• In hippocampal neurons, long-lasting down-regulation of ligation mRNA levels occurs via post-transcriptional RNA processing following glutamate receptor activation. (wikipedia.org)
  • Anti-PrP antibodies targeting epitopes in the C-terminal domain induce currents, and cause degeneration of dendrites on murine hippocampal neurons, effects that entirely dependent on the effector function of the N-terminus. (elifesciences.org)
  • In one, published December 28 last year, first author Sabrina Simoes and colleagues reported that neurons rely on vacuolar protein sorting ortholog 26b (VPS26b), a retromer component. (alzforum.org)
  • In the January 18 issue, Small, Beth Stevens at Boston Children's Hospital, and colleagues reported that knocking out a different retromer protein, VPS35, in hippocampal neurons in mice not only jammed neuronal endosome traffic but also caused microglia to assume shapes resembling those seen in AD. (alzforum.org)
  • Adding VPS35 back into the neurons restored both protein trafficking and microglial morphology. (alzforum.org)
  • A functional role for intra-axonal protein synthesis during axonal regeneration from adult sensory neurons. (uiowa.edu)
  • This gene encodes a protein receptor that localizes phosphoglycoproteins within endosomes and at the cell periphery. (wikipedia.org)
  • This trafficking receptor for phosphoglycoproteins may play a role in neuroplasticity by modulating cell-cell interactions, intracellular adhesion, and protein binding at membrane surfaces. (wikipedia.org)
  • When they tried to induce LTD with a glycine blocker (glycine is an obligatory co-agonist for NMDAR), they could again induce LTD. Their working hypothesis is that glutamate binding to NMDAR is necessary for LTD, but not ion flow through the receptor. (trailofpapers.net)
  • Knocking it out in mice slowed glutamate receptor recycling and weakened synaptic transmission, but only in the transentorhinal cortex, hinting at why this region is so vulnerable to AD pathology in people. (alzforum.org)
  • Indeed, LTP weakened and glutamate receptor GluA1 expression was lower in TEC brain slices, while both were normal in the medial entorhinal cortex. (alzforum.org)
  • VEGF-induced pMF was attenuated by the MEK/ERK inhibitor U0126 [1,4-diamino-2,3-dicyano-1,4-bis( o -aminophenylmercapto)butadiene] and was abolished by the phosphotidinositol 3 kinase/Akt inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-1(4 H )-benzopyran-4-one hydrochloride], demonstrating that ERK mitogen-activated protein kinases and Akt are both required for full expression of VEGF-induced pMF. (jneurosci.org)
  • The expression of HMGB1, c-Jun N-terminal kinase (JNK), extracellular-signal-regulated kinase (ERK), and p38 mitogen-activated protein kinase (p38 MAPK) was assessed with immunofluorescence and western blot analysis. (molvis.org)
  • LKB1 itself is a constitutively active kinase, which is regulated by posttranslational modifications and direct binding to phospholipids of the plasma membrane. (sdbonline.org)
  • This study reports that LKB1 binds to Phosphoinositide-dependent kinase (PDK1) by a conserved binding motif. (sdbonline.org)
  • Furthermore, Western blot pulldowns showed that CNIH binds to GluA1, but not GluA2. (trailofpapers.net)
  • Thus it appears the CNIH selectively bind to GluA1. (trailofpapers.net)
  • The VEGF-A protein and mRNA levels in conditioned medium of RGC-5 cells incubated with AGE-modified BSA (AGE-BSA) were examined with real-time PCR and enzyme-linked immunosorbent assay (ELISA), and BSA-treated cells were used as controls. (molvis.org)
  • In contrast, if zinc binding cysteine residues of MT3 are oxidized, MT3 may release zinc and result in much more cell death. (ilreceptor.com)
  • With the advent, development and refining of single-molecule nanomechanical techniques that enable the conformational dynamics of individual proteins under the effect of a calibrated force to be probed, we have begun to acquire a comprehensive knowledge of the diverse physicochemical principles that regulate the elasticity of single proteins. (ibecbarcelona.eu)
  • Fluorescent probes for conformational states of proteins. (academicinfluence.com)
  • In this review we will highlight mechanisms that control targeting of PSD-95 at the synapse, and discuss how this molecule influences the retention and clustering of diverse synaptic proteins to regulate synaptic structure and strength. (frontiersin.org)
  • Excitatory synaptic transmission in the brain is predominantly mediated by the neurotransmitter glutamate, while inhibitory transmission is mediated mainly by the neurotransmitter gamma-amino butyric acid (GABA). (frontiersin.org)
  • Hippocampal Synaptic Alterations Associated with Tau Pathology in Primary Age-Related Tauopathy. (neurotree.org)
  • The experiments showed that one end of the protein, called the N-terminus, is involved in the movement of electrical charges across the cell membrane and is able to cause cell degeneration. (elifesciences.org)
