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Programmed cell death (PCD) has become a topic of widespread interest and experimentation over the past decade. Written by experts in the field,Apoptosis: Pharmacological Implications and Therapeutic Opportunities concentrates on presenting an overview of PCD pathways as they are currently understood, and strives to identify important unanswered questions as well as other therapeutic possibilities suggested by recent biochemical discoveries. Understanding the biochemical pathways that participate in the cell death process has become an important goal in developmental biology, neurobiology, cardiology, and infectious disease research. The control of apoptosis has also become a major area of investigation in the field of cancer biology.Apoptosis: Pharmacological Implications and Therapeutic Opportunities contains an overview for those with a general interest in apoptosis, and provides discussions of sufficient depth to be useful for specialists in the field.
1. Communication, awareness and access to information: Given the complexity of the field and the fact that data pertaining to each particular aspects of p53 biology or deregulation are scattered in many different publications, it is extremely difficult to access the full scale of relevant information of any specific p53-related topic. Review arcticles, despite their fundamental role in disseminating knowledge, usually focus only on general mechanisms and do not discuss in detail the many variations that can occur with respect to cell type, particular mutation type, as well as biological activation context. Books such as this one may help in this task by putting into perspective both general ...
The income that supports the activities of the National Academy of Sciences (NAS) comes from two major sources: program revenue received from sponsors to pay for the myriad studies and other activities undertaken each year by the National Research Council (NRC), and a much smaller sum that is obtained from our endowment under the endowment spending policies adopted by the Council. The goal of the endowment is to provide stable support for the Academy's programs and activities. To achieve this goal, the Council, acting on the recommendations of the Finance Committee, has historically authorized spending from the portfolio at a rate designed to maintain the purchasing power of the endowment over time. This Report of the Treasure of the National Academy of Sciences presents the financial position and results of operations as well as a review of the endowment, trust, and other long-term investments portfolio activities of our Academy for the year ended December 31, 2012. While this book provides essential financial summary to key personnel, it also serves as a vital informative resource for various members of the public, private, and governmental sectors
The income that supports the activities of the National Academy of Sciences (NAS) comes from two major sources: program revenue received from sponsors to pay for the myriad studies and other activities undertaken each year by the National Academies of Sciences, Engineering, and Medicine, and a much smaller sum that is obtained from our endowment under the endowment spending policies adopted by the Council. The goal of the endowment is to provide stable support for the Academy's programs and activities. To achieve this goal, the Council, acting on the recommendations of the Finance Committee, has historically authorized spending from the portfolio at a rate designed to maintain the purchasing power of the endowment over time. This Report of the Treasurer of the National Academy of Sciences presents the financial position and results of operations as well as a review of the endowment, trust, and other long-term investments portfolio activities of our Academy for the year ended December 31, 2016. While this book provides essential financial summary to key personnel, it also serves as a vital informative resource for various members of the public, private, and governmental sectors.
Intracellular checkpoint controls constitute a network of signal transd- tion pathways that protect cells from external stresses and internal errors. Ext- nal stresses can be generated by the continuous assault of DNA-damaging agents, such as environmental mutagens, ultraviolet (UV) light, ionizing radiation, or the reactive oxygen species that can arise during normal cellular metabolism. In response to any of these assaults on the integrity of the genome, the activation of the network of checkpoint control pathways can lead to diverse cellular responses, such as cell cycle arrest, DNA repair, or elimination of the cell by cell death (apoptosis) if the damage cannot be repaired. Moreover, in...
Volume 71 of Advances in Cancer Research begins with Morgan and Kastan presenting data on the roles of p53 and ATM in cell cycle progression and cell death in response to DNA damage and how this information may lead to targets for improved cancer therapies. Kok et all. Review the methodological advantages and limitations to localizing tumor suppressor genes, especially those on the short arm of chromosome 3. Peltomaki and de la Chapelle describe research on mismatch repair genes and their effects on colorectal cancer. McKenna and Cotter present findings on the functions and failures of apoptosis in the hematopoietic system. Ravitz and Wenner review TGF-B and how it controls and affects cell ...
1 2 D. FITZGERALDI, I. PASTAN , and J. ROBERTUS Introduction . . . . . . . . . . . . . I 2 Toxin Structure-Function Properties 2 2. 1 Functions. . . . . . . . . . . . . . . . . . . . . . . . 2 2. 2 Binding. . . . . . . . . . . . . . . . . . . . . . . . . 3 3 Intracellular Processing - Cleavage and Reduction . . . . . . 4 3. 1 Cytosolic Activity . . . . . . . . . . . . . . . . 5 4 Immunotoxin Design and Testing. 6 5 Conclusion. . 8 References. . . . . 8 1 Introduction While various treatment approaches for cancer include reversal of the transformed phenotype, stimulation of immune responses, inhibition of metastatic spread and deprivation of key nutrients, the goal of immunotoxin treatment is...
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