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Topic Review
REST/NRSF in Health and Disease
Chromatin modifications play a crucial role in the regulation of gene expression. The repressor element-1 (RE1) silencing transcription factor (REST), also known as neuron-restrictive silencer factor (NRSF) and X2 box repressor (XBR), was found to regulate gene transcription by binding to chromatin and recruiting chromatin-modifying enzymes. Earlier studies revealed that REST plays an important role in the development and disease of the nervous system, mainly by repressing the transcription of neuron-specific genes. Subsequently, REST was found to be critical in other tissues, such as the heart, pancreas, skin, eye, and vascular. Dysregulation of REST was also found in nervous and non-nervous system cancers. In parallel, multiple strategies to target REST have been developed. 
  • 824
  • 13 Nov 2023
Topic Review
Lin28/let-7 Axis
An RNA-binding protein, Lin28, in regulating cancer cell stemness to drive tumour progression. Lin28 blocks the synthesis of let-7, a tumour-suppressor microRNA, and acts as a global regulator of cell differentiation and proliferation. Lin28also targets messenger RNAs and regulates protein translation. 
  • 824
  • 13 Oct 2022
Topic Review
ALS2-Related Motor Neuron Diseases
Mutations of the ALS2 gene, which encodes for the protein Alsin, are linked to three recessive motor neuron diseases characterized by early onset. Alsin is an intriguing protein characterized by several structured domains with distinct functions. 
  • 823
  • 20 Jan 2022
Topic Review
Insights into N-Glycanase 1
The cytosolic PNGase (peptide:N-glycanase), also known as peptide-N4-(N-acetyl-β-glucosaminyl)-asparagine amidase, is a well-conserved deglycosylation enzyme (EC 3.5.1.52) which catalyzes the non-lysosomal hydrolysis of an N(4)-(acetyl-β-d-glucosaminyl) asparagine residue (Asn, N) into a N-acetyl-β-d-glucosaminyl-amine and a peptide containing an aspartate residue (Asp, D). This enzyme (NGLY1) plays an essential role in the clearance of misfolded or unassembled glycoproteins through a process named ER-associated degradation (ERAD). Accumulating evidence also points out that NGLY1 deficiency can cause an autosomal recessive (AR) human genetic disorder associated with abnormal development and congenital disorder of deglycosylation.
  • 822
  • 20 Jun 2022
Topic Review
SLO3
Sperm cells must undergo a complex maturation process after ejaculation to be able to fertilize an egg. One component of this maturation is hyperpolarization of the membrane potential to a more negative value. The ion channel responsible for this hyperpolarization, SLO3, was first cloned in 1998, and since then much progress has been made to determine how the channel is regulated and how its function intertwines with various signaling pathways involved in sperm maturation. 
  • 822
  • 17 Jul 2023
Topic Review
Biochemical Mechanisms Associating Alcohol Use Disorders with Cancers
Of all yearly deaths attributable to alcohol consumption globally, approximately 12% are due to cancers, representing approximately 0.4 million deceased individuals. Ethanol metabolism disturbs cell biochemistry by targeting the structure and function of essential biomolecules (proteins, nucleic acids, and lipids) and by provoking alterations in cell programming that lead to cancer development and cancer malignancy. 
  • 822
  • 25 Jul 2023
Topic Review
Poly(ADP-ribose) Polymerase 1
Poly(ADP-ribose) (PAR) Polymerase 1 (PARP-1), also known as ADP-ribosyl transferase with diphtheria toxin homology 1 (ARTD-1), is a critical player in DNA damage repair, during which it catalyzes the ADP ribosylation of self and target enzymes. While the nuclear localization of PARP-1 has been well established, recent studies also suggest its mitochondrial localization.
  • 822
  • 28 Aug 2023
Topic Review
Transcription Factor 21 and Chicken Adipocyte Differentiation
Transcription factor 21 (TCF21) could promote chicken preadipocytes differentiation at least in part via activating MAPK/JNK pathway. 
