Topic Review
Golgi Proteostasis
The Golgi apparatus is a central hub for cellular protein trafficking and signaling. Golgi structure and function is tightly coupled and undergoes dynamic changes in health and disease. A crucial requirement for maintaining Golgi homeostasis is the ability of the Golgi to target aberrant, misfolded, or otherwise unwanted proteins to degradation. Recent studies have revealed that the Golgi apparatus may degrade such proteins through autophagy, retrograde trafficking to the ER for ER-associated degradation (ERAD), and locally, through Golgi apparatus-related degradation (GARD).
  • 440
  • 02 Mar 2022
Topic Review
GPCR, ER Stress, and EMT
Endoplasmic reticular stress (ERS) is a dynamics adaptive mechanism that is triggered upon perturbations in ER homeostasis. Hence unfolded protein response (UPR) is activated by ERS as a distress signal. UPR is involved in cancer progression by aiding cells to adapt harsh environments and evading cell death. We have made a significant discovery in the area of ERS and cell death in colonic epithelial cells where have previously unraveled the relationship between ERS and anti- apoptotic protein Survivin in colon cancer cells. We established a time point for an aggressive ERS environment with the help of ERS dynamics thereby creating a perfect environment for testing drugs. However, the role of ERS in cancer is still perplexing. G-protein coupled receptors (GCPR) are another large family of cell surface receptors that respond to a variety of external signals. GPCRs are said to have an active association with ERS in order to trigger some key processes like epithelial mesenchymal transition (EMT) which is a prime step in metastasis. However, there are some essential candidates that play a role in hindering cancer progression through numerous pathways. We therefore wish to provide the readers with an exhaustive views and insights of ER stress biology.
  • 1.0K
  • 12 Oct 2020
Topic Review
GPCRs In Intracellular Compartments: Implications For Drug Discovery
The architecture of eukaryotic cells is defined by extensive membrane-delimited compartments, which entails separate metabolic processes that would otherwise interfere with each other, leading to functional differences between cells. G protein-coupled receptors (GPCRs) are the largest class of cell surface receptors, and their signal transduction is traditionally viewed as a chain of events initiated from the plasma membrane. Furthermore, their intracellular trafficking, internalization, and recycling were considered only to regulate receptor desensitization and cell surface expression. On the contrary, accumulating data strongly suggest that GPCRs also signal from intracellular compartments. GPCRs localize in the membranes of endosomes, nucleus, Golgi and endoplasmic reticulum apparatuses, mitochondria, and cell division compartments. Importantly, from these sites they have shown to orchestrate multiple signals that regulate different cell pathways. 
  • 510
  • 08 Oct 2022
Topic Review
GPR15 in Vascular Tissue
GPR15 as a member of the Class A (rhodopsin) orphan G protein-coupled receptor (GPCR) family  has been recently deorphanized by identification of two endogenous receptor-activating ligands in human. Interestingly, in vascular tissue they interact apparently with different cell types. While one ligand triggers a cytoprotective effect on endothelial cells from the luminal site of vessels, the other ligand is rather responsible for the homing of GPR15-expressing lymphocytes into the colon. Thus, in addition to the role of GPR15 as a co-receptor for the human immunodeficiency virus (HIV) or to the expansion of GPR15-expressing lymphocytes in blood by chronic smoking this review will summarize findings to the role of GPR15 for vascular tissue based on new described receptor-ligand interactions.
  • 421
  • 21 Oct 2021
Topic Review
Gq Signaling in Autophagy Control
All processes in human physiology relies on homeostatic mechanisms which require the activation of specific control circuits to adapt the changes imposed by external stimuli. One of the critical modulators of homeostatic balance is autophagy, a catabolic process that is responsible of the destruction of long-lived proteins and organelles through a lysosome degradative pathway. Identification of the mechanism underlying autophagic flux is considered of great importance as both protective and detrimental functions are linked with deregulated autophagy. At the mechanistic and regulatory levels, autophagy is activated in response to diverse stress conditions (food deprivation, hyperthermia and hypoxia), even a novel perspective highlight the potential role of physical forces in autophagy modulation. To understand the crosstalk between all these controlling mechanisms could give people new clues about the specific contribution of autophagy in a wide range of diseases including vascular disorders, inflammation and cancer.
