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

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:
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

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 hydroxylase and factor...
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,...
Role of Matrix Metalloproteases in Degradation of ECM01:23

Role of Matrix Metalloproteases in Degradation of ECM

Matrix metalloproteases (MMPs) are enzymes involved in the hydrolysis of proteins and glycoproteins of the extracellular matrix. MMPs are essential for the migration and proliferation of cells through the dense matrix network, throughout embryonic development, and throughout morphogenesis. The first MMP activity discovered was a collagenase in a tadpole's tail undergoing metamorphosis. The active collagen deposition and modifications lead to the morphogenesis of tadpoles into the adult body.
A...
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...

You might also read

Related Articles

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

Sort by
Same author

Novel anticoagulant-preservative solution maintained the hemostatic function of cold stored whole blood for 56 days.

Transfusion·2025
Same author

Nuclear Vav3 is required for polycomb repression complex-1 activity in B-cell lymphoblastic leukemogenesis.

Nature communications·2022
Same author

The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors.

Nature communications·2019
Same author

Red blood cell concentrates treated with the amustaline (S-303) pathogen reduction system and stored for 35 days retain post-transfusion viability: results of a two-centre study.

Vox sanguinis·2017
Same author

The DEK oncogene promotes cellular proliferation through paracrine Wnt signaling in Ron receptor-positive breast cancers.

Oncogene·2014
Same author

Klf5 controls bone marrow homing of stem cells and progenitors through Rab5-mediated β1/β2-integrin trafficking.

Nature communications·2013

Related Experiment Video

Updated: May 12, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

p190-B RhoGAP regulates the functional composition of the mesenchymal microenvironment.

R Raman1, R S Kumar, A Hinge

  • 1Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH, USA.

Leukemia
|April 9, 2013
PubMed
Summary

Deletion of p190-B GTPase-activating protein (p190-B) in mice leads to hematopoietic failure by disrupting the bone marrow microenvironment. This highlights p190-B

More Related Videos

TGF-β-mediated Endothelial to Mesenchymal Transition (EndMT) and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing
07:05

TGF-β-mediated Endothelial to Mesenchymal Transition (EndMT) and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Related Experiment Videos

Last Updated: May 12, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

TGF-β-mediated Endothelial to Mesenchymal Transition (EndMT) and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing
07:05

TGF-β-mediated Endothelial to Mesenchymal Transition (EndMT) and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Area of Science:

  • * Hematology
  • * Developmental Biology
  • * Stem Cell Biology

Background:

  • * Hematopoiesis, the process of blood cell formation, is critically dependent on the bone marrow (BM) microenvironment, also known as the niche.
  • * The mesenchymal stem cell (MSC) compartment within the BM niche plays a crucial role in regulating hematopoietic stem and progenitor cell function.
  • * Understanding the molecular mechanisms that govern the interplay between MSCs and hematopoietic cells is essential for comprehending normal blood development and identifying causes of hematopoietic failure.

Purpose of the Study:

  • * To investigate the role of p190-B GTPase-activating protein (p190-B) in regulating the hematopoietic microenvironment and its impact on hematopoiesis.
  • * To determine whether p190-B deficiency affects hematopoietic stem cells directly or influences the supportive capacity of the niche.
  • * To elucidate the cellular and molecular mechanisms by which p190-B loss impairs the BM niche and consequently affects hematopoiesis.

Main Methods:

  • * Generation and analysis of p190-B knockout (p190-B(-/-)) and heterozygous (p190-B(+/-)) mice to assess hematopoietic function.
  • * Transplantation assays using p190-B(-/-) hematopoietic cells into wild-type (WT) hosts to evaluate cell-autonomous versus non-cell-autonomous effects.
  • * Coculture experiments involving WT bone marrow (BM) cells and p190-B(-/-) mesenchymal stem cells (MSCs) to assess MSC function.
  • * Analysis of BM niche composition, including colony-forming unit (CFU) assays for fibroblasts, adipocytes, and osteoblasts.
  • * Examination of MSC lineage fate specification towards osteoblast and adipocyte lineages.

Main Results:

  • * p190-B deletion in mice results in significant hematopoietic failure during ontogeny and in adult stages, affecting fetal liver, bone, spleen, and BM.
  • * Hematopoietic defects are non-cell autonomous, as p190-B(-/-) hematopoietic cells exhibit normal hematopoiesis when transplanted into WT hosts.
  • * p190-B(-/-) MSCs are functionally impaired in supporting hematopoiesis due to defective Wnt signaling.
  • * Loss of p190-B leads to altered BM niche composition, characterized by abnormal numbers of CFU-fibroblast, CFU-adipocyte, and CFU-osteoblast.
  • * MSCs lacking p190-B show aberrant lineage fate specification towards osteoblast and adipocyte differentiation.

Conclusions:

  • * p190-B is essential for maintaining a functional mesenchymal microenvironment that supports normal hematopoiesis during development.
  • * p190-B regulates MSC lineage fate and signaling pathways, including Wnt signaling, which are critical for niche integrity.
  • * The study identifies p190-B as a key regulator of the bone marrow niche, whose dysfunction leads to hematopoietic failure.