Genetic interactions between the Drosophila tumor suppressor gene ept and the stat92E transcription factor.

In order to validate the importance of the methylation profile in the regulation of gene expression, the transcription of tumor suppressor genes was performed in two

the genetic framework; Genetic and molecular analysis of programmed cell death in Drosophila; The caspases: consequential cleavage; Regulation of apoptosis by the bcl-2 family

the genetic framework; Genetic and molecular analysis of programmed cell death in Drosophila; The caspases: consequential cleavage; Regulation of apoptosis by the bcl-2 family

In the process of apoptosis, cell death is induced by the activation of a genetically and biochemically regulated cell death system, involving the participation of

Nuclear transfer, cell fusion and transcription factor (TF)-transduction have provided means to induce in vitro reprogramming of defined and specialized cells either into

Tumor-infiltrating macrophages induce apoptosis in activated CD8(+) T cells by a mecha- nism requiring cell contact and mediated by both the cell- associated form of TNF and

Studies in B16-F10 melanoma and MCF-7 breast cancer cell lines indicated that PHOS-S can induce tumor cell apoptosis regardless of blocking of the Bcl-2 protein.. Loss of

Objectives: To evaluate the association between the genetic polymorphism of the tumor necrosis factor-alpha (TNF- α ) gene and the development of sepsis and septic shock in