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

Molecular Factors Affecting Cell Division01:27

Molecular Factors Affecting Cell Division

Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...
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...
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...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...

You might also read

Related Articles

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

Sort by
Same author

PP2A catalytic subunit alpha is critically required for CD8<sup>+</sup> T-cell homeostasis and antibacterial responses.

European journal of immunology·2024
Same author

Diversity of post-translational modifications and cell signaling revealed by single cell and single organelle mass spectrometry.

Communications biology·2024
Same author

Culture-Free Whole Genome Sequencing of <i>Mycobacterium tuberculosis</i> Using Ligand-Mediated Bead Enrichment Method.

Open forum infectious diseases·2024
Same author

Multicolumn Nanoflow Liquid Chromatography with Accelerated Offline Gradient Generation for Robust and Sensitive Single-Cell Proteome Profiling.

Analytical chemistry·2024
Same author

Metabolome-wide association identifies altered metabolites and metabolic pathways in the serum of patients with cholangiocarcinoma.

JHEP reports : innovation in hepatology·2024
Same author

Dysregulated Cerebrospinal Fluid Proteome of Spinocerebellar Ataxia Type 2 and its Clinical Implications.

Movement disorders : official journal of the Movement Disorder Society·2024

Related Experiment Video

Updated: May 11, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

FAM190A deficiency creates a cell division defect.

Kalpesh Patel1, Francesca Scrimieri, Soma Ghosh

  • 1Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA.

The American Journal of Pathology
|May 14, 2013
PubMed
Summary
This summary is machine-generated.

The FAM190A gene, often deleted in cancer, is crucial for normal cell division. Its disruption causes defects in mitosis and multinuclearity, contributing to cancer

More Related Videos

Simultaneous Assessment of Kinship, Division Number, and Phenotype via Flow Cytometry for Hematopoietic Stem and Progenitor Cells
10:20

Simultaneous Assessment of Kinship, Division Number, and Phenotype via Flow Cytometry for Hematopoietic Stem and Progenitor Cells

Published on: March 24, 2023

Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo
10:10

Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo

Published on: July 15, 2016

Related Experiment Videos

Last Updated: May 11, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Simultaneous Assessment of Kinship, Division Number, and Phenotype via Flow Cytometry for Hematopoietic Stem and Progenitor Cells
10:20

Simultaneous Assessment of Kinship, Division Number, and Phenotype via Flow Cytometry for Hematopoietic Stem and Progenitor Cells

Published on: March 24, 2023

Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo
10:10

Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo

Published on: July 15, 2016

Area of Science:

  • Molecular Biology
  • Cancer Genetics
  • Cell Biology

Background:

  • FAM190A (alias CCSER1) is located at a common genomic deletion site in human cancers.
  • FAM190A transcripts frequently exhibit in-frame deletions of conserved exons in various cancers.
  • The precise function of FAM190A in cellular processes remained largely unknown prior to this study.

Purpose of the Study:

  • To elucidate the function of FAM190A in cell division and its potential role in cancer.
  • To investigate the consequences of FAM190A alterations on mitosis and multinuclearity.

Main Methods:

  • Analysis of FAM190A gene deletions in pancreatic cancer.
  • Experimental knockdown of FAM190A expression using shRNA.
  • Time-lapse microscopy to observe cell division.
  • Immunofluorescence and immunoblot assays for protein localization and detection.
  • Co-immunoprecipitation to identify interacting proteins.

Main Results:

  • FAM190A knockdown induced focal cytokinesis defects, multipolar mitosis, and multinuclearity.
  • FAM190A localizes to the gamma-tubulin ring complex during early mitosis and the midbody during cytokinesis.
  • FAM190A interacts with EXOC1 and Ndel1, proteins involved in cytoskeletal organization and cell division.
  • FAM190A protein levels peak during M-phase, with phosphorylated forms accumulating before cytokinesis.

Conclusions:

  • FAM190A is essential for normal mitosis and cytokinesis.
  • Disruptions in FAM190A, including deletions and mutations, can lead to mitotic dysregulation and multinuclearity in cancer.
  • FAM190A alterations may contribute to chromosomal instability, a hallmark of cancer.