The complexity of p53 modulation: emerging patterns from divergent signals

Article Abstract:

Functional inactivation of p53, a cellular protein critical in malignant disease and other situations, a tumor suppressor gene, makes a mammal cell susceptible to environmental hazards and oncogenic stimuli that promote malignant progression and growth deregulation. Inactivation can be achieved by protein degradation, viral oncogene binding, or gene mutation/deletion. The protein protects a cell against neoplastic transformation. A number of mechanisms have evolved to regulate activity of p53, not surprising, since it is a very important to the cell, responds to stress, such as UV radiation, decreased rNTP, and hypoxia, and to DNA damaging agents.

Analysis, DNA damage, Cancer, Genetic regulation, Cancer genetics, Ubiquitin

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Defective potassium currents in ataxia telangiectasia fibroblasts

Article Abstract:

Defective potassium ion channel activity has been implicated in ataxia telangiectasia (AT) cells. In comparison with control fibroblasts, AT fibroblasts have less ability to depolarize in the presence of increasing concentrations of extracellular K+. A lack of outward rectifier K+ currents in AT fibroblasts is indicated by electrophysiological measurements. Transfection with full-length ATM cDNA corrects the K+ current abnormalities in AT fibroblasts.

Research, Physiological aspects, Potassium channels, Ataxia telangiectasia, Fibroblasts

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CDK inhibitors p18INK4c and p27Kip1 mediate two separate pathways to collaboratively suppress pituitary tumorigenesis

Article Abstract:

CIP/KIP and INK4 are distinct families of cyclin-dependent kinase (CDK) inhibitors. They are implicated in mediation of a wide range of cell growth control signals. Mice that lack p18INK4c develop widespread organomegaly and gigantism. CDK inhibitors p18INK4c and p27Kip1 mediate two pathways to suppress pituitary tumorigenesis in collaboration.

Growth regulators, Protein kinases, Tumors, Pituitary gland tumors, Pituitary tumors

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