptosis. MTr assay type c-Jun over-expression cell resistance to vinblastine. Vinblastine on c-jun √ J + cells Ic50 a greater than l0mnol · L, while on the c. jun + / cells in the IC5o for the 0.8nmol · L '. Can be seen, c-Jun over-expression-based cell resistance to vinblastine compared with wild-type cells of l2 times. These results show that, c-Jun in vinblastine sensitivity of cells to mitotic arrest and regulation of cell death play an important role in changing the c. Jun's expression or function will help to overcome drug resistance of tumor cells. (Abstract Min Wei Shao Yin School) 019 body hidden HIV. 1 Clear [English] / BartonS / / NatureRevDrugDiscov. A 2005,4 (11). A 886 highly active antiretroviral therapy (HAART), based on targeting various stages of the virus life cycle combination of drugs can effectively suppress viral replication, but can not completely eradicate the virus. CIMT cells as a dormant period before the virus replication persists after treatment is stopped,[link widoczny dla zalogowanych], the virus began a new round of replication. Use of IL. 2 (IL-2) activation of latent infected cells, although their number can be greatly reduced, but when treatment stopped, the virus database has been filled. In the meantime, I 【Canton 2 T cells induced extensive activation will increase the side effects of treatment. Lehrman and other reports in the journal Lancet,[link widoczny dla zalogowanych], a strategy with a well-known anticonvulsant valproic acid, cell targeting latent infection with HIV-1 enzyme is closely related to persistent infection, selective induction of recessive genes before the virus expression, remove dormant HIV-1 cells, but not non-specific activation of T cells. On one of the four were HIV 1 infected adult volunteers conducted a study with valproic acid treatment and strengthen the HARRT 16 ~ l8 weeks after treatment,[link widoczny dla zalogowanych], three patients significantly reduced the number of infected CD4 cells (mean reduction of 75 %), indicating that the drug targeting HIV. A potential molecular requirements is feasible to eliminate the virus reservoir strategies. However, more research needs to address this strategy in the many problems, such as there are two patients in the low-level viremia, are not very clear that this is originated from resting cells or cells because the drugs did not arrive Copy all the small room. (Zhang Di He Junlin Abstract) 020-specific enzyme to promote cleavage of amyloid precursor protein into l1. Amyloid protein [English] / SeniorK / / DrugDiscovroar. A 2005,11 (10). A 1408J3 a deposition of amyloid is Alzheimer's disease (AD) pathogenesis of origin factors, the formation of senile plaques is the most basic pathological changes. Therefore,[link widoczny dla zalogowanych], the targeting. AD amyloid measures are the most promising treatment for AD is also a research focus. Amyloid precursor protein (APP) in the 7 secretase-mediated cleavage into the mouth. Amyloid protein, such as a secreted enzyme can inhibit the activity of _y, you can help the treatment of AD patients. However,[link widoczny dla zalogowanych], 7. Secretase is a large complex molecules with important physiological functions, can be cracked at least 30 kinds of working-type membrane protein, such as the complete inhibition of enzyme activity, it will inhibit the effect of other substrates, resulting in adverse reactions, is clearly not wise. Researchers recently found to promote APP cleavage, a new B-amyloid protein into the mechanism. . A fragment of the enzyme secreted nlcrastin and J3. Directly related to the formation of amyloid protein. nicrastin has two functional areas: outside the functional area, identify the type I transmembrane protein produced after cleavage of functional areas outside of the short amino-terminal residues; transmembrane transport area, in the assembly during the formation of secreted enzyme complex work. APl】 hydrolysis of extracellular amino-terminal and the emergence of new functional areas outside nicrastin combination, then, APP as substrate in the formation of 7. Secretase complex. nicrastin 7. Secretase complex role and how substrate recognition is still unclear. In vitro, nicrastin mutations outside the functional areas or functional areas outside after the reduction of APP cleavage can be specified and the secretion of enzymes with a combination of 7, suggesting that the mechanism based on the design or the first block or filter specific cleavage of APP N-terminal compound or antibody derivatives, cleavage of APP is to identify a lead compound targeting a good strategy, but there is no doubt that this is a complex task. (Abstract WU Xiang Liu Nian root of school)
Post został pochwalony 0 razy
|
|
