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  • 1
    Online Resource
    Online Resource
    Trifurcate Feed-Forward Regulation of Age-Dependent Cell Death Involving miR164 in Arabidopsis
    American Association for the Advancement of Science (AAAS) ; 2009
    In:  Science Vol. 323, No. 5917 ( 2009-02-20), p. 1053-1057
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 323, No. 5917 ( 2009-02-20), p. 1053-1057
    Abstract: Aging induces gradual yet massive cell death in higher organisms, including annual plants. Even so, the underlying regulatory mechanisms are barely known, despite the long-standing interest in this topic. Here, we demonstrate that ORE1, which is a NAC (NAM, ATAF, and CUC) transcription factor, positively regulates aging-induced cell death in Arabidopsis leaves. ORE1 expression is up-regulated concurrently with leaf aging by EIN2 but is negatively regulated by miR164. miR164 expression gradually decreases with aging through negative regulation by EIN2 , which leads to the elaborate up-regulation of ORE1 expression. However, EIN2 still contributes to aging-induced cell death in the absence of ORE1 . The trifurcate feed-forward pathway involving ORE1, miR164 , and EIN2 provides a highly robust regulation to ensure that aging induces cell death in Arabidopsis leaves.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1166386
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2009
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  • 2
    Online Resource
    Online Resource
    Learning-Related Synaptic Growth Mediated by Internalization of Aplysia Cell Adhesion Molecule Is Controlled by Membrane Phosphatidylinositol 4,5-Bisphosphate Synthetic Pathway
    Society for Neuroscience ; 2012
    In:  The Journal of Neuroscience Vol. 32, No. 46 ( 2012-11-14), p. 16296-16305
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 32, No. 46 ( 2012-11-14), p. 16296-16305
    Abstract: Long-term facilitation in Aplysia is accompanied by the growth of new synaptic connections between the sensory and motor neurons of the gill-withdrawal reflex. One of the initial steps leading to the growth of these synapses is the internalization, induced by 5-HT, of the transmembrane isoform of Aplysia cell-adhesion molecule (TM–apCAM) from the plasma membrane of sensory neurons (Bailey et al., 1992). However, the mechanisms that govern the internalization of TM–apCAM and how this internalization is coupled to the molecular events that initiate the structural changes are not fully understood. Here, we report that the synthesis of membrane phosphatidylinositol 4,5-bisphosphate [PI(4,5)P 2 ], which is known to be mediated by a signaling cascade through Aplysia Sec7 protein (ApSec7) and phosphatidylinositol-4-phosphate 5-kinase type I α (PIP5KIα) is required for both the internalization of TM–apCAM and the initiation of synaptic growth during 5-HT-induced long-term facilitation. Pharmacological blockade of PI(4,5)P 2 synthesis by the application of the inhibitor phenylarsine oxide blocked the internalization of apCAM. Furthermore, perturbation of the endogenous activation of ApSec7 and its downstream target PIP5KIα also blocked 5-HT-mediated internalization of TM–apCAM and synaptic growth. Finally, long-term facilitation was specifically impaired by blocking the ApSec7 signaling pathway at sensory-to-motor neuron synapses. These data indicate that the ApSec7/PIP5KIα signaling pathway is actively recruited during learning-related 5-HT signaling and acts as a key regulator of apCAM internalization associated with the formation of new synaptic connections during long-term facilitation.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1872-12.2012
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2012
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    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Identification of a serotonin receptor coupled to adenylyl cyclase involved in learning-related heterosynaptic facilitation in Aplysia
    Proceedings of the National Academy of Sciences ; 2009
    In:  Proceedings of the National Academy of Sciences Vol. 106, No. 34 ( 2009-08-25), p. 14634-14639
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 106, No. 34 ( 2009-08-25), p. 14634-14639
