Although sympathetic neurons are a well-studied model for neuronal apoptosis, the role of the apoptosome in activating caspases in these neurons remains debated. We find that the ability of sympathetic neurons to undergo apoptosis in response to nerve growth factor (NGF) deprivation is completely dependent on having an intact apoptosome pathway. Genetic deletion of Apaf-1, caspase-9, or caspase-3 prevents apoptosis after NGF deprivation, and importantly, allows these neurons to recover and survive long-term following readdition of NGF. The inability of caspase-3 deficient sympathetic neurons to undergo apoptosis is particularly striking, as apoptosis in dermal fibroblasts and cortical neurons proceeds even in the absence of caspase-3. Our results show that in contrast to dermal fibroblasts and cortical neurons, sympathetic neurons express no detectable levels of caspase-7. The strict requirement for an intact apoptosome, coupled with a lack of effector caspase redundancy, provides sympathetic neurons with a markedly increased control over their apoptotic pathway.
We present an analysis of the publicly available HARPS radial velocity (RV)
Measurements for Alpha Cen B, a star hosting an Earth-mass planet candidate in
A 3.24 day orbit. The goal is to devise robust ways of extracting low-amplitude
RV signals of low mass planets in the presence of activity noise....
We calculate the expected rate of double-neutrino
Interactions from a single cosmic-ray air shower. The rate is small, about 0.07
Events/year for a 1 km$^3$ detector like IceCube, with only a small dependence
On the assumed cosmic-ray composition and hadronic interaction model. For a
We present a possible mechanism to account for
The inverse magnetic catalysis at finite temperature found in lattice
Calculations which so far cannot be reproduced in the context of effective
Chiral models. Such mechanism is based on the use of the EPNJL model with a
Magnetic field dependent scale p...
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