Can I please get help on proposing the next experiment (future direction) for the information provided below? One potential next experiment? Reference: MicroRNA-9 regulates neural apoptosis in methylmalonic acidemia via targeting BCL2L11
Can I please get help on proposing the next experiment (future direction) for the information provided below? One potential next experiment? Reference: MicroRNA-9 regulates neural apoptosis in methylmalonic acidemia via targeting BCL2L11
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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Can I please get help on proposing the next experiment (future direction) for the information provided below? One potential next experiment?
Reference: MicroRNA-9 regulates neural apoptosis in methylmalonic acidemia via targeting BCL2L11

Transcribed Image Text:Abstract
Methylmalonic acidemia (MMA) is an autosomal-recessive
inborn metabolic disorder that results from a deficiency in
methylmalonyl-coenzyme A mutase or its cofactor,
adenosylcobalamin. Currently, neurological manifestations in
MMA are thought to be associated with neural apoptosis.
BCL2L11, which is a proapoptotic Bcl-2 family member, is
resident in the outer mitochondrial membrane, where this
protein acts as a central regulator of the intrinsic apoptotic
cascade and mediates excitotoxic apoptosis. MicroRNAS
(miRNAs) are a class of non-coding RNAS that function as
endogenous triggers of the RNA interference pathway.
Currently, little is known regarding the role of miRNA in
MMA. In our previous study, we preliminarily found that the
expression of miR-9 was significantly down-regulated in
MMA patient plasma and sensitively changed after VitB12
treatment, which may act as a potential "competitor" of gas
chromatography-mass spectrometry for the diagnosis of
MMA. In the present study, we first confirmed that miR-9
inhibited BCL2L11 expression by directly targeting its 3'-
untranslated region, and the up-regulation of miR-9 reduced
neural apoptosis induced by methylmalonate via targeting
BCL2L11. Taken together, our results suggested that miR-9
might act as a monitor of changes in MMA and might
provide new insights into a therapeutic entry point for
treating MMA.
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