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Related Concept Videos

Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Cell Polarization by Rho Proteins01:21

Cell Polarization by Rho Proteins

Cell polarity is the asymmetric distribution of cellular and membrane components, making one side of the cell different from the other. This polarity is essential to many processes such as embryogenesis, axon migration, glucose transport across epithelial cells, and directional cell migration. A migrating cell responds to intracellular or extracellular signals via molecular cascades that reorganize the actin cytoskeleton to establish this polarity. In these cells, the Rho family proteins Cdc42,...
Rab Cascades01:25

Rab Cascades

Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.

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Related Experiment Video

Updated: May 28, 2026

RhoC GTPase Activation Assay
09:58

RhoC GTPase Activation Assay

Published on: August 22, 2010

High glucose-induced RhoA activation requires caveolae and PKCβ1-mediated ROS generation.

Y Zhang1, F Peng, B Gao

  • 1Division of Nephrology, McMaster University, Hamilton, Ontario, Canada.

American Journal of Physiology. Renal Physiology
|October 7, 2011
PubMed
Summary
This summary is machine-generated.

High glucose activates RhoA in kidney cells via PKCβ and reactive oxygen species (ROS) within caveolae, leading to matrix buildup in diabetic nephropathy.

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RhoC GTPase Activation Assay
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07:33

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS

Published on: December 21, 2011

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Diabetic nephropathy is characterized by glomerular matrix accumulation.
  • Previous research linked high glucose-induced RhoA activation in mesangial cells (MC) to matrix upregulation.

Purpose of the Study:

  • To elucidate the mechanism of RhoA activation by high glucose in MC.
  • To investigate the roles of protein kinase C beta (PKCβ), reactive oxygen species (ROS), and caveolae in this process.

Main Methods:

  • Utilized primary rat MC and caveolin-1 knockout cells.
  • Employed PKC inhibitors, small interfering RNA (siRNA) for PKCβ, ROS scavengers (N-acetylcysteine), NADPH oxidase inhibitors (apocynin, DPI), and chemical disruption of caveolae.
  • Assessed RhoA, PKCβ1, ROS generation, activator protein-1 (AP-1) activation, and transforming growth factor-β1 (TGF-β1) upregulation.

Main Results:

  • Glucose-induced RhoA activation required glucose metabolism and was blocked by PKCβ inhibition.
  • PKCβ inhibition abrogated ROS generation, which was prevented by ROS scavengers and NADPH oxidase inhibitors.
  • RhoA and PKCβ1 activation, ROS generation, and downstream AP-1 and TGF-β1 upregulation were dependent on caveolae and caveolin-1.
  • These effects were absent in caveolin-1 knockout cells and rescued by reexpression.

Conclusions:

  • High glucose activates RhoA in MC through a pathway involving PKCβ1-induced ROS generation, likely via NADPH oxidase.
  • Caveolae are essential for PKCβ1 activation and subsequent signaling, including AP-1 and TGF-β1 upregulation.
  • Caveolae play a critical role in mediating the profibrotic processes in diabetic nephropathy.