  • and group 4 (late-elderly, 75-85).Protein levels and deregulated protein phosphorylation linked to similar biological terms/functions, but involving different individual proteins, are found in FC with age. (ibecbarcelona.eu)
  • Embryonic poly(A)-binding protein (ePAB) phosphorylation is required for Xenopus oocyte maturation. (uiowa.edu)
  • This Review addresses single-molecule force spectroscopy experiments conducted on proteins with a known role in mechanosensing and mechanotransduction in eukaryotic cells. (ibecbarcelona.eu)
  • Kinetics of homophilic binding by embryonic and adult forms of the neural cell adhesion molecule. (academicinfluence.com)
  • Prion diseases are a group of degenerative illnesses of the brain caused when a molecule called the prion protein (PrP for short) adopts the wrong shape. (elifesciences.org)
  • Glycation, the result of a protein or lipid molecule bonding with sugar molecules, is a consequence of the aging process. (molvis.org)
  • Cytotactin, an extracellular matrix protein of neural and non-neural tissues that mediates glia-neuron interaction. (academicinfluence.com)
  • Binding of neural cell adhesion molecules (N-CAMs) to the cellular prion protein. (academicinfluence.com)
  • MK-801 is a competitive antagonist that binds to NMDARs differently than APV, and blocks NMDAR currents. (trailofpapers.net)
  • Ligands binding to the N-terminal domain abolish the spontaneous ionic currents associated with neurotoxic mutants of PrP, and the isolated N-terminal domain induces currents when expressed in the absence of the C-terminal domain. (elifesciences.org)
  • In the metallothioneins, MT3 is especially enriched while in the brain, Some MT3 zinc binding web sites are redox modulated, making it possible for MT3 to accept and release zinc in response to changes in oxidative standing, Mainly because MT3 can induce or minimize zinc toxicity based on context, it could improve or reduce brain damage, based on the specific state of MT3. (ilreceptor.com)
  • Although inhibitory postsynaptic sites lack PSDs, they also consist of complex protein matrices. (frontiersin.org)
  • PrP C , the cellular isoform of the prion protein, serves to transduce the neurotoxic effects of PrP Sc , the infectious isoform, but how this occurs is mysterious. (elifesciences.org)
  • However, protein levels of components of cell membranes, vesicles and synapses, RNA modulation, and cellular structures (including tau and tubulin filaments) are markedly altered from the age of 75. (ibecbarcelona.eu)
  • Mechanical force modulates the conformation and function of individual proteins, and this underpins many mechanically driven cellular processes. (ibecbarcelona.eu)
  • These diseases are caused by refolding of the cellular prion protein (PrP C ) into an infectious isoform (PrP Sc ) that catalytically templates its abnormal conformation onto additional molecules of PrP C ( Prusiner, 1998 ). (elifesciences.org)
  • It had been shown that certain altered PrP proteins caused the death of brain cells by allowing excessive electrical charges to cross the membranes of the cell. (elifesciences.org)
  • The main groups include sodium channel blockers, calcium current inhibitors, gamma-aminobutyric acid (GABA) enhancers, glutamate blockers, carbonic anhydrase inhibitors, hormones, and drugs with unknown mechanisms of action (see the image below). (medscape.com)
  • This protein contains single PUA and SUI1 domains and these domains may function in RNA binding and translation initiation, respectively. (wikipedia.org)
  • In two recent Cell Reports papers, scientists led by Scott Small, Columbia University, New York, detail new insights into the function of the retromer, an endosome protein complex linked to Alzheimer's disease. (alzforum.org)
  • Ligatin, otherwise known as eIF2D, is a protein that in humans is encoded by the LGTN gene. (wikipedia.org)
  • A viral nuclear noncoding RNA binds re-localized poly(A) binding protein and is required for late KSHV gene expression. (uiowa.edu)
  • By contrast, the other end of the protein, the C-terminus, acts as a regulator for the N-terminus and can prevent cell degeneration. (elifesciences.org)
  • Noteworthy, protein levels of large clusters of hierarchically-related protein expression levels are stable until 70. (ibecbarcelona.eu)
  • Compared with the BSA controls, the RGC-5 cells incubated with AGE-BSA showed a dose- and time-dependent increase in VEGF-A mRNA and VEGF-A protein secretion in the supernatant, with the highest levels achieved at 24 h. (molvis.org)
  • Here, we review the major advances underpinning our current understanding of how the elasticity of single proteins regulates mechanosensing and mechanotransduction. (ibecbarcelona.eu)
  • Effects of ovarian steroids and raloxifene on proteins that synthesize, transport, and degrade serotonin in the raphe region of macaques. (jamanetwork.com)
  • Each protein co-localized with VPS35 (not shown). (alzforum.org)
  • One guy (specific names withheld) talked about potential drugs for glutamate receptors, which consisted of showing chemical structures of existing drugs, and 3D reconstructions of receptors. (trailofpapers.net)