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Topic Review
NLRP3
The NLRP3 inflammasome (NOD-, LRR-, and pyrin domain-containing protein 3) is an intracellular, multiprotein signalling complex implicated in a plethora of inflammatory diseases. These integral elements include the sensor NLRP3 protein, an adaptor protein called adaptor molecule apoptosis-associated speck-like protein containing a CARD (ASC) and procaspase-1. The sensor NLRP3 protein can be triggered by PAMPs, DAMPs, and a range of diverse external stimuli such as infection and injury.
  • 873
  • 03 Nov 2021
Topic Review
Heat Shock Proteins in Colorectal Carcinoma
Cancer cells can reprogram their metabolic activities and undergo uncontrolled proliferation by utilizing the power of heat shock proteins (HSPs). HSPs are highly conserved chaperones that facilitate the folding of intracellular proteins under stress. Constitutively, HSPs are expressed at low levels, but their expression upregulates in response to a wide variety of insults, including anticancer drugs, allowing cancer cells to develop chemoresistance.
  • 496
  • 01 Nov 2021
Topic Review
Heat Shock Proteins in Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) is a multifactorial human intestinal disease that arises from numerous, yet incompletely defined, factors. Two main forms, Crohn’s disease (CD) and ulcerative colitis (UC), lead to a chronic pathological form. Heat shock proteins (HSPs) are stress-responsive molecules involved in various pathophysiological processes.
  • 704
  • 01 Nov 2021
Topic Review
Dysregulation of miRNA in Leukemia
Micro RNAs (miRNAs) are a class of small non-coding RNAs that have a crucial role in cellular processes such as differentiation, proliferation, migration, and apoptosis. miRNAs may act as oncogenes or tumor suppressors; therefore, they prevent or promote tumorigenesis, and abnormal expression has been reported in many malignancies. The role of miRNA in leukemia pathogenesis is still emerging, but several studies have suggested using miRNA expression profiles as biomarkers for diagnosis, prognosis, and response to therapy in leukemia.
  • 642
  • 29 Oct 2021
Topic Review
Extracellular Vesicles for Diffuse Large B-Cell Lymphoma
The role of extracellular vesicles (EVs) proteome in diffuse large B-cell lymphoma (DLBCL) pathology, subclassification, and patient screening is unexplored. Here, we used an in vitro model of Germinal center B-cell like (GCB - good prognosis) and activated B-cell (ABC - poor prognosis) subtypes to propose potential drug targets and biomarkers. 
  • 429
  • 29 Oct 2021
Topic Review
Post-Ischemic Tau Protein
Recent data suggest that post-ischemic brain neurodegeneration in humans and animals is associated with the modified tau protein in a manner typical of Alzheimer’s disease neuropathology. Pathological changes in the tau protein, at the gene and protein level due to cerebral ischemia, can lead to the development of Alzheimer’s disease-type neuropathology and dementia. Some studies have shown increased tau protein staining and gene expression in neurons following ischemia-reperfusion brain injury. Recent studies have found the tau protein to be associated with oxidative stress, apoptosis, autophagy, excitotoxicity, neuroinflammation, blood-brain barrier permeability, mitochondrial dysfunction, and impaired neuronal function. In this review, we discuss the interrelationship of these phenomena with post-ischemic changes in the tau protein in the brain. The tau protein may be at the intersection of many pathological mechanisms due to severe neuropathological changes in the brain following ischemia. The data indicate that an episode of cerebral ischemia activates the damage and death of neurons in the hippocampus in a tau protein-dependent manner, thus determining a novel and important mechanism for the survival and/or death of neuronal cells following ischemia. In this review, we update our understanding of proteomic and genomic changes in the tau protein in post-ischemic brain injury and present the relationship between the modified tau protein and post-ischemic neuropathology and present a positive correlation between the modified tau protein and a post-ischemic neuropathology that has characteristics of Alzheimer’s disease-type neurodegeneration. 
