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Topic Review
Adipose Tissue Development
Despite developing prenatally, the adipose tissue is unique in its ability to undergo drastic growth even after reaching its mature size. Proper adipose tissue development relies on tightly regulated processes that require careful coordination and cooperation between many different cell types and their matrix cues.
  • 786
  • 25 Oct 2022
Topic Review
B-Cell Maturation Antigen (BCMA)
During the past two decades there has been a major shift in the choice of agents to treat multiple myeloma, whether newly diagnosed or in the relapsed/refractory stage. The introduction of new drug classes, such as proteasome inhibitors, immunomodulators, and anti-CD38 and anti- SLAMF7 monoclonal antibodies, coupled with autologous stem cell transplantation, has approximately doubled the disease’s five-year survival rate. However, this positive news is tempered by the realization that these measures are not curative and patients eventually relapse and/or become resistant to the drug’s effects. Thus, there is a need to discover newer myeloma- driving molecular markers and develop innovative drugs designed to precisely regulate the actions of such putative targets. B cell maturation antigen (BCMA), which is found almost exclusively on the surfaces of malignant plasma cells to the exclusion of other cell types, including their normal counterparts, has emerged as a specific target of interest in this regard. Immunotherapeutic agents have been at the forefront of research designed to block BCMA activity. These agents encompass monoclonal antibodies, such as the drug conjugate belantamab mafodotin; bispecific T-cell engager strategies exemplified by AMG 420; and chimeric antigen receptor (CAR) T-cell therapeutics that include idecabtagene vicleucel (bb2121) and JNJ-68284528.
  • 782
  • 16 Sep 2020
Topic Review
KRAS
The RAS family consists of membrane-associated small GTPases which play essential roles in cell survival, proliferation, and differentiation. There are four RAS protein isoforms in humans: HRAS, NRAS, and two splice variants, KRAS4A and KRAS4B. 
  • 781
  • 12 Oct 2021
Topic Review
The Gut–Brain Axis
The gut–brain axis (GBA) it is a complex network in which the CNS and the enteric nervous system (ENS) interact with each other in a bilateral manner by several mechanisms, including nervous, hormonal, metabolic, and immunological ones. Recently, this relationship has been described as the ‘microbiota–gut–brain axis’ because of the known role of the gut microbiota in maintaining a physiological brain–gut relationship and its participation in the pathogenesis of several diseases. In this complex network, a plethora of interactions take place.
  • 780
  • 15 Sep 2021
Topic Review
Homologous Recombination Repair Deficiency
Homologous recombination repair deficiency (HRD) can be observed in virtually all cancer types. Cells possess a complex set of non-redundant and partially overlapping pathways to detect and repair DNA damage. In cancer, DNA damage repair (DDR) is frequently disrupted, leading to genomic instability. One of the pathways that is regularly altered in cancer is HR. HR is an important pathway for the repair of double-strand DNA breaks (DSBs) during the S and G2 phase of the cell cycle, i.e., after DNA replication has occurred. HR is considered a relatively error-free process because it uses an intact sister chromatid to guide DNA repair. HR deficiency (HRD) leads to enhanced reliance on alternative pathways involved in DSB repair, i.e., classical NHEJ, alternative end joining, and single-strand annealing. These pathways repair DSBs without a homologous DNA template, resulting in characteristic genomic scars across the genome.
  • 779
  • 25 May 2021
Topic Review
Exosomes in Motor Neurone Disease
Exosomes are attractive as vehicle systems for small therapeutic molecules and/or biomolecules including nucleic acids and proteins because of their lipid nature, presence of specific surface ligands (CD11b and CD18 receptors, integrins, tetraspanins) and ability to cross the blood–brain barrier. When compared to other drug delivery systems, exosomes have the distinct advantages of blood–brain barrier penetrance, longer duration in systemic circulation, tissue specificity that minimizes unwanted toxicity or off-target effects, stability of content, desirable biocompatibility and minimal toxicity issues. Techniques such as fusion expression, exosome membrane surface display and anchoring platforms have been used to attach peptides and biological ligands of interest to adhesion molecules, tetraspanins or integrins on exosome surface to ensure targeted delivery and enhanced uptake into desired cells.