    Abstract: Serotonin (5-HT) plays a critical role in modulating synaptic plasticity in the marine mollusc Aplysia and in the mammalian nervous system. In Aplysia sensory neurons, 5-HT can activate several signal cascades, including PKA and PKC, presumably via distinct types of G protein-coupled receptors. However, the molecular identities of these receptors have not yet been identified. We here report the cloning and functional characterization of a 5-HT receptor that is positively coupled to adenylyl cyclase in Aplysia neurons. The cloned receptor, 5-HT apAC1 , stimulates the production of cAMP in HEK293T cells and in Xenopus oocytes. Moreover, the knockdown of 5-HT apAC1 expression by RNA interference blocked 5-HT-induced cAMP production in Aplysia sensory neurons and blocked synaptic facilitation in nondepressed or partially depressed sensory-to-motor neuron synapses. These data implicate 5-HT apAC1 as a major modulator of learning related synaptic facilitation in the direct sensory to motor neuron pathway of the gill withdrawal reflex.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0907502106
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2009
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    SSG: 11
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  • 4
    Online Resource
    Online Resource
    AU-rich element-binding protein negatively regulates CCAAT enhancer-binding protein mRNA stability during long-term synaptic plasticity in Aplysia
    Proceedings of the National Academy of Sciences ; 2012
    In:  Proceedings of the National Academy of Sciences Vol. 109, No. 38 ( 2012-09-18), p. 15520-15525
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 109, No. 38 ( 2012-09-18), p. 15520-15525
    Abstract: The consolidation of long-term memory for sensitization and synaptic facilitation in Aplysia requires synthesis of new mRNA including the immediate early gene Aplysia CCAAT enhancer-binding protein ( ApC/EBP ). After the rapid induction of ApC/EBP expression in response to repeated treatments of 5-hydroxytryptamine (5-HT), ApC/EBP mRNA is temporarily expressed in sensory neurons of sensory-to-motor synapses. However, the molecular mechanism underlying the rapid degradation of ApC/EBP transcript is not known. Here, we cloned an AU-rich element (ARE)-binding protein, ApAUF1, which functions as a destabilizing factor for ApC/EBP mRNA. ApAUF1 was found to bind to the 3′ UTR of ApC/EBP mRNA that contains AREs and subsequently reduces the expression of ApC/EBP 3′ UTR-containing reporter genes. Moreover, overexpression of ApAUF1 inhibited the induction of ApC/EBP mRNA in sensory neurons and also impaired long-term facilitation of sensory-to-motor synapses by repetitive 5-HT treatments. These results provide evidence for a critical role of the posttranscriptional modification of ApC/EBP mRNA during the consolidation of synaptic plasticity.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1116224109
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2012
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Synaptic Protein Degradation Underlies Destabilization of Retrieved Fear Memory
    American Association for the Advancement of Science (AAAS) ; 2008
    In:  Science Vol. 319, No. 5867 ( 2008-02-29), p. 1253-1256
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 319, No. 5867 ( 2008-02-29), p. 1253-1256
    Abstract: Reactivated memory undergoes a rebuilding process that depends on de novo protein synthesis. This suggests that retrieval is dynamic and serves to incorporate new information into preexisting memories. However, little is known about whether or not protein degradation is involved in the reorganization of retrieved memory. We found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after retrieval of contextual fear memory. Moreover, the infusion of proteasome inhibitor into the CA1 region immediately after retrieval prevented anisomycin-induced memory impairment, as well as the extinction of fear memory. This suggests that ubiquitin- and proteasome-dependent protein degradation underlies destabilization processes after fear memory retrieval. It also provides strong evidence for the existence of reorganization processes whereby preexisting memory is disrupted by protein degradation, and updated memory is reconsolidated by protein synthesis.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1150541
