Nat,
The big big problem is to define precisely the molecular etiology of diverse forms of
dysferlinopathies and their numberless regulation networks.
Theoretically this is possible thank to the microarrays of the whole human genome
already commercially available, and later at least essential relating proteomes, either
in control (physiological state) and progressive evolutions steps of diseases.
The task is daunting but very exciting, and needs all efforts worldwide.
Sophareth
natalisan <natalisan@...> a écrit :
--- In dysferlin@y..., "sophareth" <sophareth@y...> wrote:
> Dear members,
>
> Since the dysferlin gene is known, why antisense/sense paradigm has
> not been used more intensively in clinical research? Ce paradigm is
> based on the RNA interference mechanism discovered some 3-4 y ago.
>
> Sophareth Camsonne
Dear Sophareth,
Thanks for answering and furthering my questions in a so unexpected
way, though.
I was thinking that antisense/ sense RNA paradigm's potential goal
was to inhibit mutated genes over-expression... acting by sample to
supress cells replication.
Wasn't it the reason why it was one research field for HIV and
cancers treatements in those times? (especially for cancer, i've
heard antisense could complete some chemotherapies for a few cancers
(lung) in clinical trials)
Knowing a " non " expression protein from a mutated gene(s)? is
responsible for dysferlinopathies,
would it mean, using antisense mecanism could "disinhibit" this non
expression?
Unfortunatly, who knows how dysferlin deficiency is regulated, as it
seems to involve many genes and multifactorial mutation factors?
I guess things would still be blurred in that pathway for now, but,
it couldn't be a bad idea to keep it in thought...
Phalevi
Ps cher Sophareth, i appreciate your interest for dysferlin which is-
for me- more than a pleasant surprise!
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