  • 779
  • 08 Nov 2021
Topic Review
3C Protease as Ferroptosis Inducer
Regulated cell death (RCD) is a fundamental process common to nearly all living beings and essential for the development and tissue homeostasis in animals and humans. A wide range of molecules can induce RCD including a number of viral proteolytic enzymes. To date, numerous data indicate that picornaviral 3C proteases can induce RCD. In most reported cases, these proteases induce classical caspase-dependent apoptosis. In contrast, the human hepatitis A virus 3C protease (3Cpro) has recently been shown to cause caspase-independent cell death accompanied by previously undescribed features. In the current topic the results of the study where 3Cpro-induced cell death was characterized morphologically and biochemically are presented. It was found that dead cells demonstrated necrosis-like morphological changes including permeabilization of plasma membrane, loss of mitochondrial potential, as well as mitochondria and nuclei swelling. Additionally, it was shown that 3Cpro-induced cell death was efficiently blocked by ferroptosis inhibitors and was accompanied by intense lipid peroxidation. Taken together, these results indicate that 3Cpro induces ferroptosis upon its individual expression in human cells. This is the first demonstration that a proteolytic enzyme can induce ferroptosis, the recently discovered and actively studied type of RCD.
  • 776
  • 22 Sep 2021
Topic Review
Sublethal Cell Death Signaling
An important role of cell death pathways is to protect tissues and minimize disease by limiting the transference of potentially oncogenic mutations to daughter clones. However, there is increasing evidence demonstrating that activation of sublethal cell death signaling pathways, in particular apoptotic signaling, in the absence of direct DNA damaging stimuli, can promote genomic instability in cells that fail to die. This may increase the risk of the formation of subsequent neoplasms. Apoptosis-mediated mutagenesis occurs indirectly via sublethal activation of caspases and apoptotic nucleases (specifically CAD). On the other hand, cells surviving sublethal necroptotic signaling did not acquire mutations, most likely due to caspase-independent pathways, although the possibility of mutagenesis under conditions of oxidative stress are still elusive. It may therefore be possible for necroptosis-inducing anti-cancer drugs to be less likely than apoptosis-inducing or DNA damaging drugs to trigger therapy-related cancers.
  • 776
  • 12 Jul 2021
Topic Review
Age-Related Alterations at Neuromuscular Junction
With advancing aging, a decline in physical abilities occurs, leading to reduced mobility and loss of independence. Although many factors contribute to the physio-pathological effects of aging, an important event seems to be related to the compromised integrity of the neuromuscular system, which connects the brain and skeletal muscles via motoneurons and the neuromuscular junctions (NMJs). NMJs undergo severe functional, morphological, and molecular alterations during aging and ultimately degenerate. The effect of this decline is an inexorable decrease in skeletal muscle mass and strength, a condition generally known as sarcopenia. Moreover, several studies have highlighted how the age-related alteration of reactive oxygen species (ROS) homeostasis can contribute to changes in the neuromuscular junction morphology and stability, leading to the reduction in fiber number and innervation. Increasing evidence supports the involvement of epigenetic modifications in age-dependent alterations of the NMJ. In particular, DNA methylation, histone modifications, and miRNA-dependent gene expression represent the major epigenetic mechanisms that play a crucial role in NMJ remodeling. It is established that environmental and lifestyle factors, such as physical exercise and nutrition that are susceptible to change during aging, can modulate epigenetic phenomena and attenuate the age-related NMJs changes.
  • 771
  • 15 Jun 2021
Topic Review
Selenomethionine
Selenium is an essential trace element. Although this chalcogen forms a wide variety of compounds, there are surprisingly few small-molecule organic selenium compounds (OSeCs) in biology. Besides its more prominent relative selenocysteine (SeCys), the amino acid selenomethionine (SeMet) is one example. SeMet is synthesized in plants and some fungi and, via nutrition, finds its way into mammalian cells. In contrast to its sulfur analog methionine (Met), SeMet is extraordinarily redox active under physiological conditions and via its catalytic selenide (RSeR’)/selenoxide (RSe(O)R’) couple provides protection against reactive oxygen species (ROS) and other possibly harmful oxidants. In contrast to SeCys, which is incorporated via an eloquent ribosomal mechanism, SeMet can enter such biomolecules by simply replacing proteinogenic Met. Interestingly, eukaryotes, such as yeast and mammals, also metabolize SeMet to a small family of reactive selenium species (RSeS). Together, SeMet, proteins containing SeMet and metabolites of SeMet form a powerful triad of redox-active metabolites with a plethora of biological implications. In any case, SeMet and its family of natural RSeS provide plenty of opportunities for studies in the fields of nutrition, aging, health and redox biology. 
  • 771
  • 23 Jun 2021
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