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Topic Review
P2X7 Variants
The human P2X7 gene is highly polymorphic, and several splice variants of the receptor have been identified in time. P2X7 single-nucleotide polymorphisms (SNPs) have been broadly analyzed by studies relating them to pathologies as different as infectious, inflammatory, nervous, and bone diseases, among which cancer is included. Moreover, in the last years, an increasing number of reports concentrated on P2X7 splice variants’ different roles and their implications in pathological conditions, including oncogenesis. Our article on P2X7 variants in oncogenesis recently published in Cells gives an overview of established and recent literature demonstrating a role for human P2X7 gene products in oncological conditions. Here you find the main structural information on P2X7 variants.
  • 621
  • 02 Feb 2021
Topic Review
P2X Receptor-Dependent Modulation
P2X receptors (P2XRs) are membrane ligand-gated ion channels and are members of the purinergic receptor family. Of the seven P2XR family members, only four of them (P2X1, P2X4, P2X6 and P2X7) have been shown to be expressed in MCs, with each of them playing an important role in regulating MC activities, such as Ca+ influx and degranulation. P2XRs are also present in neurons and glial cells, where their engagement may affect the development of neuroinflammatory pathologies such as the Alzheimer’s disease (AD), Parkinson’s disease (PD) and Multiple sclerosis (MS).
  • 369
  • 14 Oct 2021
Topic Review
P27Kip1
The Cyclin-dependent kinase (CDK) regulator p27Kip1 is a gatekeeper of G1/S transition. It also regulates G2/M progression and cytokinesis completion, via CDK-dependent or -independent mechanisms. Recently, other important p27Kip1 functions have been described, including the regulation of cell motility and migration, the control of cell differentiation program and the activation of apoptosis/autophagy.
  • 407
  • 13 Sep 2021
Topic Review
P-21 Activated Kinases in Liver Disorders
The p21 Activated Kinases (PAKs) are serine threonine kinases and play important roles in many biological processes, including cell growth, survival, cytoskeletal organization, migration, and morphology. PAKs have emerged in the process of liver disorders, including liver cancer, hepatic ischemia-reperfusion injury, hepatitis, and liver fibrosis, owing to their effects in multiple signaling pathways in various cell types. Activation of PAKs promotes liver cancer growth and metastasis and contributes to the resistance of liver cancer to radiotherapy and chemotherapy, leading to poor survival of patients. PAKs also play important roles in the development and progression of hepatitis and other pathological processes of the liver such as fibrosis and ischemia-reperfusion injury.
  • 445
  • 10 Mar 2023
Topic Review
Oxysterols
Oxysterols are cholesterol oxidation products, which can be absorbed from the diet, or generated by auto-oxidation or by enzymatic mechanisms. Oxysterols result from oxidation of cholesterol on the sterol rings, the side chain, or both. This generates a diverse range of oxysterol congeners that have distinct biophysical properties.
  • 362
  • 27 Aug 2021
Topic Review
Oxygen Homeostasis
The unique biology of the intestinal epithelial barrier is linked to a low baseline oxygen pressure (pO2), characterised by a high rate of metabolites circulating through the intestinal blood and the presence of a steep oxygen gradient across the epithelial surface. These characteristics require tight regulation of oxygen homeostasis, achieved in part by hypoxia-inducible factor (HIF)-dependent signalling. Furthermore, intestinal epithelial cells (IEC) possess metabolic identities that are reflected in changes in mitochondrial function. In recent years, it has become widely accepted that oxygen metabolism is key to homeostasis at the mucosae. In addition, the gut has a vast and diverse microbial population, the microbiota. Microbiome–gut communication represents a dynamic exchange of mediators produced by bacterial and intestinal metabolism. The microbiome contributes to the maintenance of the hypoxic environment, which is critical for nutrient absorption, intestinal barrier function, and innate and/or adaptive immune responses in the gastrointestinal tract.
  • 529
  • 22 Sep 2021
Topic Review
Oxidative Stress in Tumorigenesis and Progression
Oxidative stress refers to the imbalance between the production of reactive oxygen species (ROS) and the endogenous antioxidant defense system. Its involvement in cell senescence, apoptosis, and series diseases has been demonstrated. Advances in carcinogenic research have revealed oxidative stress as a pivotal pathophysiological pathway in tumorigenesis and to be involved in lung cancer, glioma, hepatocellular carcinoma, leukemia, and so on.
  • 152
  • 07 Mar 2024
Topic Review
Oxidative Stress and Retinitis Pigmentosa
Degenerative retina in RP is exposed to high-level O2 and thereby damaged by ROS. Microglia as well as photoreceptor cells are injured by ROS. Oxidative microglial activation promotes microgliosis and photoreceptor cell death in RP. Oxidative DNA damage mediates MUTYH-SSBs-PARP signaling to induce microglial activation.
  • 717
  • 26 Oct 2020
Topic Review
Oxidative Stress and Redox-Dependent Pathways in Cholangiocarcinoma
Cholangiocarcinoma (CCA) is a fatal tumor, accounting for 2% of all cancer-related mortalities worldwide yearly due to its high aggressiveness and poor response to current therapies. Furthermore, over the past few decades, CCA mortality has increased globally.
  • 143
  • 12 Jan 2024
Topic Review
Oxidative Stress and Laminopathies Caused by LMNA Mutations
Mutations in the genes that encode for lamins, predominantly lamin A/C, cause a wide spectrum of human diseases, referred to as laminopathies, including muscular dystrophy, lipodystrophy, and systemic premature aging syndrome. HGPS, one of the most severe laminopathies, is a rare genetic disorder characterized by multisystem abnormalities, including premature aging. The most frequent mutation causing HGPS is c.1842C>T (p.G608G) in exon 11 of LMNA, resulting in cryptic splicing between an abnormal donor site in the middle of exon 11 and the usual acceptor of exon 12. This change causes a 50-amino acid deletion in the carboxyl-terminal tail of prelamin A, producing a truncated protein referred to as progerin. The 50 missing amino acids include the recognition sites for the prelamin A-cleaving enzyme ZMPSTE24. Consequently, progerin is normally farnesylated but cannot be further processed because of the lack of docking sites for ZMPSTE24. The farnesylated domain of progerin is firmly anchored to the nuclear membrane, leading to nuclear deformation and deleterious effects in HGPS cells. Blocking the farnesylation of progerin with a farnesyltransferase inhibitor (FTI) successfully reduced the cytotoxic effects of progerin in vitro; however, a clinical trial of FTIs did not yield promising results. A study showed that the interaction between progerin and wild-type lamin A/C was also a critical cause of nuclear deformation in HGPS and normal aging cells, providing a new therapeutic target for HGPS. Progerin expression in various cell types induces excessive ROS production and reduces the activities of the antioxidant system. Oxidative stress is also implicated in other types of laminopathies, such as Dunnigan-type familial partial lipodystrophy (FPLD), amyotrophic quadricipital syndrome with cardiac involvement, autosomal dominant Emery–Dreifuss muscular dystrophy (AD-EDMD), and restrictive dermopathy (RD).
  • 326
  • 25 May 2023
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