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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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The Equilibrium Binding Constant and Binding Strength02:18

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The equilibrium binding constant (Kb) quantifies the strength of a protein-ligand interaction. Kb can be calculated as follows when the reaction is at equilibrium:
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Drug binding to proteins is a key aspect of pharmacokinetics and can influence a drug's distribution, absorption, and elimination in the body. Several factors, including the drug's physiochemical properties, protein concentration, disease states, and the number of binding sites on the protein, influence this process.
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Drugs predominantly attach to plasma proteins, with only a small percentage remaining unbound. The unbound portion can be calculated as one minus the bound fraction. Acidic drugs form large, inactive complexes by reversibly binding to plasma albumin, which prevents them from diffusing across biological barriers. These drug-protein complexes act as reservoirs for the drugs. As the concentration of unbound drugs decreases, these complexes quickly dissociate to release the free drug, maintaining...
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Protein-Drug Binding: Determination Methods01:22

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Determining protein-drug binding can be achieved through indirect and direct methods, each providing valuable insights into the interaction between proteins and drugs.
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Single-Strand DNA Binding Proteins01:03

Single-Strand DNA Binding Proteins

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For successful DNA replication, the unwinding of double-stranded DNA must be accompanied by stabilization and protection of the separated single strands of the DNA. This crucial task is performed by single-strand DNA-binding (SSB) proteins. They bind to the DNA in a sequence-independent manner, which means that the nitrogenous bases of the DNA need not be present in a specific order for binding of SSB proteins to it. The binding of SSB proteins straightens single-stranded DNA (ssDNA) and makes...
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Techniques to Induce and Quantify Cellular Senescence
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IGF Binding Protein-5 Induces Cell Senescence.

Fumihiro Sanada1, Yoshiaki Taniyama1,2, Jun Muratsu1,2

  • 1Department of Clinical Gene Therapy, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Frontiers in Endocrinology
|March 9, 2018
PubMed
Summary

Insulin-like growth factor-binding protein-5 (IGFBP-5) drives cellular senescence and inflammation. This protein is upregulated during aging, impacting organ function and potentially linking to age-related hyper-coagulation.

Keywords:
IGF binding protein-5age-related diseasecell senescencecoagulation systeminflammation

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Area of Science:

  • Gerontology
  • Cell Biology
  • Molecular Biology

Background:

  • Cellular senescence is a key driver of organismal aging and organ dysfunction.
  • Senescence involves irreversible growth arrest, often triggered by telomere shortening or stress.
  • Senescent cells are linked to age-related inflammation and hyper-coagulation.

Purpose of the Study:

  • To review the role of Insulin-like Growth Factor-binding Protein-5 (IGFBP-5) in cellular senescence and inflammation.
  • To highlight the upregulation of IGFBP-5 during senescence, mediated by the tumor suppressor p53.
  • To explore the implications of IGFBP-5 in age-related conditions.

Main Methods:

  • Review of existing literature on cellular senescence and IGFBP-5.
  • Analysis of studies demonstrating IGFBP-5 upregulation in various senescence models.
  • Examination of the link between IGFBP-5, inflammation, and coagulation.

Main Results:

  • IGFBP-5 is upregulated during cellular senescence, induced by p53.
  • This upregulation mediates premature senescence in fibroblasts and endothelial cells (ECs).
  • IGFBP-5 is implicated in age-related inflammation and hyper-coagulation.

Conclusions:

  • IGFBP-5 plays a critical role in regulating cellular senescence and inflammation.
  • The protein's involvement in senescence is independent of IGF-I and IGF-II.
  • IGFBP-5 represents a potential therapeutic target for age-related diseases.