DNA REPARATION ELISA OROZCO
-
Upload
elisa-orozco -
Category
Science
-
view
44 -
download
1
Transcript of DNA REPARATION ELISA OROZCO
Non-homologus joining and
homologus recombination are
mechanisms for reparing damaged
DNA.
Researchers recently found out
that enzymes act in the
damaged ends with the
purpose of replacing the lost
information with a copy before
the joining happens
Researchers thinks that knowing
about these enzymes it may be
useful for preventing hereditary
diseases such as cancer, by using
gene therapy.
This research is really important because
as many parts of the DNA can be
damaged by different factors and in the
future develop different diseases,
RESECTION IN THE LINGO might be the
solution that we have been waiting for our
DNA survival
p53 is known as a tumor
suppressor or the “guardian of the
genome” because this protein
avoids the mutation of our
genome by arresting the cell
cycle in the G1/S regulation point.
Research shows that statins such as
Lipitor, Crestor and Mevacor are the
key for preventing damage caused
by mutated p53.
DNAJA1 protects the mutated p53
with the purpose of avoiding its
destruction by enzymes, statins
prevents that DNAJA1 binds to the
mutated p53.
As the title of the research says, statins
might be the key for treating cancer, this
pills that so many people take for
lowering their cholesterol levels, have
more to offer to our organism, this would
avoid metastasis in cancer patients.
The reparation of the DNA by the
mechanisms and the different proteins that
were mentioned, can lead us to control
several diseases and develop prevention,
detection and treatment in our patients.
The research of statins
helped scientists to
understand how mutated
p53 is destroyed by statins,
and how it is protected
from destruction by
DNAJA1.
We are often exposed to
environmental and metabolic
changes that can damage our DNA,
the key to our survival are might be
just in front of our eyes: STATINS.
Statins that are so common in our
era, can avoid resistance to
chemotherapy and metastasis in
cancer patients, a disease that
affects any person of any social
group.
BIBLIOGRAPHY
1. Ronja Biehs, Monika Steinlage, Olivia Barton, Szilvia
Juhász, Julia Künzel, Julian Spies, Atsushi Shibata,
Penny A. Jeggo, Markus Löbrich. DNA Double-Strand
Break Resection Occurs during Non-homologous End
Joining in G1 but Is Distinct from Resection during
Homologous Recombination. Molecular Cell, 2017;
DOI: 10.1016/j.molcel.2016.12.016
2. Alejandro Parrales, Atul Ranjan, Swathi V. Iyer,
Subhash Padhye, Scott J. Weir, Anuradha Roy, Tomoo
Iwakuma. DNAJA1 controls the fate of misfolded mutant
p53 through the mevalonate pathway. Nature Cell
Biology, 2016; 18 (11): 1233 DOI: 10.1038/ncb3427