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Topic Review
PPARs and Vitamin D Receptor in Cancer
Peroxisome proliferator-activated receptors (PPARs) are members of the superfamily of nuclear hormone receptors, which respond to specific ligands such as polyunsaturated fatty acids by altering gene expression. Three subtypes of this receptor have been discovered, each evolving to achieve different biological functions. Like other nuclear receptors, the transcriptional activity of PPARs is affected not only by ligand-stimulation, but also by cross-talk with other molecules. For example, both PPARs and the RXRs are ligand-activated transcription factors that coordinately regulate gene expression. In addition, PPARs and vitamin D receptor (VDR) signaling pathways regulate a multitude of genes that are of importance for cellular functions including cell proliferation and cell differentiation. Interaction of the PPARs and VDR signaling pathways has been shown at the level of molecular cross-regulation of their transcription factor. A variety of ligands influencing the PPARs and VDR signaling pathways have been shown to reveal chemopreventive potential by mediating tumor suppressive activities in human cancers.
  • 263
  • 08 Sep 2023
Topic Review
Interplay of Kinases Involved in Autisms and ADHD
A brain-enriched multi-domain scaffolding protein, neurobeachin has been identified as a candidate gene for autism patients. Mutations in the synaptic adhesion protein cell adhesion molecule 1 (CADM1) are also associated with autism spectrum disorder, a neurodevelopmental disorder of uncertain molecular origin. Potential roles of neurobeachin and CADM1 have been suggested to a function of vesicle transport in endosomal trafficking. It seems that protein kinase B (AKT) and cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) have key roles in the neuron membrane trafficking involved in the pathogenesis of autism. Attention deficit hyperactivity disorder (ADHD) is documented to dopaminergic insufficiencies, which is attributed to synaptic dysfunction of dopamine transporter (DAT). AKT is also essential for the DAT cell-surface redistribution.
  • 172
  • 08 Sep 2023
Topic Review
BRCA1 and p53 Tumor Suppressor Molecules in AD
Tumor suppressor molecules play a pivotal role in regulating DNA repair, cell proliferation, and cell death, which are also important processes in the pathogenesis of Alzheimer’s disease (AD). Generally, onset of neurodegenerative diseases including Alzheimer’s disease may be delayed with use of dietary neuro-protective agents against oxidative stresses. Studies suggest that dietary antioxidants are also beneficial for brain health in reducing disease-risk and in slowing down disease-progression. 
  • 139
  • 08 Sep 2023
Topic Review
PTEN with DNA Repair in Parkinson’s Disease
Oxidative stress is considered to play key roles in aging and pathogenesis of many neurodegenerative diseases such as Parkinson’s disease, which could bring DNA damage by cells. The DNA damage may lead to the cell apoptosis, which could contribute to the degeneration of neuronal tissues. Evidence suggests that PTEN (phosphatase and tensin homolog on chromosome 10) may be involved in the pathophysiology of the neurodegenerative disorders. Since PTEN expression appears to be one dominant determinant of the neuronal cell death, PTEN should be a potential molecular target of novel therapeutic strategies against Parkinson’s disease. In addition, defects in DNA damage response and DNA repair are often associated with modulation of hormone signaling pathways. Especially, many observations imply a role for estrogen in a regulation of the DNA repair action.
  • 169
  • 08 Sep 2023
Topic Review
PTEN-p53-AKT-MDM2 Loop in Mesenchymal Stem/Stromal Cells Regulation
Mesenchymal stromal/stem cells (MSCs) are multipotent cells that can differentiate to various specialized cells, which have the potential capacity to differentiate properly and accelerate recovery in damaged sites of the body. This stem cell technology has become the fundamental element in regenerative medicine. As reactive oxygen species (ROS) have been reported to adversely influence stem cell properties, it is imperative to attenuate the extent of ROS to the promising protective approach with MSCs’ regenerative therapy. Oxidative stress also affects the culture expansion and longevity of MSCs. Therefore, there is great need to identify a method to prevent oxidative stress and replicative senescence in MSCs. Phosphatase and tensin homologue deleted on chromosome 10/Protein kinase B, PKB (PTEN/AKT) and the tumor suppressor p53 pathway have been proven to play a pivotal role in regulating cell apoptosis by regulating the oxidative stress and/or ROS quenching.
