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Centipede Envenomation Effects on Human Beings and Scientific Research on Traditional Antivenom Agents
Published in Parimelazhagan Thangaraj, Medicinal Plants, 2018
Dhivya Sivaraj, Revathi Ponnusamy, Rahul Chandran, Parimelazhagan Thangaraj
Enzyme PLA2 is found only in Scolopendrid venom (Gonzàlez-Morales et al. 2009; Liu et al. 2012; Malta et al. 2008; Undheim et al. 2014). PLA2 hydrolyse glycerophospholipids at the sn-2 position release lysophospholipids and fatty acids, such as arachidonic acids, thereby inducing skin diseases and prostrate cancer (Eividin et al. 2011). However, neofunctionalisation of snake venom PLA2 often removes the ability to catalyse the reaction (Fry et al. 2009; Low et al. 2013) and this may also be the case for PLA2 in scolopendrid venom. Local necrosis, hemorrhages and respiratory arrest or paralysis are due to PLA2 (an anticoagulant enzyme which inhibits the prothrombinase complex by its binding to coagulation factor Xa) and cardiotoxin (Fry et al. 2009; King and Hardy 2013).
Diagnosis and Pathobiology
Published in Franklyn De Silva, Jane Alcorn, The Elusive Road Towards Effective Cancer Prevention and Treatment, 2023
Franklyn De Silva, Jane Alcorn
All human cells are composed of either two X chromosomes in females or single X and Y chromosomes in males, along with the 22 pairs of autosomal chromosomes [297–299]. Drawings of human chromosomes first appeared in the late 19th century [300], (Table 2.3), likely by Arnold who was the first to observe human chromosomes in cancer cells in 1879 [300, 301]. Painter in 1923 and Tjio and Levan in 1956 confirmed the exact number of chromosomes as 46 [298, 301]. Chromosomes are made up of chromatin, a complex composed of macromolecular genomic DNA and nuclear proteins [297, 298, 302]. In 2003, the “Human Genome Project” completed mapping the human genome, all genes on the 23 pairs of chromosomes, and this set the stage for the “1000 Genomes Project”, which conducted a whole-genome sequence analysis of a total of 2504 individuals representing 26 different populations covering five continents [297, 303, 304]. This project identified ~88 million genome variants of which single nucleotide polymorphisms (SNPs) accounted for ~84.7 million of the 88 million variants while short insertion/deletions (indels) accounted for ~3.6 million variants and larger number of copy variants accounted for ~60,000 variants [297, 303, 304]. On average, around 150 variants cause protein truncation, ~10,000 variants cause changes in amino acid sequences, about 500,000 influence transcription factor binding sites [297, 303, 304]. (Peri)centromeric repetitive sequences constitute a substantial proportion of the human genomic component [305]. Furthermore, repetitive segments of DNA, such as long interspersed elements (LINEs, 500–8000 bp, representing 21% by frequency), retrotransposons (long terminal repeats or LTRs, 200–5000 bp, representing 8% by frequency), DNA transposons (200–2000 bp, representing 3% by frequency), short interspersed elements (SINEs, 100–300 bp, representing 21% by frequency), and minisatellite, microsatellite, or major satellite (2–100 bp, representing 3% by frequency) all account in total for ~50% of the human genome sequence [297, 303, 304, 306–308]. It is now established that over 98% of the human genome does not encode proteins [309–311]. Furthermore, noncoding DNA accounts for the majority of heterochromatin, and almost all noncoding DNA is transcribed into a repertoire consisting mostly of noncoding ribonucleic acids (RNAs), including small RNAs [311]. These nonprotein-coding sequences parts (i.e., nongenic DNA) were initially considered as junk DNA or parasitic DNA, or selfish DNA. Therefore, they were thought to be redundant and having insignificant selective pressure, and thus tolerated the accretion of mutations to give rise to a new gene (i.e., neofunctionalization) without the ability to encode a functional protein (i.e., pseudogene) and generally harmless to the organism [308–310, 312]. Over the years, research into noncoding DNA has resulted in extensive recharacterization and now suggests these noncoding DNA sequences can regulate gene expression and are vital for the function and survival of the cell [309, 311, 313, 314].
Integration of transcriptomic and proteomic approaches for snake venom profiling
Published in Expert Review of Proteomics, 2021
Cassandra M. Modahl, Anthony J. Saviola, Stephen P. Mackessy
Snake venoms are complex oral secretions, composed of many proteins and peptides that function individually and/or synergistically to target multiple physiological systems in prey or predators [1]. Through the process of gene duplication and neofunctionalization, a single toxin family can have dozens of isoforms with different activities, all dependent on amino acid residue substitutions within a conserved family scaffold [2,3]. Profiling and characterizing the blend of toxins present in a venom and determining their sequences can be a daunting task, especially considering the documented variation in toxin diversity between individual snakes at both the transcriptome [4] and the proteome levels [5–8]. However, advances in sensitivity and high-throughput technology in the fields of genomics, transcriptomics, and proteomics have provided powerful approaches to address these challenges [9]. The integration of these -omic fields in venom research has been termed ‘venomics’ [10–12].
Scorpion venomics: a 2019 overview
Published in Expert Review of Proteomics, 2020
Jimena I. Cid-Uribe, José Ignacio Veytia-Bucheli, Teresa Romero-Gutierrez, Ernesto Ortiz, Lourival D. Possani
Peptides in the venom are responsible for the envenomation phenomenon caused by scorpion sting. These toxins interact with ion channels, modulating the electrical properties of cell membranes [8]. In addition, enzymes found in the venom facilitate the biodistribution of venom components [9] and generate post-translational modifications, such as amidation of the peptides, that improve their function and increase their stability [10]. Proteins found in venoms are the result of toxin recruitment events in which an ordinary protein gene, typically one involved in a regulatory process, is duplicated, and the new gene is selectively expressed in the venom gland. Such toxin genes are amplified to obtain multigene families with extensive neofunctionalization, followed by the deletion of some copies and degradation of others to nonfunctional copies or pseudogenes. The newly created toxin multigene families often preserve the molecular scaffold of the ancestral protein, but key functional residues outside the core scaffold are modified to acquire a myriad of newly derived activities [1,11].
Hematopoietic growth factors: the scenario in zebrafish
Published in Growth Factors, 2018
Vahid Pazhakh, Graham J. Lieschke
Gene duplication, not least in part the legacy of a whole genome duplication in the teleost radiation, has left its legacy on the zebrafish genome (Braasch et al., 2016; Postlethwait et al., 1998). While gene duplication can be considered to be an added complexity, it has also provided nature with an opportunity to explore biologically feasible variations that can provide biological insight when they are understood. Diversification processes including gene loss, subfunctionalization and neofunctionalization can eliminate or segregate biological functions between duplicates, or assign new functions to individual duplicates. These processes can create new private single ligand/receptor pairs, or regionally isolate components of promiscuous ligand/receptor groups to achieve highly specific anatomically-localized effects. Amongst model organisms, zebrafish are not unique in the diversity of their HGF ligand/receptor configurations: even between humans and mice, significant differences exist. For example, interleukin-3 receptor structure is more complex in the mouse than human, there being an extra mouse-specific alternative beta subunit (Geijsen et al., 2001; Hara & Miyajima, 1992).