GLORIA

GEOMAR Library Ocean Research Information Access

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Autophagy: Biology and Diseases : Basic Science (2019)
    Singapore : Springer
    Details Availability
    Keywords: Molecular Medicine ; Molecular biology ; Cell biology ; Biochemistry
    Description / Table of Contents: History and current status of autophagy research -- Regulation of ATG and autophagy initiation -- Regulation of autophagy by mTOR signaling pathway -- AMPK and autophagy -- Beclin 1, Bcl-2 and autophagy -- TP53, TP53 target genes (DRAM, TIGAR) and autophagy -- Ca(2+) ion and autophagy -- Endoplasmic reticulum stress and autophagy -- Oxidative stress and autophagy -- Noncoding RNAs and atophagy -- Epigenetic regulation of autophagy -- Protein modification and autophagy activation -- Other molecular mechanisms regulating Autophagy -- The role of nanomaterials in autophagy -- Structural basis of autophagy regulatory proteins -- Autophagy and energy metabolism -- Autophagy and lipid metabolism -- Autophagy and the metabolism of misfolding protein -- Autophagy in mitochondrial quality control -- Chaperone-mediated autophagy -- Autophagy in reproduction -- Autophagy in development and differentiation -- Autophagy in normal stem cells and specialized cells -- Autophagy, aging and longevity -- Autophagy and the ubiquitin-proteasome system -- Immuno-signal and autophagy regulation -- Autophagy and the immune response -- Autophagy and immune tolerance -- Autophagy and cell survival and death -- Coordination of autophagy and other cellular activities
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource (XV, 727 p. 91 illus., 83 illus. in color)
    Edition: 1st ed. 2019
    ISBN: 9789811506024
    Series Statement: Advances in Experimental Medicine and Biology 1206
    URL: https://doi.org/10.1007/978-981-15-0602-4
    DOI: 10.1007/978-981-15-0602-4
    Language: English
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    GEOMAR CATALOGUE
    Link to Library Catalog
    get availability status
  • 2
    Electronic Resource
    Electronic Resource
    Lesions of Mouse Striatum Induced by 6-Hydroxydopamine Differentially Alter the Density, Rate of Synthesis, and Level of Gene Expression of D1 and D2 Dopamine Receptors (1994)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 62 (1994), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: To study the effects of altering dopaminergic input on the levels and rate of synthesis of dopamine receptors, corpora striata of mice were lesioned unilaterally with 6-hydroxydopamine (6-OHDA), and the densities and levels of the mRNAs for D1 and D2 dopamine receptors were determined. The results showed that 6-OHDA caused significant reductions in D1 dopamine receptors and in D1 dopamine receptor mRNA in dorsolateral and dorsomedial regions of the lesioned striatum. By contrast, 6-OHDA lesions caused significant increases in D2 dopamine receptors and in D2 dopamine receptor mRNA in dorsolateral and ventrolateral regions of the lesioned striatum. To assess the effects of 6-OHDA lesions on the rate of synthesis of D1 and D2 dopamine receptors, the irreversibly acting dopamine receptor antagonist 2-ethoxy-1-ethoxycarbonyl-1,2-dihydroquinoline (EEDQ) was administered, and the rate of recovery of these receptors determined. The lesions decreased the rate of synthesis of D1 dopamine receptors in dorsolateral striatum but increased the rate of synthesis of D2 dopamine receptors in dorsolateral striatum. Correlation of these molecular events with dopaminergic behaviors showed that the rate of recovery from EEDQ-induced cataleptic activity and the recovery from inhibition of quinpirole-induced rotational behavior was more rapid than the recovery of either the D1 or D2 dopamine receptor. These results suggest that dopaminergic denervation differentially affects the rate of synthesis of D1 and D2 dopamine receptors in mouse striatum, and that these alterations in the rates of synthesis of the receptors may be explained by corresponding alterations in the levels of the respective transcripts for these receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1994.62020411.