Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...
Type IV Collagen of Basal Lamina01:05

Type IV Collagen of Basal Lamina

Type IV collagen is a 400 nm long, network-forming collagen that acts as a barrier between the epithelial and endothelial cells. Type IV collagen  forms the backbone of the basement membrane by scaffolding with laminin, entactin, proteoglycans, and fibronectin. Apart from rendering structural support to the basement membrane, it also helps entail signaling potentials necessary for both pathological and physiological functions.
A type IV collagen molecule has six alpha chains which can exist in...
Fibril-associated Collagen01:11

Fibril-associated Collagen

Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Glucose Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Bimodality of local structural ordering in extremely confined hard disks.

The Journal of chemical physics·2025
Same author

Measurement of femtosecond incoherent XUV pulses using shot-noise-driven fluctuations in plasma betatron sources.

Physical review. E·2025
Same author

Resiliency of fast-growing and slow-growing genotypes of broiler chickens submitted to different environmental temperatures: growth performance and meat quality.

Poultry science·2024
Same author

The real-world use and effectiveness of avacopan in routine practice for the treatment of ANCA vasculitis. First experiences in Spain.

Rheumatology (Oxford, England)·2024
Same author

Dietary fat content and supplementation with sodium butyrate: effects on growth performance, carcass traits, meat quality, and myopathies in broiler chickens.

Poultry science·2024
Same author

Dietary supplementation with Chlorella vulgaris in broiler chickens submitted to heat-stress: effects on growth performance and meat quality.

Poultry science·2024

Related Experiment Video

Updated: Jun 3, 2026

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
06:39

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

Published on: August 19, 2020

Familial collapsing focal segmental glomerulosclerosis.

V Liakopoulos1, A Huerta, S Cohen

  • 1Departments of Medicine and Division of Nephrology of Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.

Clinical Nephrology
|March 24, 2011
PubMed
Summary
This summary is machine-generated.

Genetic analysis identified a TRPC6 gene defect in one family with collapsing focal segmental glomerular sclerosis (FSGS). However, the other family showed no known inherited podocyte defects, highlighting varied genetic causes for this kidney disease.

Related Experiment Videos

Last Updated: Jun 3, 2026

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
06:39

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

Published on: August 19, 2020

Area of Science:

  • Nephrology
  • Genetics
  • Molecular Biology

Background:

  • Collapsing focal segmental glomerular sclerosis (FSGS) is a severe kidney disease often idiopathic.
  • Genetic causes of FSGS are rarely identified, typically linked to rare syndromes.
  • Understanding the genetic basis of FSGS is crucial for diagnosis and treatment.

Observation:

  • Two families presented with multiple affected members exhibiting collapsing FSGS without secondary causes.
  • Genetic investigations revealed a TRPC6 gene mutation in one family.
  • The second family's FSGS was not explained by known inherited podocyte gene defects.

Findings:

  • Familial collapsing FSGS can arise from distinct genetic underpinnings, including TRPC6 mutations.
  • The absence of known podocyte gene defects in one family suggests novel genetic factors may be involved.
  • Clinical presentation and treatment response varied significantly even within affected families.

Implications:

  • This study expands the known genetic landscape of familial collapsing FSGS.
  • Identifying specific genetic defects may enable tailored therapeutic strategies for FSGS patients.
  • Further research is needed to uncover the genetic basis of FSGS in families without identified mutations.