  • 821
  • 21 Dec 2021
Topic Review
Hydrogen Sulfide as a Regulator of Autophagy
The term “autophagy”, (from the Greek words auto, meaning “self” and phagein, meaning “to eat”)—literally, eating one’s self—was first created by Christian de Duve over 40 years ago, who discovered lysosomes and provided clear proof of their participation in this process. It is an evolutionarily conserved process of degradation and recycling in eukaryotic organisms. H2S is already considered a physiological mediator involved in many physiological and pathological processes in animals and plants, including autophagy.
  • 821
  • 11 Apr 2022
Topic Review
Carbon-Supported Noble-Metal Nanoparticles
Noble-metal nanoparticles (NMNPs), with their outstanding properties, have been arousing the interest of scientists for centuries. Although our knowledge of them is much more significant today, and people can obtain NMNPs in various sizes, shapes, and compositions, our interest in them has not waned. When talking about noble metals, gold, silver, and platinum come to mind first. Still, people cannot forget about elements belonging to the so-called platinum group, such as ruthenium, rhodium, palladium, osmium, and iridium, whose physical and chemical properties are very similar to those of platinum. It makes them highly demanded and widely used in various applications. The current knowledge on the preparation of all noble metals is presented in the form of nanoparticles and their assembling with carbon supports.
  • 821
  • 27 Sep 2023
Topic Review
TNFα
About 60 years ago, it was reported that bacterial endotoxin administration to mice resulted in the release of a serological protein with necrotic anti-tumor activity at high concentrations. Due to the latter characteristic, this protein was termed tumor necrosis factor (TNF)  and considered a breakthrough for cancer therapy. Today, the TNF superfamily consists of 19 members and 29 TNF receptors .Within this family, functional TNFα is represented by a trimer of 17.35 kDa monomers, folded into a rigid bell-shaped “jelly roll” composed of antiparallel filaments. It exists in two forms: a transmembrane form (tmTNFα) next to a soluble (sTNFα) form. The latter one is cleaved from tmTNFα by the metalloproteinase TNF-alpha-converting enzyme (TACE).
  • 820
  • 18 Aug 2021
Topic Review
Proto-Oncogene ETS-Related Gene in Prostate Cancer
The ETS-related gene (ERG) is proto-oncogene that is classified as a member of the ETS transcription factor family, which has been found to be consistently overexpressed in about half of the patients with clinically significant prostate cancer (PCa). The overexpression of ERG can mostly be attributed to the fusion of the ERG and transmembrane serine protease 2 (TMPRSS2) genes, and this fusion is represented about 85% of all gene fusions observed in prostate cancer. Clinically, individuals with ERG gene fusion are mostly documented to have advanced tumor stages, increased mortality, and higher rates of metastasis in non-surgical cohorts.
  • 820
  • 13 May 2022
Topic Review
Non-Alcoholic Steatohepatitis and Organokines
Non-alcoholic steatohepatitis (NASH) is characterized by steatosis, lobular inflammation, and enlargement of the diameter of hepatocytes (ballooning hepatocytes), with or without fibrosis. It affects 20% of patients with non-alcoholic fatty liver disease (NAFLD). Due to liver dysfunction and the numerous metabolic changes that commonly accompany the condition (obesity, insulin resistance, type 2 diabetes, and metabolic syndrome), the secretion of organokines is modified, which may contribute to the pathogenesis or progression of the disease. 
  • 820
  • 23 Jul 2023
Topic Review
Protein Ser/Thr Phosphatase Folding
Post-translational modification (PTM) is a key mechanism providing the functional diversity of proteins in cellular signaling and physiology and changing the functions or stability of proteins. 
  • 820
  • 25 Jul 2023
Topic Review
Alzheimer’s Disease and Choroid Plexus
The choroid plexus (CP), located in each of the four ventricles of the brain, is formed by a monolayer of epithelial cells that surrounds a highly vascularized connective tissue with permeable capillaries. These cells are joined by tight junctions forming the blood–cerebrospinal fluid barrier (BCSFB), which strictly regulates the exchange of substances between the blood and cerebrospinal fluid (CSF). 
