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

Nucleosome Remodeling02:54

Nucleosome Remodeling

Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
Cell Motility through Blebbing01:16

Cell Motility through Blebbing

Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
Blebbing Through the Matrix
In multicellular...
Cytoskeletal Coordination in Cell Migration01:32

Cytoskeletal Coordination in Cell Migration

A migrating cell changes its shape during the cyclic events of attachment and detachment from the substratum and repositions the cell organelles correspondingly. These complex events are orchestrated by the dynamic cytoskeletal network comprising actin filaments, intermediate filaments, and microtubules. Cytoskeletal crosstalk — the direct and indirect communication between the different components — is crucial for this coordination. Direct communication involves various linker proteins that...

You might also read

Related Articles

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

Sort by
Same author

Editorial Expression of Concern: Discovery of a BTK/MNK dual inhibitor for lymphoma and leukemia.

Leukemia·2026
Same author

Distinct alterations in probabilistic reversal learning across at-risk mental state, first episode psychosis and persistent schizophrenia.

Scientific reports·2024
Same author

Correction: Precision weighting of cortical unsigned prediction error signals benefits learning, is mediated by dopamine, and is impaired in psychosis.

Molecular psychiatry·2020
Same author

Precision weighting of cortical unsigned prediction error signals benefits learning, is mediated by dopamine, and is impaired in psychosis.

Molecular psychiatry·2020
Same author

Correction: AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL.

British journal of cancer·2019
Same author

Discovery of a highly potent FLT3 kinase inhibitor for FLT3-ITD-positive AML.

Leukemia·2016
Same journal

Extracellular matrix reprogramming by the YAP/TAZ- TGF-ß2 axis drives immune exclusion in cholangiocarcinoma models.

The Journal of clinical investigation·2026
Same journal

Tumor cell-derived extracellular vesicles foster the immunosuppressive landscape of pancreatic cancer.

The Journal of clinical investigation·2026
Same journal

Julie Zikherman receives the ASCI/Marian W. Ropes, MD, Award.

The Journal of clinical investigation·2026
Same journal

Targeted degradation of MDM2 overcomes feedback regulation of p53 signaling in Merkel cell carcinoma models.

The Journal of clinical investigation·2026
Same journal

SGLT2 inhibitors enhance ketogenesis by acting as allosteric activators of the mitochondrial enzyme HMGCS2.

The Journal of clinical investigation·2026
Same journal

MDM2 degraders for Merkel cell carcinoma: round peg in a round hole.

The Journal of clinical investigation·2026
See all related articles

Related Experiment Video

Updated: May 7, 2026

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
10:27

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

BCR/ABL induces multiple abnormalities of cytoskeletal function

R Salgia1, J L Li, D S Ewaniuk

  • 1Division of Hematologic Malignancies, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA. Ravi_Salgia@dfci.harvard.edu

The Journal of Clinical Investigation
|July 1, 1997
PubMed
Summary
This summary is machine-generated.

The BCR/ABL oncogene drives chronic myelogenous leukemia (CML) by increasing hematopoietic cell motility and altering cytoskeletal function. Alpha-interferon treatment partially reverses these abnormal cell motility defects.

More Related Videos

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
10:54

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations

Published on: September 17, 2012

In Vivo Modeling of the Morbid Human Genome using Danio rerio
12:31

In Vivo Modeling of the Morbid Human Genome using Danio rerio

Published on: August 24, 2013

Related Experiment Videos

Last Updated: May 7, 2026

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
10:27

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
10:54

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations

Published on: September 17, 2012

In Vivo Modeling of the Morbid Human Genome using Danio rerio
12:31

In Vivo Modeling of the Morbid Human Genome using Danio rerio

Published on: August 24, 2013

Area of Science:

  • Hematology
  • Cell Biology
  • Oncology

Background:

  • The BCR/ABL oncogene is the primary driver of human chronic myelogenous leukemia (CML).
  • BCR/ABL transforms hematopoietic cells, leading to cytokine-independence, enhanced viability, and altered cytoskeletal dynamics.
  • Previous studies suggest p210(BCR/ABL) interacts with actin and affects cytoskeletal protein phosphorylation, but its role in cell motility is not fully understood.

Purpose of the Study:

  • To investigate the impact of BCR/ABL on hematopoietic cell motility and cytoskeletal function.
  • To determine if BCR/ABL-induced cytoskeletal abnormalities are linked to tyrosine kinase activity.
  • To assess the potential of these functional changes as biomarkers for BCR/ABL activity and therapeutic response.

Main Methods:

  • Time-lapse video microscopy was employed to analyze cell motility and morphology on fibronectin-coated surfaces.
  • Cell lines, including those transformed by a temperature-sensitive BCR/ABL mutant, were utilized.
  • Hematopoietic progenitor cells from CML patients and healthy donors were compared.

Main Results:

  • BCR/ABL transformation significantly increased spontaneous cell motility, membrane ruffling, filopodia formation, and pseudopodia dynamics.
  • BCR/ABL-transformed cells exhibited persistent motility, contrasting with the sessile nature of untransformed cells.
  • These motility defects were dependent on BCR/ABL tyrosine kinase activity and were observed in primary CML cells.
  • Alpha-interferon treatment demonstrated a capacity to partially normalize the abnormal motility phenotype.

Conclusions:

  • BCR/ABL oncogene profoundly enhances hematopoietic cell motility and alters cytoskeletal function, contributing to CML pathogenesis.
  • The observed motility abnormalities are direct consequences of BCR/ABL tyrosine kinase activity.
  • These functional changes serve as valuable biological markers for BCR/ABL's effects in hematopoietic cells and may indicate therapeutic responsiveness.