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Related Concept Videos

Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
Formation of Muscle Fibers from Myoblasts01:13

Formation of Muscle Fibers from Myoblasts

De novo myogenesis, or the formation of muscle fibers, begins during the early embryonic stages. The skeletal muscle is formed from somites– blocks of embryonic cell layers. The somites are further divided into dermatomes, myotomes, sclerotomes, and syndetomes. Among these, the myotomes give rise to muscle fibers.
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription factors...
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...
Satellite Stem Cells and Muscular Dystrophy01:21

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Differentiation of Common Myeloid Progenitor Cells

Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
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Receptor Downregulation in MVBs

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Related Experiment Video

Updated: Jul 8, 2026

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
14:47

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Published on: May 17, 2016

c-Myb-dependent smooth muscle cell differentiation.

Karolina M Kolodziejska1, M H Noyan-Ashraf, Andras Nagy

  • 1Heart & Stroke Richard Lewar Center of Excellence in Cardiovascular Research, Department of Medicine, University of Toronto, Canada.

Circulation Research
|January 12, 2008
PubMed
Summary
This summary is machine-generated.

The transcription factor c-Myb is crucial for vascular smooth muscle cell (SMC) differentiation. Studies show c-Myb deficiency impairs SMC development from stem cells and in vivo, highlighting its role in vascular health.

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08:28

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Stem Cell Biology

Background:

  • The transcription factor c-Myb is known to influence vascular smooth muscle cell (SMC) proliferation and hematopoiesis.
  • Its specific role in the differentiation and maturation of contractile SMCs has remained largely unexplored.

Purpose of the Study:

  • To investigate the role of c-Myb in the differentiation of vascular smooth muscle cells (SMCs) from embryonic stem cells (ESCs).
  • To determine if c-Myb is essential for the development of contractile SMCs and their contribution to vascular tissues in vivo.

Main Methods:

  • Utilized c-myb(-/-) and wild-type embryonic stem cells (ESCs) to generate embryoid bodies (EBs).
  • Assessed SMC differentiation using quantitative real-time RT-PCR for SMC-specific genes (myocardin, smooth muscle alpha-actin, SM22alpha, smooth muscle myosin heavy chain).
  • Quantified SMC populations via fluorescence-activated cell sorting (FACS) and analyzed in vivo contribution in chimeric embryos.

Main Results:

  • c-myb(-/-) ESCs failed to produce embryoid bodies (EBs) with spontaneously contracting SMCs, while cardiomyocyte differentiation was unaffected.
  • Expression of SMC differentiation markers, including myocardin, smooth muscle alpha-actin, SM22alpha, and smooth muscle myosin heavy chain, was significantly reduced in c-myb(-/-) EBs.
  • In vivo studies demonstrated a reduced contribution of c-myb(-/-) cells to the SMC lineage in chimeric embryos and adult aortas, particularly in the visceral SMC population.

Conclusions:

  • c-Myb is essential for the differentiation of vascular smooth muscle cells (SMCs) from precursor stem cell populations.
  • The absence of c-Myb impairs the development of contractile SMCs and their in vivo contribution to vascular tissues.
  • These findings implicate c-Myb in SMC phenotypic modulation and suggest its potential role in vascular diseases.