  • 819
  • 29 Jan 2022
Topic Review
Tetraoctylammonium
Alkylammonium salts have been used extensively to study the structure and function of potassium channels. Here, we use the long-chain, hydrophobic tetraoctylammonium (TOA+) to shed light on the structure of the inactivated state of KcsA, a tetrameric prokaryotic potassium channel. By the combined use of a thermal denaturation assay and the analysis of homo-Förster resonance energy transfer in a mutant channel containing a single tryptophan (W67) per subunit, we found that TOA+ binds the channel cavity with high affinity, either with the inner gate open or closed. Moreover, bound TOA+ induces a decrease in the affinity for K+ in the two characteristic K+ binding events to the channel selectivity filter at pH 7.0, when the channel inner gate is in the closed conformation. This is similar to that observed in the absence of TOA+ upon acidic-pH-induced channel inactivation. Therefore, this suggests that TOA+ binding by itself causes inactivation at pH 7.0 when the inner gate is closed. Furthermore, in apparent agreement with such conclusion, the presence of bound TOA+ in the pH 4.0 samples has only modest effects on the affinity of the two binding events for K+, likely because the channel is already inactivated. Finally, we also observed that TOA+ bound at the cavity, allosterically modifies the conformation of the pore helices, leading to longer W67-W67 intersubunit distances at any K+ concentration and both at pH 7.0 and pH 4.0. The changes in the pore helix conformation, along with the decreased affinity for K+ at pH 7.0 caused by TOA+, seen in both homo-FRET and thermal denaturation experiments, are very similar to those effects caused by inactivation at pH 4.0.
  • 818
  • 30 Apr 2021
Topic Review
STAMP2 in Diabetes, Inflammatory Diseases and Cancers
STAMP2 plays a pivotal role in the pathogenesis of  type II diabetes, inflammation and cancers. The six transmembrane protein of prostate 2 (STAMP2), a metalloreductase involved in iron and copper homeostasis, is well known for its critical role in the coordination of glucose/lipid metabolism and inflammation in metabolic tissues. STAMP2 is a critical modulator for coordinating metabolism and inflammation. Although STAMP2 has been widely studied focusing on the inhibitory role in inflammation and metabolism, the underlying mechanism is not fully understood. In addition to its role in metabolism and inflammation, STAMP2 is also associated with tumorigenesis. For example, STAMP2 overexpression may increase ROS, which may contribute to increased mutational rates and further progression of prostate cancer.
  • 817
  • 02 Sep 2022
Topic Review
Biological Roles of miR-199a in Lung Cancer
Lung cancer is the leading cause of cancer death worldwide. miR-199a, which has two mature molecules: miR-199a-3p and miR-199a-5p, plays an important biological role in the genesis and development of tumors. There has been increasing evidence that the aberrant expression of miR-199a is closely related to lung cancer, affecting its proliferation, apoptosis, autophagy, glucose metabolism, etc.
  • 817
  • 16 Sep 2022
Topic Review
Novel Therapies for T1D
It is well established that genetic and environmental factors contribute to the initiation and progression of type 1 diabetes, but recent studies show that epigenetic modifications are also important.  Key epigenetic modifications associated with type 1 diabetes pathogenesis and the ways to harness epigenetic mechanisms to prevent, reverse, or manage T1D have been discussed in details. 
  • 816
  • 20 Nov 2020
Topic Review
Chronic Muscle Disuse
Periods of muscle disuse promote diminished muscle quality along with muscle atrophy that is characterized by reductions in muscle fiber cross-sectional area (CSA). Skeletal muscle disuse may be brought about by chronic sedentarism, periods of immobilization due to injury, bed rest as result of illness, or even exposure to microgravity. Such inactivity elicits functional and metabolic derangements in the affected tissue including marked mitochondrial alterations that contribute to the impaired metabolic health and degree of atrophy in the muscle. These impairments within the tissue prompt a net increase in catabolic processes in conjunction with reductions in skeletal muscle protein synthesis. Skeletal muscle mitochondrial decline and atrophy are underlying features of many diseases and they exacerbate disease progression and reduced mobility with aging. Thus, understanding the molecular underpinnings of muscle mitochondrial deficits with prolonged inactivity is of considerable interest.
  • 816
  • 21 May 2021
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