نتایج جستجو برای: melanoma inhibitor of apoptosis ml
تعداد نتایج: 21218902 فیلتر نتایج به سال:
The release of molecules from injured tissue leads to produce inflammatory response that can result in apoptosis and cell death. Preconditioning (PC) can decrease the inflammatory response, increase neuroprotective mechanism on different levels. So, we investigated the role of PC as a suitable preventative approach in neurodegenerative disease in and inflammatory oncogenic factors in PC12 cells...
In previous studies we have shown that the sensitivity of melanoma cell lines to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis was determined largely by the level of expression of death receptor TRAIL receptor 2 on the cells. However, approximately one-third of melanoma cell lines were resistant to TRAIL, despite expression of high levels of TRAIL receptor 2....
In previous studies we have shown that the sensitivity of melanoma cell lines to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)induced apoptosis was determined largely by the level of expression of death receptor TRAIL receptor 2 on the cells. However, approximately one-third of melanoma cell lines were resistant to TRAIL, despite expression of high levels of TRAIL receptor 2. ...
Staurosporine has long been used in vitro as an initiator of apoptosis in many different cell types, but the mechanism involved remains poorly understood. In the present study, we have examined the apoptosis-inducing potential of staurosporine in cultured melanoma cell lines and dissected the staurosporine-induced apoptotic signaling pathway. We report that although staurosporine activated Bax ...
Homologue of Slimb (HOS)/beta-transducin repeats containing proteins up-regulate nuclear factor kappaB activity by targeting its inhibitor (IkappaB) for ubiquitination and subsequent degradation. We investigated whether inhibition of HOS function may modulate apoptosis in human melanoma cells. Forced expression of the dominant negative HOSdeltaF construct inhibited IkappaB degradation and led t...
Homologue of Slimb (HOS)/b-transducin repeats containing proteins up-regulate nuclear factor kB activity by targeting its inhibitor (IkB) for ubiquitination and subsequent degradation. We investigated whether inhibition of HOS function may modulate apoptosis in human melanoma cells. Forced expression of the dominant negative HOS construct inhibited IkB degradation and led to sensitization of me...
Intrinsic cross-resistance to inhibition of different signaling pathways may hamper development of combinatorial treatments in melanoma, but the relative frequency of this phenotype and the strategies to overcome this hurdle remain poorly understood. Among 49 BRAF-mutant melanoma cell lines from patients not previously treated with target therapy, 21 (42.9%) showed strong primary resistance (IC...
Abstract Staphylococcus aureus is the most common cause of wound infections. Infected wounds increase severity and have a slower rate healing. Moreover, emergence multiple‐drug resistant bacteria such as methicillin‐resistant S. (MRSA) limited treatment options. This study was therefore aimed to evaluate antibacterial activity against pathogen wound‐healing properties green synthesized ZnO nano...
We found previously that restriction of tyrosine (Tyr) and phenylalanine (Phe) inhibited growth and metastasis of B16BL6 murine melanoma and arrested these cells in the G0-G1 phase of the cell cycle. Here, we report that deprivation of these two amino acids in vitro induces apoptosis in B16BL6 and in human A375 melanoma cells but not in nontransformed, neonatal murine epidermal cells or human i...
BACKGROUND Several inhibitor of apoptosis proteins (IAPs) are cleaved during apoptosis. Studies of the melanoma-associated IAP (ML-IAP) Livin, using recombinant molecules, have implicated both caspases 3/7 and the serine protease Omi/HtrA2 in its proteolytic cleavage. OBJECTIVE To characterize the apoptotic cleavage of Livin in melanocytic cells, and evaluate the role of known proteases. ME...
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