  • 358
  • 02 Sep 2022
Topic Review
Graviperception and Graviresponses in Euglena gracilis
The genus Euglena contains unicellular eukaryotic flagellates. In addition to light and chemicals, the cells perceive the gravitational field of the Earth and orient themselves paralell to the gravivector to optimize their position in the water column. The perception is based on transient receptor proteins in the membrane which are stimulated by the pressure of the cell content onto the lower membrane. Upon stimulation these proteins open and allow the influx of calcium from the outer medium which binds to a specific calmodulin. In turn this enzyme activates a adenylyl cyclase which produces cAMP believed to stimulate a phosphodiesterase A which finally modifies a flagellar protein which results in a course correction. Since Euglena is photosynthetic it absorbs carbon dioxide and produces oxygen and is thus an excellent candidate for a bioregenerative life support system during long-term space flights.
  • 408
  • 04 Nov 2022
Topic Review
GRKs
G protein-coupled receptor (GPCR) kinases (GRKs) play an important role in the regulation of signaling of GPCRs that bind neurotransmitters. The canonical model of GPCR desensitization posits that GRKs phosphorylate ligand-activated GPCRs, and this phosphorylation prepares receptors for the high-affinity binding of arrestin proteins. Arrestin binding prevents further G protein coupling, promotes receptor internalization, and initiates and/or facilitates specific branches of signaling. Existing data suggest that the role of GPCR phosphorylation by GRKs is distinct in different receptors. The relationship between G protein- and arrestin-mediated signaling on the one hand, and therapeutic and side effects of drugs on the other, is more complex than is widely believed. Also, the relationship between rapid (minutes to hours) GRK/arrestin-mediated regulation and long-term (days to weeks) neural plasticity remains to be elucidated. 
  • 1.1K
  • 19 Jan 2021
Topic Review
Growth and Division of Peroxisomes
The identification and molecular characterization of peroxisomal division proteins, microscopic observations and the analysis of patient fibroblasts have contributed to a refined growth and division model for peroxisomes. In mammalian cells, peroxisome formation by membrane growth and division represents a multi-step process involving the remodelling of the peroxisomal membrane, membrane expansion/elongation (growth), membrane constriction and final scission (fission). Peroxisomal growth and division results in the formation of new peroxisomes (multiplication/proliferation), which import matrix and membrane proteins to maintain functionality.
  • 265
  • 23 Jun 2022
Topic Review
Growth Hormone-Releasing Hormone
Growth hormone-releasing hormone (GHRH) is secreted primarily from the hypothalamus, but other tissues, including the lungs, produce it locally. GHRH stimulates the release and secretion of growth hormone (GH) by the pituitary and regulates the production of GH and hepatic insulin-like growth factor-1 (IGF-1). Pituitary-type GHRH-receptors (GHRH-R) are expressed in human lungs, indicating that GHRH or GH could participate in lung development, growth, and repair. The goal of thisentry is to present and critically evaluate new findings regarding growth hormone-releasing hormone (GHRH) and its actions in the settings of lung inflammation, fibrosis, and cancer. The essential, unanswered question we address is whether GHRH, as revealed by synthetic peptide probes that activate or inhibit its receptor, plays key roles in lung pathophysiology that are distinct from its effects on growth and metabolism. It provides background on the physiology of GHRH in the lung, which was elucidated using recently developed GHRH receptor peptide agonists and antagonists as mechanistic probes.
  • 1.0K
  • 09 Nov 2020
Topic Review
GRP78 Autoantibodies in Immune-Mediated Neurological Diseases
The 78 kDa glucose-regulated protein (GRP78), a member of the 70 kDa heat-shock family of molecular chaperones (HSP70), is essential for the regulation of the unfolded protein response (UPR) resulting from cellular endoplasmic reticulum (ER) stress. During ER stress, GRP78 evades retention mechanisms and is translocated to the cell surface (csGRP78) where it functions as an autoantigen. Autoantibodies to GRP78 appear in prostate, ovarian, gastric, malignant melanoma, and colorectal cancers. They are also found in autoimmune pathologies such as rheumatoid arthritis (RA), neuromyelitis optica (NMO), anti-myelin oligodendrocyte glycoprotein antibody-associated disorder (AMOGAD), Lambert-Eaton myasthenic syndrome (LEMS), multiple sclerosis (MS), neuropsychiatric systemic lupus erythematosus (NPSLE) and type 1 diabetes (T1D). 
  • 420
  • 16 Jun 2022
  • Page
  • of
  • 161
Video Production Service