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Telomeres and Telomerase02:41

Telomeres and Telomerase

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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded...
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Replicative Cell Senescence02:15

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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...
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Replication in Eukaryotes01:29

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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
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Replication in Eukaryotes02:31

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Cancer Stem Cells and Tumor Maintenance02:40

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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Related Experiment Video

Updated: Jan 10, 2026

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
12:08

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Published on: May 22, 2013

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Telomere Maintenance and Oncogenesis.

Antonio Torres-Montaner1

  • 1Independent Researcher, 22400 Monzon, Spain.

International Journal of Molecular Sciences
|November 27, 2025
PubMed
Summary
This summary is machine-generated.

Telomere shortening, typically cancer-protective, may paradoxically aid malignant transformation. This occurs when Rap1 protein releases from telomeres, interacting with Zscan4 to promote cell immortalization.

Keywords:
PI3K/AKT pathwayRap1Zscan4telomeres

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Author Spotlight: Advanced Single-Molecule Techniques for Investigating Telomeric Protein-DNA Interactions
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Author Spotlight: Advanced Single-Molecule Techniques for Investigating Telomeric Protein-DNA Interactions

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Most cancers show reduced telomere length and post-stem cell origins.
  • Telomere shortening usually prevents cancer by inducing apoptosis, but this is less effective in p53-deficient cancers.
  • Telomere shortening can alter chromatin structure, potentially aiding tumor maintenance.

Purpose of the Study:

  • To investigate the paradoxical role of telomere shortening in cancer development.
  • To explore the mechanism by which telomere shortening might promote malignant transformation.
  • To propose a novel pathway involving Rap1 and Zscan4 in cancer immortalization.

Main Methods:

  • Analysis of cancer cell differentiation markers and telomere length.
  • Investigation of apoptosis pathways, including p53 function.
  • Examination of telomeric chromatin alterations and the telomere position effect.
  • Study of signaling pathways leading to Rap1 release from telomeres.
  • Assessment of Rap1 interaction with Zscan4 and its effect on cell immortalization.

Main Results:

  • Telomere shortening, while generally protective, may contribute to cancer in specific contexts, such as p53 deficiency.
  • Telomere shortening can induce chromatin changes supporting telomere maintenance in tumors.
  • A proposed mechanism involves signaling pathways causing Rap1 release from telomeres.
  • Released Rap1 may interact with Zscan4, promoting cell immortalization and malignant transformation.

Conclusions:

  • Telomere shortening can play a dual role in cancer, potentially promoting it under certain conditions.
  • The interaction between Rap1 and Zscan4 is a novel proposed mechanism for cancer cell immortalization.
  • This pathway may be crucial for understanding cancer development, particularly in tumors with altered apoptotic functions.