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About Biomedical Basics
Biomedical Basics are AI-generated explanations prepared with access to the complete collection, human-reviewed prior to publication. Short and simple, covering biomedical and life sciences fundamentals.
Topics Covered
- Telomere structure and function
- Telomere shortening and aging
- Telomerase role in maintenance
- Telomere dynamics in disease
- Telomerase activation in cancer
Talk Citation
(2026, March 31). Telomeres and telomerase [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 18, 2026, from https://doi.org/10.69645/HVQC9876.Export Citation (RIS)
Publication History
- Published on March 31, 2026
Financial Disclosures
A selection of talks on Oncology
Transcript
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0:00
The topic of telomeres and
telomerase will be
explored through
the structure and function of
telomeres as protective
chromosome caps,
the consequences of telemere
shortening during
cell division and
the role of telomerase in
counteracting this erosion
in select cell types.
We will explore how telomere
dynamics drive
cellular aging and
contribute to diseases
linked to tissue
degeneration and inherited
telomere disorders.
Additionally, we
will discuss how
cancer cells exploit
telomerase to achieve
limitless replication
and the challenges
this presents for developing
targeted therapies.
Telmrs and telomerase are
crucial players in
genome stability,
cell aging, and disease.
Telmrs found at our
chromosome ends
are repeated TTAGGG
sequences in humans,
acting as protective caps,
much like plastic tips on
shoelaces, safeguarding
genetic material.
They prevent chromosomes
from fraying or fusing,
thus maintaining
genome integrity,
especially in frequently
dividing cells.
Telomeres with
shelter in proteins
protect DNANs and prevent
cell repair errors.
Telmrs protect chromosome ends,
but they're not permanent.
With each cell division,
the end replication problem
prevents complete duplication
of the lagging strand,
causing telomeres to shorten by
about 50 to 100 base
pairs per division.
When telmrs reach
a critical length,
cells recognize this as
DNA damage and trigger
permanent arrest or replicative
senescence or cell death.