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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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Nephrotic Syndrome II : Assessment and Medical Management01:26

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IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document...
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Acute Kidney Injury II: Pathophysiology01:29

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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Notch2 activation ameliorates nephrosis.

Eriko Tanaka1, Katsuhiko Asanuma2, Eunhee Kim3

  • 11] Division of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan [2] Department of Pediatrics and Developmental Biology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.

Nature Communications
|February 15, 2014
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Summary

Notch2 activation prevents podocyte loss in kidney disease. Activating Notch2 with antibodies protected damaged podocytes and reduced disease in mice, suggesting a new treatment strategy for nephrosis.

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Immunology

Background:

  • Notch1 and Notch2 signaling are implicated in human glomerular diseases.
  • Podocyte injury and loss are key features of nephrotic syndrome.

Purpose of the Study:

  • To investigate the role of Notch2 in preventing podocyte loss.
  • To evaluate Notch2 activation as a therapeutic strategy for nephrosis and glomerulosclerosis.

Main Methods:

  • Utilized a mouse model of nephrosis and focal segmental glomerulosclerosis.
  • Administered a Notch2 agonistic monoclonal antibody.
  • Performed in vitro podocyte apoptosis assays with Notch2 knockdown and agonistic antibodies.
  • Investigated the involvement of the Akt pathway using triciribine.

Main Results:

  • Notch2 activation prevented podocyte loss and ameliorated proteinuria and glomerulosclerosis in mice.
  • Notch2 knockdown increased apoptosis in damaged podocytes.
  • Notch2 agonistic antibodies protected podocytes by activating the Akt pathway.
  • Akt inhibition abolished the protective effects of Notch2 activation.
  • A positive correlation was observed between activated Notch2 and residual podocytes in human samples.

Conclusions:

  • Specific activation of Notch2 rescues damaged podocytes.
  • Targeting Notch2 activation represents a potential novel clinical strategy for treating nephrosis and glomerulosclerosis.