Cellular function control with

CDKs are central mediators of cell proliferation and their roles in various aspects of cell growth and development have been extensively characterized and explored for the treatment of various oncological conditions. CDKs 1, 2, 4, and 6 are associated with cell division and control the cell cycle through the Gl, S, G2, and M phases. Other cellular functions controlled by specific... 

In concordance with the central role of ubiquitin modification in multiple cellular functions perturbations of this system are associated with a variety of diseases. Defects in the control of cell cycle regulators by the ubiquitin proteasome system are connected to cancer progression and many E3 ligases were originally identified as oncogenes. 

Although the importance of a systemic perspective on metabolism has only recently attained widespread attention, a formal frameworks for systemic analysis has already been developed since the late 1960s. Biochemical Systems Theory (BST), put forward by Savageau and others [142, 144 147], seeks to provide a unified framework for the analysis of cellular reaction networks. Predating Metabolic Control Analysis, BST emphasizes three main aspects in the analysis of metabolism [319] (i) the importance of the interconnections, rather than the components, for cellular function (ii) the nonlinearity of biochemical rate equations (iii) the need for a unified mathematical treatment. Similar to MCA, the achievements associated with BST would warrant a more elaborate treatment, here we will focus on BST solely as a tool for the approximation and numerical simulation of complex biochemical reaction networks. 

In recent years the psychopharmacologist has paid increasing attention to the examination of brain proteins with which psychotropic drugs react, and also the molecular mechanisms that control the synthesis and cellular function of these proteins. For this reason, any understanding of psychopharmacology requires some knowledge of the basic techniques of molecular genetics. 

An increase in lung lesions, as compared to controls, was observed in rats exposed to 0.7 mg nickel/m as nickel subsulfide for 78 weeks (6 hours/day, 5 days/week), followed by a 30-week observation period (Ottolenghi et al. 1974). The lung lesions included pneumonitis, atelectasis, bronchitis, bronchiectasis, and emphysema. Morphological alterations in alveolar macrophages (hyperplasia and lamellated material in the cytoplasm) were associated with impaired cellular function in rabbits exposed to 0.2 mg nickel/m as metallic nickel or nickel chloride for 8 months (Johansson and Camner 1986 Johansson et al. 1981). An increase in volume density of alveolar type II cells was also observed in rabbits exposed to 0.2 mg nickel/m as metallic nickel or nickel chloride for 1 month (Johansson and Camner 1986 Johansson et al. 1981). 

The second messenger molecules Ca2+ and cyclic AMP (cAMP) provide major routes for controlling cellular functions. In many instances, calcium (Ca2+) achieves its intracellular effects by binding to the receptor protein calmodulin. Calmodulin has the ability to associate with and modulate different proteins in a Ca2+-dependent and reversible manner. Calmodulin-dependent cyclic nucleotide phosphodiesterase (CaMPDE, EC 3.1.4.17) is one of the key enzymes involved in the complex interactions that occur between the cyclic-nucleotide and Ca2+ second messenger systems (see Figure 13.2). CaMPDE exists in different isozymic forms, which exhibit distinct molecular and catalytic properties. The differential expression and regulation of individual phosphodiesterase (PDE) isoenzymes in different tissues relates to their function in the body. 

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