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

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.7K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.7K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.4K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.4K
The Ras Gene02:38

The Ras Gene

6.2K
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...
6.2K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

5.2K
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...
5.2K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

7.2K
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...
7.2K

You might also read

Related Articles

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

Sort by
Same author

Fusion-positive rhabdomyosarcoma oncofusions share a common interactome.

Nature communications·2026
Same author

Binding orientation of weakly associating membrane peripheral proteins via membrane paramagnetic relaxation enhancement NMR.

Communications chemistry·2026
Same author

NAPRT expression and epigenetic regulation in pediatric rhabdomyosarcoma as a potential biomarker for NAMPT inhibition.

Molecular cancer therapeutics·2026
Same author

Biological Advances and Current Challenges for Pediatric Rhabdomyosarcoma.

Cancers·2026
Same author

Combined Inhibition of HRAS and MEK Induces Tumor Regression and Restores Myogenic Differentiation in HRAS-Mutant Rhabdomyosarcoma.

Cancer research·2026
Same author

Wide Ranging Neurobehavioral Phenotype in Individuals With Costello Syndrome.

American journal of medical genetics. Part A·2026

Related Experiment Video

Updated: Jun 8, 2025

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
11:32

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

6.7K

ASAP1 and ARF1 Regulate Myogenic Differentiation in Rhabdomyosarcoma by Modulating TAZ Activity.

Katie E Hebron1,2,3, Olivia L Perkins2,3,4, Angela Kim1

  • 1Laboratory of Cell and Developmental Signaling, National Cancer Institute, National Institutes of Health, Frederick, Maryland.

Molecular Cancer Research : MCR
|November 4, 2024
PubMed
Summary

ASAP1 and ARF1 are crucial for rhabdomyosarcoma differentiation. Targeting these proteins and WWTR1 (TAZ) may improve differentiation therapy for advanced rhabdomyosarcoma, offering new hope for patients.

More Related Videos

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

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

Published on: May 17, 2016

9.8K
Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas
09:21

Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas

Published on: September 13, 2019

7.1K

Related Experiment Videos

Last Updated: Jun 8, 2025

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
11:32

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

6.7K
Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
14:47

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

Published on: May 17, 2016

9.8K
Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas
09:21

Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas

Published on: September 13, 2019

7.1K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Differentiation

Background:

  • Prognosis for refractory/recurrent rhabdomyosarcoma (RMS) remains poor despite aggressive treatments.
  • Differentiation therapy is a potential strategy for advanced RMS, given its resemblance to muscle precursor cells.
  • MEK1/2 inhibition (MEKi) shows promise in preclinical models but has limited efficacy.

Purpose of the Study:

  • To investigate the molecular mechanisms regulating differentiation in RAS-mutant PAX fusion-negative RMS (FN-RMS).
  • To identify novel therapeutic targets for improving MEKi-induced differentiation in FN-RMS.

Main Methods:

  • Utilized preclinical FN-RMS models.
  • Performed knockdown studies of ASAP1, ARF1, and ARF5.
  • Assessed myogenic transcription factor expression.
  • Analyzed WWTR1 (TAZ) phosphorylation and activity.
  • Investigated the impact of dual knockdown of ASAP1 and WWTR1.

Main Results:

  • ASAP1, ARF1, and ARF5 are necessary for FN-RMS differentiation.
  • Loss of ASAP1 or ARF1/ARF5 inhibits myogenic transcription factor expression.
  • MEKi induces WWTR1 (TAZ) inactivation, which is blocked by ASAP1/ARF1 loss.
  • Dual knockdown of ASAP1 and WWTR1 rescued MEKi-induced differentiation.

Conclusions:

  • ASAP1 and ARF1 are essential regulators of MEKi-induced myogenic differentiation in FN-RMS.
  • The ASAP1-ARF pathway modulates WWTR1 (TAZ) activity, impacting differentiation.
  • Targeting YAP1/TAZ signaling in conjunction with ASAP1/ARF1 modulation presents a promising strategy for FN-RMS differentiation therapy.