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2008
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 6
    Online Resource
    Online Resource
    Discovery of a dual-action small molecule that improves neuropathological features of Alzheimer’s disease mice
    Proceedings of the National Academy of Sciences ; 2022
    In:  Proceedings of the National Academy of Sciences Vol. 119, No. 3 ( 2022-01-18)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 119, No. 3 ( 2022-01-18)
    Abstract: Alzheimer’s disease (AD) is characterized by complex, multifactorial neuropathology, suggesting that small molecules targeting multiple neuropathological factors are likely required to successfully impact clinical progression. Acid sphingomyelinase (ASM) activation has been recognized as an important contributor to these neuropathological features in AD, leading to the concept of using ASM inhibitors for the treatment of this disorder. Here we report the identification of KARI 201, a direct ASM inhibitor evaluated for AD treatment. KARI 201 exhibits highly selective inhibition effects on ASM, with excellent pharmacokinetic properties, especially with regard to brain distribution. Unexpectedly, we found another role of KARI 201 as a ghrelin receptor agonist, which also has therapeutic potential for AD treatment. This dual role of KARI 201 in neurons efficiently rescued neuropathological features in AD mice, including amyloid beta deposition, autophagy dysfunction, neuroinflammation, synaptic loss, and decreased hippocampal neurogenesis and synaptic plasticity, leading to an improvement in memory function. Our data highlight the possibility of potential clinical application of KARI 201 as an innovative and multifaceted drug for AD treatment.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2115082119
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2022
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    SSG: 11
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  • 7
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    Clinical feasibility of brain‐computer interface based on steady‐state visual evoked potential in patients with locked‐in syndrome: Case studies
    Wiley ; 2017
    In:  Psychophysiology Vol. 54, No. 3 ( 2017-03), p. 444-451
    Details
    In: Psychophysiology, Wiley, Vol. 54, No. 3 ( 2017-03), p. 444-451
    Abstract: Although the feasibility of brain‐computer interface (BCI) systems based on steady‐state visual evoked potential (SSVEP) has been extensively investigated, only a few studies have evaluated its clinical feasibility in patients with locked‐in syndrome (LIS), who are the main targets of BCI technology. The main objective of this case report was to share our experiences of SSVEP‐based BCI experiments involving five patients with LIS, thereby providing researchers with useful information that can potentially help them to design BCI experiments for patients with LIS. In our experiments, a four‐class online SSVEP‐based BCI system was implemented and applied to four of five patients repeatedly on multiple days to investigate its test‐retest reliability. In the last experiments with two of the four patients, the practical usability of our BCI system was tested using a questionnaire survey. All five patients showed clear and distinct SSVEP responses at all four fundamental stimulation frequencies (6, 6.66, 7.5, 10 Hz), and responses at harmonic frequencies were also observed in three patients. Mean classification accuracy was 76.99% (chance level = 25%). The test‐retest reliability experiments demonstrated stable performance of our BCI system over different days even when the initial experimental settings (e.g., electrode configuration, fixation time, visual angle) used in the first experiment were used without significant modifications. Our results suggest that SSVEP‐based BCI paradigms might be successfully used to implement clinically feasible BCI systems for severely paralyzed patients.