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Kainic Acid-Induced Apoptosis in Rat Striatum Is Associated with Nuclear Factor-κB Activation (2000)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 74 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present study evaluated whether nuclear factor-κB (NF-κB) activation contributes to the apoptotic-like death of striatal neurons induced by kainic acid (KA) receptor stimulation. Intrastriatally infused KA (1.25-5.0 nmol) produced substantial neuronal loss as indicated by an 8-73% decrease in 67-kDa glutamic acid decarboxylase (p 〈 0.05). KA (1.25-5.0 nmol) elicited internucleosomal DNA fragmentation that was inhibited by the AMPA/KA receptor antagonist NBQX (1,2,3,4-tetrahydro-6-nitro-2,3-dibenzo[f]quinoxaline-7-sulfonamide) but not by the NMDA receptor antagonist MK-801. A decrease in IκB-α protein levels, which was accompanied by an increase in NF-κB binding activity, was found from 6 to 72 h after KA (2.5 nmol) infusion. NF-κB was composed mainly of p65 and c-Rel as revealed by supershift assay. In addition, c-Myc and p53 increased from five- to sevenfold from 24 to 72 h after KA (2.5 nmol) administration. Immunohistochemistry revealed high levels of c-Myc and p53 immunoreactivity, mainly in medium-sized striatal neurons. Pretreatment with the cell-permeable recombinant peptide NF-κB SN50 (5-20 μg) blocked NF-κB nuclear translocation, but had no effect on AP-1 binding. NF-κB SN50 also inhibited the KA-induced up-regulation of c-Myc and p53, as well as internucleosomal DNA fragmentation. The apoptotic-like destruction of rat striatal neurons induced by KA receptor stimulation thus appears to involve biochemical mechanisms similar to those mediating the excitotoxic response to NMDA receptor stimulation. The present results provide additional support for the view that NF-κB activation contributes to c-Myc and p53 induction and subsequent apoptosis in an excitotoxic model of Huntington’s disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.740647.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Prostaglandin A1 inhibits rotenone-induced apoptosis in SH-SY5Y cells (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 83 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The degeneration of nigral dopamine neurons in Parkinson's disease (PD) reportedly involves a defect in brain mitochondrial complex I in association with the activation of nuclear factor-κB (NF-κB) and caspase-3. To elucidate molecular mechanisms possibly linking these events, as well as to evaluate the neuroprotective potential of the cyclopentenone prostaglandin A1 (PGA1), an inducer of heat shock proteins (HSPs), we exposed human dopaminergic SH-SY5Y cells to the complex I inhibitor rotenone. Dose-dependent apoptosis was preceded by the nuclear translocation of NF-κB and then the activation of caspase-3 over the ensuing 24 h. PGA1 increased the expression of HSP70 and HSP27 and protected against rotenone-induced apoptosis, without increasing necrotic death. PGA1 blocked the rotenone-induced nuclear translocation of NF-κB and attenuated, but did not abolish, the caspase-3 elevation. Unexpectedly, the caspase-3 inhibitor, Ac-DEVD.CHO (DEVD), at a concentration that completely prevented the caspase-3 elevation produced by rotenone, failed to protect against apoptosis. These results suggest that complex I deficiency in dopamine cells can induce apoptosis by a process involving early NF-κB nuclear translocation and caspase-3 activation. PGA1 appears to protect against rotenone-induced cell death by inducing HSPs and blocking nuclear translocation of NF-κB in a process that attenuates caspase-3 activation, but is not mediated by its inhibition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2002.01224.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Regulation of c-Jun N-terminal kinase, p38 kinase and AP-1 DNA binding in cultured brain neurons: roles in glutamate excitotoxicity and lithium neuroprotection (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 84 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In rat cerebellar granule cells, glutamate induced rapid activation of c-Jun N-terminal kinase (JNK) and p38 kinase to phosphorylate c-Jun (at Ser63) and p53 (at Ser15), respectively, and a subsequent marked increase in activator protein-1 (AP-1) binding that preceded apoptotic death. These glutamate-induced effects and apoptosis could largely be prevented by long-term (7 days) pretreatment with 0.5–2 mm lithium, an antibipolar drug. Glutamate's actions could also be prevented by known blockers of this pathway, MK-801 (an NMDA receptor blocker), SB 203580 (a p38 kinase inhibitor) and curcumin (an AP-1 binding inhibitor). The concentration- and time-dependent suppression of glutamate's effects by lithium and curcumin correlated well with their neuroprotective effects. These results suggest a prominent role of JNK and p38, as well as their downstream AP-1 binding activation and p53 phosphorylation in mediating glutamate excitotoxicity. Moreover, the neuroprotective effects of lithium are mediated, at least in part, by suppressing NMDA receptor-mediated activation of the mitogen-activated protein kinase pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.01548.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...