The tyrosine hydroxylase plays a key role in the catecholamine synthesis responding to many stimuli disturbing homeostasis. In this part we described the posttranscriptional levels of the gene and the protein regulation including: alternative splicing, isoform specificity, feedback inhibition, protein phosphorylation and dephosphorylation, protein stability, translational regulation.
In recent years there was a growing number of reports of new non-protein-coding RNAs which are implicated in the regulation of many cellular processes. They differ in many respects from already known housekeeping RNA species involved in protein biosynthesis (tRNA, rRNA) and RNA maturation or modification (RNase P RNA, snRNAs, snoRNAs). Regulatory RNAs (riboregulators) are expressed only in certain cell types, at particular stages of organism development or cell differentiation or in response to biotic and abiotic stimuli. Their expression is usually accompanied by the alteration of patterns of the expression of other genes. The mechanisms employed by riboregulators can affect transcription, pre-mRNA processing and translation. In the post-genomic era, the noncoding regulatory RNAs emerge as key determinants of organismal complexity, providing efficient and highly specific means for integration of various cellular processes.
The control of eucaryotic class II genes transcription is unusually complicated because it is the first stage of their expression in the cell. The assortment of specific gene coding sequence as a process of selection of submission for expression genes particularly essential is. In this process, beside RNA polymerase II, the basic transcription initiation factors that form different initiation complexes with enzyme and DNA take part, as well as other protein factors, often tissue specific that interact with fragment of DNA located in the distant place of the start of transcription. The formation of transcription complex, its components and possible interaction are discussed. The control of this process are discussed on the example of contribution of protein kinases and phosphatases modifying individual proteins, influencing the change of their mutual interactions and, in consequence, differentiating transcription level of specific genes.
Transplant rejection, like tolerance, is a T cell-dependent event. There is compelling evidence to suggest that induction of transplant tolerance is an actively learned process in which T cells need to engage the alloantigens in order to learn to tolerate the allograft. A family of cytokines whose receptors use the same IL-2 receptor gamma chain (also called the common gamma c) plays an important role in regulating multiple aspects of the allograft response (i.e. rejection vs. tolerance). It is undeniable that gamma c-cytokines can drive clonal expansion and effector maturation of alloreactive T cells, and therefore, targeting such cytokines or their receptor components remains an attractive way of blocking transplant rejection. However, we just started to appreciate that gamma c-cytokines also regulate the acquisition of transplant tolerance via programming activated T cells for apoptotic cell death and via guiding the evolution of regulatory T cells. Thus, understanding precisely the role of gamma c-cytokines in regulating T cell homeostasis and T cell regulation is critically important in the induction of transplant tolerance.
In this paper we present a theoretical framework for novelty based feedback regulation in artificial neural networks. Novelty is assessed on the basis of monitoring the coherence of network dynamics. The result of novelty detection is dynamically coupled to parameters that control the dynamics of the recognition process. The paper presents a new measure of novelty detection - the strength of the local field - and presents new simulation results concerning novelty detection. It also integrates previously published models and simulation results into a general dynamical model of feedback regulation.
Essential differences between the innate and acquired branches of immunity are described. These differences concern the detection system (receptors and pathogen structures) and the cells engaged in both systems as well as the effectory mechanisms. In contrast to those of the acquired system, receptors of the innate system, which developed during evolution, recognize unchanged structures on large groups of pathogens (e.g. lipopolysaccharide in Gram-negative bacteria). Two lineages, natural killer (NK) and dendritic cells (DCs), play important roles in the innate system. Phenotypic and functional differentiation is observed among NKs and DCs, so each of their sublineages plays a different role in the innate system. Every lineage of cells of the innate immune system express different stimulatory and sometimes also inhibitory receptors on their surfaces (e.g. NK cells). Among the stimulatory are Toll-like receptors (TLRs), mannose and scavenger receptors, and the stimulatory receptors of NK cells. All TLRs show similarity in structure and in the kind of molecules involved in intracellular signaling. The immune reactions of the innate system involve cytokine-dependent resistance of cells against infection with pathogen, production of cytokines (tumor necrosis factor, interferons, interleukins, chemokines) and MHC-independent killing. Although these reactions protect the host from invasion by microorganisms, they can also be responsible for significant tissue damage or may stimulate the development of autoimmunity. Therefore innate immunity must be under rigorous control. The possible regulatory mechanisms of innate immunity are discussed.
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