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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
In order to divide successfully, a cell must copy its DNA so that each daughter cell receives its full set of chromosomes. This is achieved by a tightly regulated mitosis following the cell cycle pathway (Figure 2.6). Passage through the cell cycle is controlled by cyclin proteins, in a cascade of phosphorylation events. Each cyclin acts as a catalytic subunit in partnership with a cyclin-dependent kinase (CDK). Upon cyclin binding, CDKs phosphorylate target proteins that are required for cell-cycle progression. CDK-specific inhibitors (CDKIs) bind cyclin–CDK complexes to regulate their activity and can themselves be regulated by other proteins. During mitosis, one member of each chromosome pair becomes attached to a centriole. Centrioles move to opposite ends of the cell, taking the chromosomes with them. In order to prevent inappropriate proliferation of cells, mitosis is tightly controlled, with various checkpoints to ensure that every part of the mitotic process is completed correctly before the next stage begins. Because uncontrolled proliferation is a hallmark of cancer, the cell cycle provides an obvious target for therapy. CDKIs often act as tumour suppressors and are potentially useful anticancer agents.
The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The centrosome is an area near the nucleus that contains a pair of rod-like structures called the centrioles. This area and the centrioles are associated with the process of cell division. They produce the mitotic spindle in dividing cells. The centrioles also form the basis of cilia and flagella. Cilia are typically found on the columnar epithelium of the lining of the respiratory tract. They are involved in the movement of dust particles and mucus up the respiratory tract. The only example found in humans of a cell with a flagellum is the sperm.
The Pineal Gland and Melatonin
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Jerry Vriend, Nancy A.M. Alexiuk
Most of the organelles of the mammalian pinealocyte do not differ substantially from those of other mammalian cells. The nucleus may be irregular in shape with indentations of the surface. A prominent nucleolus is present. Both smooth and rough endoplasmic reticulum are consistently reported;72 but Wolfe70 pointed out that in the rat the endoplasmic reticulum is not typical and has referred to it as intergrade endoplasmic reticulum. Clusters of ribosomes, not associated with membranes, are found throughout the cytoplasm. Although mitochondria are generally reported as normal in mammalian pinealocytes, considerable variation in size and shape have been documented.70,73–75 They are relatively numerous in most pinealocytes. Centrioles, although not present in great numbers, have been reported to differentiate into structures called microtubular sheaves (microtubules arranged in sheaves).70–76 The presence of cilia depends on the species studied and on the developmental stage examined. Clabough77 observed cilia in pinealocytes of fetal and neonatal rats, but cilia were absent or very rare in pinealocytes of adult rats.70,78 In some species, such as the mole, cilia may be a characteristic feature of each pinealocyte.54 In this species, the cilia were reported as having filaments in a 9 + 0 arrangement in the shaft, an arrangement also found in photoreceptor cells.
Prevalence and natural history of variants in the ANKRD26 gene: a short review and update of reported cases
Published in Platelets, 2022
Hrushikesh Vyas, Ahmad Alcheikh, Gillian Lowe, William S Stevenson, Neil V Morgan, David J Rabbolini
As suggested by its localization, ANKRD26 appears to play a role in centriole biology [41]. Centrioles are important in ciliogenesis and motility. They are components of centrosomes that have been implicated in cancer pathogenesis [56,57]. Centrosome amplification triggers p53-dependent apoptosis through activation of a multiprotein complex known as the PIDDosome [56]. In centrosome amplification (e.g. cytokinesis failure), ANKRD26 recruits the p53-induced death domain protein 1 (PIDD1) to the centriole distal appendages to form part of the PIDDosome [57–59]. When ANKRD26 is inactivated, cells cannot sustain PIDDosome assembly and show enhanced growth following centrosome amplification [57,59]. Whether these actions of ANKRD26 protein play any role in the pathogenesis of ANKRD26-RT is unknown.
Indomethacin: an exploratory study of antiviral mechanism and host-pathogen interaction in COVID-19
Published in Expert Review of Anti-infective Therapy, 2022
Nishant Shekhar, Harpinder Kaur, Phulen Sarma, Ajay Prakash, Bikash Medhi
Centrosome-associated protein CEP250 is involved in the synthesis of core centrosomal protein required for centriole–centriole cohesion, during interphase. Its activity can be rendered crucial for centriole dynamics and cell cycle regulation. In a recent study by Shigdel et al. (2020), the authors discuss the human-SARS-CoV-2 interactome network from Gordon & Jang et al. (2020), where CEP250 interacts with the CoV protein Nsp13 [43]. The AvgSpec value of CEP250-Nsp13 complex detection was 151.0, which was the 2nd most strongest interaction in the human-SARS-CoV-2 interactome in addition to a 1.43-fold increase in expression level upon SAR-CoV-2 infection. Shigdel et al. (2020) report from their study that the small molecule of their interest WDB002 which directly targets CEP250 can lead to SARS-CoV-2 inhibition. According to the CTD database, co-treatment of Indomethacin with Insulin, dexamethasone, 1-Methyl-3-isobutylxanthine, and bisphenol F decreases. Similar CEP250-Nsp13 interaction was also found in SARS & MERS virus-human protein interactome. The strong interaction of Nsp13 helicase with CEP250 protein raises questions on the comprehensive explanation about its function and how it influences host cell viability.
A homozygous POC1B variant causes recessive cone-rod dystrophy
Published in Ophthalmic Genetics, 2021
Ann-Marie C. Peturson, Nicole C. L. Noel, Ian M. MacDonald
Inherited retinal dystrophies are diverse groups of photoreceptor disorders, with many genetic etiologies. Cone dystrophies are characterized by the dysfunction and loss of cone photoreceptors. An initial diagnosis of cone dystrophy can progress to cone-rod dystrophy as rod photoreceptors degenerate. Variants in components of the photoreceptor cilium are common causes of photoreceptor dystrophies. The POC1 centriolar protein B (POC1B) gene encodes a component of the centrosome and basal body of the photoreceptor cilium (Figure 1) (1). The centrosome, which is comprised of two centrioles surrounded by a protein mass, forms the primary cilia basal body. POC1B has been reported to play essential roles in centriole duplication and length, centriole integrity, cell proliferation, primary ciliogenesis, and retinal integrity (2–5). Pathogenic variants in POC1B have been associated with autosomal recessive cone dystrophy, cone-rod dystrophy, and syndromic retinal dystrophy (1,5–8). Here, we present a cone-rod dystrophy patient with a homozygous POC1B variant, further expanding the clinical findings for patients with POC1B variants.