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Related Concept Videos

Laminins are the Adhesive Proteins of Basal Lamina00:55

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Laminins are heterotrimeric proteins with high molecular mass found in the extracellular matrix. Each laminin molecule is composed of three chains, viz. alpha, beta, and gamma, coded by five, four, and three paralogous genes, respectively. Laminins are categories based on the compositions of the three chains.
In humans, the five forms of alpha chains are LAMA 1, LAMA 2, LAMA 3, LAMA 4, and LAMA 5. The four forms of beta chains are LAMB 1, LAMB 2, LAMB 3, and LAMB 4. The three forms of gamma...
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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Plakins are large proteins with binding domains for microtubules, microfilaments, intermediate filaments, and membrane-associated protein complexes at cell junctions. Plakin functions are evolutionarily conserved and are primarily involved in organizing the different components of the cytoskeleton by crosslinking them to each other and connecting them to the cell-matrix and cell adhesion complexes. They are also known to interact with signal transducers, serve as scaffolds for signaling...
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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Intracellular Signaling Affects Focal Adhesions01:17

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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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A Link between Replicative Stress, Lamin Proteins, and Inflammation.

Simon Willaume1, Emilie Rass1, Paula Fontanilla-Ramirez1

  • 1Université de Paris and Université Paris-Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité, Génétique Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.

Genes
|April 30, 2021
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Summary

Double-strand breaks (DSB) are toxic DNA lesions. DNA damage accumulation can trigger inflammation, impacting aging and cancer, but new insights offer therapeutic strategies.

Keywords:
DNA replication stressHutchinson-Gilford progeria syndromeagingcGAS-STING pathwaycancerdouble-strand break repairgenome instabilityinflammationlaminssenescence

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Area of Science:

  • Molecular Biology
  • Genetics
  • Immunology

Background:

  • Double-stranded breaks (DSB) are highly toxic DNA lesions arising from endogenous or exogenous sources.
  • Replicative stress, a major driver of genome instability, necessitates complex mechanisms for replication fork restart.
  • Emerging evidence links DNA damage accumulation to inflammation via cytosolic DNA sensing.

Purpose of the Study:

  • To review mechanisms of DSB repair and replicative stress management.
  • To explore the connection between DNA damage, inflammation, and cellular fate.
  • To highlight the role of nuclear envelope components, like lamins, in these processes.

Main Methods:

  • Literature review of DNA repair pathways.
  • Analysis of replication stress response mechanisms.
  • Synthesis of recent findings on DNA damage-induced inflammation.

Main Results:

  • DSB repair and replication fork management are critical for genome integrity.
  • Cytosolic DNA release due to DNA repair or replication defects triggers inflammatory responses.
  • Chronic inflammation from DNA damage contributes to aging and cancer progression.

Conclusions:

  • Understanding DNA damage response, replication stress, and inflammation is key for novel therapies.
  • The nuclear envelope, particularly lamins, plays a newly recognized role in DNA repair, replication stress, and inflammation.
  • Targeting these pathways could offer new treatments for cancer and age-related inflammatory diseases.