    Type of Medium: Online Resource
    ISSN: 0048-5772 , 1469-8986
    URL: Issue
    URL: Article
    DOI: 10.1111/psyp.2017.54.issue-3
    DOI: 10.1111/psyp.12793
    RVK:
    CL 1000
    Language: English
    Publisher: Wiley
    Publication Date: 2017
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    SSG: 5,2
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  • 8
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    Ultrasensitive detection of malignant melanoma using PET molecular imaging probes
    Proceedings of the National Academy of Sciences ; 2020
    In:  Proceedings of the National Academy of Sciences Vol. 117, No. 23 ( 2020-06-09), p. 12991-12999
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 117, No. 23 ( 2020-06-09), p. 12991-12999
    Abstract: Malignant melanoma has one of the highest mortality rates of any cancer because of its aggressive nature and high metastatic potential. Clinical staging of the disease at the time of diagnosis is very important for the prognosis and outcome of melanoma treatment. In this study, we designed and synthesized the 18 F-labeled pyridine-based benzamide derivatives N -(2-(dimethylamino)ethyl)-5-[ 18 F]fluoropicolinamide ([ 18 F]DMPY2) and N -(2-(dimethylamino)ethyl)-6-[ 18 F]fluoronicotinamide ([ 18 F]DMPY3) to detect primary and metastatic melanoma at an early stage and evaluated their performance in this task. [ 18 F]DMPY2 and [ 18 F]DMPY3 were synthesized by direct radiofluorination of the bromo precursor, and radiochemical yields were ∼15–20%. Cell uptakes of [ 18 F]DMPY2 and [ 18 F]DMPY3 were 〉 103-fold and 18-fold higher, respectively, in B16F10 (mouse melanoma) cells than in negative control cells. Biodistribution studies revealed strong tumor uptake and retention of [ 18 F]DMPY2 (24.8% injected dose per gram of tissue [ID/g] at 60 min) and [ 18 F]DMPY3 (11.7%ID/g at 60 min) in B16F10 xenografts. MicroPET imaging of both agents demonstrated strong tumoral uptake/retention and rapid washout, resulting in excellent tumor-to-background contrast in B16F10 xenografts. In particular, [ 18 F]DMPY2 clearly visualized almost all metastatic lesions in lung and lymph nodes, with excellent image quality. [ 18 F]DMPY2 demonstrated a significantly higher tumor-to-liver ratio than [ 18 F]fluorodeoxyglucose ([ 18 F]FDG) and the previously reported benzamide tracers N -[2-(diethylamino)-ethyl]-5-[ 18 F]fluoropicolinamide ([ 18 F]P3BZA) and N -[2-(diethylamino)-ethyl]-4-[ 18 F]fluorobenzamide ([ 18 F]FBZA) in B16F10-bearing or SK-MEL-3 (human melanoma)-bearing mice. In conclusion, [ 18 F]DMPY2 might have strong potential for the diagnosis of early stage primary and metastatic melanoma using positron emission tomography (PET).
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1922313117
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2020
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    detail.hit.zdb_id: 1461794-8
    SSG: 11
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  • 9
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    Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer’s disease via H2O2− production
    Springer Science and Business Media LLC ; 2020
    In:  Nature Neuroscience Vol. 23, No. 12 ( 2020-12), p. 1555-1566
    Details
    In: Nature Neuroscience, Springer Science and Business Media LLC, Vol. 23, No. 12 ( 2020-12), p. 1555-1566
    Type of Medium: Online Resource
    ISSN: 1097-6256 , 1546-1726
    URL: Article
    DOI: 10.1038/s41593-020-00735-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 1494955-6
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  • 10
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    Ion-to-ion amplification through an open-junction ionic diode
    Proceedings of the National Academy of Sciences ; 2019
    In:  Proceedings of the National Academy of Sciences Vol. 116, No. 28 ( 2019-07-09), p. 13807-13815
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 28 ( 2019-07-09), p. 13807-13815
    Abstract: As biological signals are mainly based on ion transport, the differences in signal carriers have become a major issue for the intimate communication between electrical devices and biological areas. In this respect, an ionic device which can directly interpret ionic signals from biological systems needs to be designed. Particularly, it is also required to amplify the ionic signals for effective signal processing, since the amount of ions acquired from biological systems is very small. Here, we report the signal amplification in ionic systems as well as sensing through the modified design of polyelectrolyte hydrogel-based ionic diodes. By designing an open-junction structure, ionic signals from the external environment can be directly transmitted to an ionic diode. Moreover, the minute ionic signals injected into the devices can also be amplified to a large amount of ions. The signal transduction mechanism of the ion-to-ion amplification is suggested and clearly verified by revealing the generation of breakdown ionic currents during an ion injection. Subsequently, various methods for enhancing the amplification are suggested.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1903900116
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2019
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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