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Parthanatos during cerebral ischemia. PSD-95 links NMDARs to nNOS. Neuronal DNA injury that is caused by oxidative or nitrosative stress activates PARP-1, which uses NAD+to synthesize PAR. PAR inhibits HK and promotes the nuclear translocation of AIF. The mPTP allows the release of AIF into t...
Briefly, mice anesthetized with 2% isofluoroalkanes were put into a stereotaxic frame (Wood Dale, USA). The skull was exposed through a midline incision in the skin at the top of the brain. A cold light source with a 2-mm-diameter fiber optic bundle (12,000 lux; World Precision ...
Maf1, a general transcriptional regulator and mTOR downstream effector, is highly expressed in the hippocampus and cortex, but the function of Maf1 in neurons is not well elucidated. Here, we first demonstrate that Maf1 plays a central role in the inhibi
may impair the structure and/or function of the postsynaptic compartment. If confirmed, this possibility, which has never been addressed before, would provide a logical frame for the protein involvement in different psychiatric diseases, characterized by defective formation and function of the postsynapti...
Enlarged pictures after the black frame. Bar = 50 µm. c Quantitative analysis of the number of neurons using ImageJ. The results are expressed as the Mean ± SD, *p < 0.05, verses D-gal+PBS groups, #p < 0.05, verses D-gal+Cell groups (n = 6). Full size ...
aLipid metabolism requires the transfer of phospholipids from the ER to mitochondria and back again at MERCS. Phosphatidylserine (PS) in the ER is transferred to mitochondria where it is converted to phosphatidylethanolamine (PE) by enzyme PS Decarboxylase (PSD). PE is shuttled back to ER where...
(PSD-95), and these interactions are critical for actin turnover and stabilization of dendritic spines [33,34,35,36]. Moreover, AMOT is indispensable for dendrite growth and arborization in developing neurons, and conditional deletion ofAmotin mouse neurons results in impaired dendritic network ...
However, an important question that still needs to be addressed concerns the time frame in which such ionic dyshomeostasis occurs in AD. Does the ionic deregulation precede or follow the onset of the pathology? Is this a cause or a consequence of the disease? In this review, we analyze the...