  • 421
  • 29 Oct 2021
Topic Review
Cofilin Signaling
Three ADF/cofilin family members are expressed in mammals: ADF, cofilin-1, and cofilin-2. The first member ADF (also known as destrin), encoded by the gene DSTN in humans, was initially identified in the chick brain. Cofilin was discovered as an actin-interacting protein in the porcine brain. Later, Ono et al. identified two mammalian variants of cofilin, non-muscle type (also known as cofilin-1 and n-cofilin) and muscle type (also known as cofilin-2 and m-cofilin). In humans, cofilin-1 and cofilin-2 are encoded by the genes CFL1 and CFL2, respectively. Different isoforms of ADF/cofilin have qualitatively similar but quantitatively different effects on actin dynamics. To be noted, both ADF and cofilin show cooperative binding with actin filaments. Interestingly, cofilin-1 comprises almost 90% of the total ADF/cofilin family in CNS. Cofilin can bind to both G-actin and F-actin, exhibiting stronger affinities for the ADP-bound actins than the ATP- or ADP-Pi-bound forms. Cofilin binding to F-actin induces actin subunit rotation, enhances Pi release along the filament, and promotes filament severing in a concentration-dependent manner.
  • 629
  • 28 Oct 2021
Topic Review
Pluripotent Stem Cells
Pluripotent stem cells (PSCs) hold great potential both in studies on developmental biology and clinical practice. Mitochondrial metabolism that encompasses pathways that generate ATP and produce ROS significantly differs between PSCs and somatic cells. Correspondingly, for quite a long time it was believed that the redox homeostasis in PSCs is also highly specific due to the hypoxic niche of their origin – within the pre-implantation blastocyst. However, recent research showed that redox parameters of cultivated PSCs have much in common with that of their differentiated progeny cells. Moreover, it has been proven that similar to somatic cells, maintaining the physiological ROS level is critical for the regulation of PSC identity, proliferation, differentiation, and de-differentiation.
  • 507
  • 28 Oct 2021
Topic Review
Protein Glycosylation
Protein glycosylation is a highly conserved post-translational modification among organisms. It plays fundamental roles in many biological processes, ranging from protein trafficking and cell adhesion to host–pathogen interactions. According to the amino acid side chain atoms to which glycans are linked, protein glycosylation can be divided into two major categories: N-glycosylation and O-glycosylation. However, there are other types of modifications such as the addition of GPI to the C-terminal end of the protein. Besides the importance of glycoproteins in biological functions, they are a major component of the fungal cell wall and plasma membrane and contribute to pathogenicity, virulence, and recognition by the host immunity. Given that this structure is absent in host mammalian cells, it stands as an attractive target for developing selective compounds for the treatment of fungal infections.
  • 1.0K
  • 27 Oct 2021
Topic Review
S100P-Induced Cell Migration and Metastasis
The presence of S100P protein in cancer cells is strongly associated with reduced survival times of patients suffering from a number of cancers. It has been shown previously that S100P is a potent inducer of metastasis in a model system and it is likely that this metastasis-inducing ability underlies its association with reduced patient survival. However, the molecular mechanisms involved in S100P-driven metastasis are only now beginning to be elucidated and the evidence points to S100P enhancing cell migration and cell invasion.  It is now shown that in the same cell system S100P enhances cell migration by two separate mechanisms. One pathway being intracellular, involves changes in the numbers of focal adhesions.  The second pathway occurs at the cell membrane and does not involve changes in the number of focal adhesions, but involves extracellular/membrane bound S100P and is inhibited by specific inhibitors of plasmin. Importantly, mutation of the C-terminal amino acid of S100P, not only abolishes both pathways, but also markedly reduces the metastasis-inducing ability of S100P, thus identifying a possible target for the reduction of S100P-induced metastasis.
  • 437
  • 27 Oct 2021
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