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Carbon Monoxide — From Tool to Neurotransmitter
Published in David G. Penney, Carbon Monoxide, 2019
Nanduri R. Prabhakar, Robert S. Fitzgerald
A good deal of information is available on the regulation of HO-1 activity. The nucleotide sequence of the HO-1 gene contains four introns and five exons. The ability of various stimuli to induce increases in enzyme levels can be explained by the presence of multiple promoters in the HO-1 gene. In eukaryotic cells, prolonged exposure to heat activates a specific set of genes resulting in induction of so-called heat-shock proteins. It has been shown that HO-1 can be induced by heat (Shibahara et al., 1987) and the biochemical properties of HO-1 suggest that it is similar to hsp-32, which is a heat shock-protein (Lindquist and Craig, 1988). Regulation of HO-1 activity resembles in many respects the control of metalothionen (Mt). Both the HO-1 and Mt gene can be induced by essentially the same type of stimuli, which include glucocorticoids, metals, hormones, and interferons that have a heat shock element in the 5’ flanking region (Shibahara et al., 1987). Compared to HO-1, relatively little is known about the regulation of HO-2. Chromosomal localization of human heme oxygenases has been recently reported (Kutty et al., 1994). HO-1 located on chromosome 22 q 12, and HO-2 to chromosome 16 p 13.3.
Naturally Occurring Polymers—Animals
Published in Charles E. Carraher, Carraher's Polymer Chemistry, 2017
One of the active agents is cyclic AMP. A protein called CREB (for CRE-binding protein; CRE is simply a specific DNA unit, part of a gene, that is called the cyclic AMP response element or site) is activated altering the shape and functioning of the synapse in our brains when exposed to cyclic AMP (10.12) or some related compound in our brains. Genes that are activated are called CRE genes with the name being the initials of cyclic AMP response elements. CREB, when phosphorylated, binds to the CREs near certain genes acting as a transcription factor and turning on or activating the genes. Animals without the CREB-producing gene are able to learn but do not possess long-term memory. It is believed by some that the CREB-related genes are in fact essential to our learning and memory and act as master switches in activating other genes necessary in our learning/memory process. The CREB gene is on chromosome 2. A related and essential gene that helps CREB perform is found on chromosome 16 and is given the name CREBBP.
Recognition of the Most Common Trisomies through Automated Identification of Abnormal Metaphase Chromosome Cells
Published in Mohamed Lahby, Utku Kose, Akash Kumar Bhoi, Explainable Artificial Intelligence for Smart Cities, 2021
Reem Bashmail, Muna Al-Kharraz, Lamiaa A. Elrefaei, Wadee Alhalabi, Mai Fadel
The research work in Keller et al. (1995) separated the foreground of metaphase image from the background by locally refined thresholding. Then, chromosomes segmentation occurred by Connected Component Analysis and Thinning Objects to One Pixel Wide 'Skeletons'. The datasets contain 23400 of 16 and 18 chromosomes and they extracted centromeric index, relative length, and banding pattern features. The fuzzy logic classifier was used to differentiate between 16 and 18 chromosomes and achieved 100% classification accuracy for chromosome 16 and 87% accuracy for chromosome 18.
Inflammatory bowel disease: why this provides a useful example of the evolving science of nutrigenomics
Published in Journal of the Royal Society of New Zealand, 2020
Familial aspects of IBD were recognised and reported as early as the 1970s (Singer et al. 1971). In their 1994 review, Satsangi et al. (1994) reported the use of genome scanning techniques using microsatellite markers, to implicate specific areas of chromosomes linked to disease, while association studies of specific genes or gene complexes, such as the human leukocyte antigen (HLA) gene complex, which encodes the major histocompatibility complex (MHC) proteins, were also linked to the risk of this disease in humans. HLA or cytokine genes were considered in early IBD studies to aid in mechanistic understandings, and this association was reinforced by subsequent findings (Satsangi et al. 1996). The possible involvement of the X chromosome was also suggested at an early stage, since there was a somewhat higher number of reported cases in women than in men (Vermeire et al. 2001). The situation appeared considerably more complex than a single gene disorder, and by the year 2000, Orchard and co-workers estimated the involvement of at least somewhere between 10 and 20 genes in disease susceptibility (Orchard et al. 2000). One gene that appeared of considerable importance in these early studies was the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) gene (Hugot et al. 2001). This gene, also known as caspase recruitment domain-containing protein 15 (CARD15) or inflammatory bowel disease protein 1 (IBD1), is a protein that is encoded by the NOD2 gene, located on chromosome 16 in humans.