Primary cortical neurons from rat embryos were transfected at DIV7 using 1µg DNA plasmid and 2µL of magnetic nanoparticles NeuroMag.
This paper shows the high efficiency of NeuroMag from OZ Biosciences to transfect primary rat cortical neurons.article reference: Hum Mol Genet. 2013 Jul 9.
Loss of c-Jun N-terminal kinase-interacting protein-1 does not affect axonal transport of the amyloid precursor protein or Aβ production.Vagnoni A, Glennon EB, Perkinton MS, Gray EH, Noble W, Miller CC.
Abstract
Disruption to
axonal transport is an early pathological feature in Alzheimer's
disease. The amyloid precursor protein (APP) is a key axonal transport
cargo in Alzheimer's disease since perturbation of its transport
increases APP processing and production of amyloid-β peptide (Aβ) that
is deposited in the brains of Alzheimer's disease patients. APP is
transported anterogradely through axons on kinesin-1 motors. One
favoured route for attachment of APP to kinesin-1 involves the
scaffolding protein c-Jun N-terminal kinase-interacting protein-1
(JIP1), which has been shown to bind both APP and kinesin-1 light chain
(KLC). However, direct experimental evidence to support a role of JIP1
in APP transport is lacking. Notably, the effect of loss of JIP1 on
movement of APP through axons of living neurons, and the impact of such
loss on APP processing and Aβ production has not been reported. To
address these issues, we monitored how siRNA mediated loss of JIP1
influenced transport of enhanced green fluorescent protein (EGFP)-tagged
APP through axons and production of endogenous Aβ in living neurons.
Surprisingly, we found that knockdown of JIP1 did not affect either APP
transport or Aβ production. These results have important implications
for our understanding of APP trafficking in Alzheimer's disease.
No comments:
Post a Comment