  • 274
  • 08 Sep 2023
Topic Review
ROS and Autophagy in Cisplatin-Induced Acute Kidney Injury
Cisplatin-induced acute kidney injury (AKI) is the main factor restraining the clinical application of cisplatin. As increased levels of reactive oxygen species (ROS) may promote the progression of the injury, the elimination of ROS has been considered as an effective method to prevent the cisplatin-induced AKI. In addition, it has been revealed that an inducer of autophagy could protect kidney cells in the autophagy dependent manner. Induction of autophagy could also modulate the production of ROS in cases of renal injury.
  • 176
  • 08 Sep 2023
Topic Review
APRO Family Proteins in Cancer Invasiveness
The APRO family members may be involved in the regulation of cell growth, migration, and/or invasion. Although an APRO protein could suppress the invasiveness of several cancer cells, it has been reported that overexpression of the same APRO protein could also promote the invasiveness and/or metastasis of the same cancer cells. In general, the invasiveness of cancer cells might be associated with the function of matrix metalloproteinases (MMPs) as well as with the function of certain exosomes. However, it has been shown that exosomes involving particular APRO proteins, MMPs, and/or microRNA could contribute to the regulation of invasiveness.
  • 187
  • 08 Sep 2023
Topic Review
Animal Models of Rheumatoid Arthritis
Rheumatoid arthritis (RA), a global health concern affecting millions, has prompted extensive research using animal models to develop effective treatments. Among these models, Adjuvant-Induced Arthritis (AIA) and Pristane-Induced Arthritis (PIA) have gained prominence. In part 2 of this series, the unique features, advantages, and limitations of AIA and PIA  were described. These models provide valuable insights into RA but also have specific constraints. By understanding their characteristics and drawbacks, their crucial role in advancing RA research and facilitating the discovery of novel therapies for this debilitating autoimmune disorder were emphasizes, which continues to challenge healthcare worldwide.
  • 215
  • 08 Sep 2023
Topic Review
Animal Models of Arthritis
This entry explores several animal models utilized in rheumatoid arthritis (RA) research. Streptococcal Cell Wall-Induced Arthritis (SCWIA) closely resembles human RA and reveals insights into the pathogenicity of bacterial cell wall components. Collagen-Induced Arthritis (CIA) replicates RA in clinical and immunological aspects, with a focus on B cell involvement. Collagen Antibody-Induced Arthritis (CAIA) offers a rapid model for understanding antibody-mediated mechanisms. Proteoglycan-Induced Arthritis (PGIA) in BALB/c mice mimics human RA, providing genetic and immunological insights unique to this model. Adjuvant-Induced Arthritis (AIA) mirrors RA's clinical and serological aspects, albeit with variability in disease intensity. Pristane-Induced Arthritis (PIA) highlights the role of environmental triggers in chronic inflammation. Collectively, these models advance our comprehension of RA, facilitating research into its pathogenesis, immune responses, and potential therapies.
  • 270
  • 08 Sep 2023
Topic Review
Inflammation
Inflammation, a vital and intricately regulated biological response, defends the body against threats like pathogens and injuries. When balanced, it supports health, but disruption can lead to chronic inflammation and diseases like cardiovascular issues and cancer. This exploration delves into inflammation's mechanisms, involving lipid-derived mediators, proinflammatory cytokines, vasoactive mediators, hydrolytic enzymes, reactive oxygen species, transcription factors, and the complement system. Understanding these elements is crucial for targeted therapies against inflammation-related diseases. Researchers continually uncover innovative strategies to restore the balance between protective and pathological inflammation, offering hope to millions with chronic inflammatory conditions. Advancements promise more effective management, a brighter future, and improved lives.
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  • 08 Sep 2023
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