Kooperativer Bibliotheksverbund

Berlin Brandenburg

and
and

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • Signal Transduction
Type of Medium
Language
Year
  • 1
    Language: English
    In: Immunologic Research, 2012, Vol.52(1), pp.157-168
    Description: Development of resistance to TRAIL-induced toxicity is one of the strategies used from tumor cells to escape destruction from the immune system. This process may occur through aberrant expression of functional receptors, overexpression of decoy receptors on tumor cell membrane, or malfunctioning of downstream signals triggered by specific ligation of TRAIL. Numerous cytostatic, but also noncytostatic, drugs like protease inhibitors and NO-hybridized molecules have been shown to revert sensitivity of neoplastic cells to TRAIL by means of different mechanisms. This paper will review the possible routes of reconstitution of sensitivity to TRAIL-mediated immune response by specific modulation of different signals responsible for the development of resistance at both the membrane and the intracellular levels. Moreover, we will review and suggest novel strategies, aimed at resetting immune cell efficiency in cancer treatment.
    Keywords: TRAIL resistance ; Death receptors ; Saquinavir-NO
    ISSN: 0257-277X
    E-ISSN: 1559-0755
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Language: English
    In: Neuroscience and Biobehavioral Reviews, October 2014, Vol.46, pp.228-241
    Description: Activation of group-I metabotropic glutamate receptors, mGlu1 and mGlu5, triggers a variety of signalling pathways in neurons and glial cells, which are differently implicated in synaptic plasticity. The earliest and much of key studies discovered abnormal mGlu5 receptor function in Fragile X syndrome (FXS) mouse models which then motivated more recent work that finds mGlu5 receptor dysfunction in related disorders such as intellectual disability (ID), obsessive-compulsive disorder (OCD) and autism. Therefore, mGlu1/5 receptor dysfunction may represent a common aetiology of these complex diseases. Furthermore, many studies have focused on dysregulation of mGlu5 signalling to synaptic protein synthesis. However, emerging evidence finds abnormal mGlu5 receptor interactions with its scaffolding proteins in FXS which results in mGlu5 receptor dysfunction and phenotypes independent of signalling to protein synthesis. Finally, both an increased and reduced mGlu5 functioning seem to be associated with ID and autism spectrum disorders, with important consequences for potential treatment of these developmental disorders.
    Keywords: Synaptic Plasticity ; Developmental Disorders ; Mental Retardation ; Fragile X ; Fmrp ; TSC ; Pten ; Neuroligin ; Homer ; Shank ; Sapap3 ; Anatomy & Physiology
    ISSN: 0149-7634
    E-ISSN: 1873-7528
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Language: English
    In: PLoS ONE, 01 January 2016, Vol.11(3), p.e0152104
    Description: BACKGROUND:Malignant melanoma is an aggressive tumor of the skin and seems to be resistant to current therapeutic approaches. Melanocytic transformation is thought to occur by sequential accumulation of genetic and molecular alterations able to activate the Ras/Raf/MEK/ERK (MAPK) and/or the...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Language: English
    In: PLoS ONE, 01 January 2011, Vol.6(1), p.e16447
    Description: The identification of mechanisms that mediate stress-induced hippocampal damage may shed new light into the pathophysiology of depressive disorders and provide new targets for therapeutic intervention. We focused on the secreted glycoprotein...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Language: English
    In: Neuropharmacology, March 2013, Vol.66, pp.24-30
    Description: The purpose of the present article is to review our actual knowledge on the desensitization of metabotropic glutamate receptors based on the literature available so far, with the attempt to emphasize all converging data and to give a possible explanation to those evidences that still remain controversial. 1. We review our knowledge on the regulation of mGlu receptors based on the available literature 2. We report converging data and we comment on issues that still remain controversial. This article is part of a Special Issue entitled ‘Metabotropic Glutamate Receptors’. ► We review our knowledge on the desensitization of mGlu receptors. ► We focus both on converging data and on issues that still remain controversial. ► GRK2 regulates mGlu1 receptor by a phosphorylation-independent mechanism. ► The mGlu2 (but not the mGlu3) receptor is resistant to homologous desensitization.
    Keywords: Metabotropic Glutamate Receptors ; Receptor Desensitization ; Grks ; Arrestins ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Language: English
    In: Current Opinion in Pharmacology, February 2018, Vol.38, pp.1-7
    Description: A dysfunction of glutamate signaling is implicated at several levels in the pathogenesis of Alzheimer's disease. Currently, metabotropic glutamate receptors, which have a wide distribution in the central nervous system and activate a multitude of cell signaling pathways, are pursued as targets for therapeutic intervention in Alzheimer's disease. Research is still limited, but results underscore the relevance of ongoing studies. Here we discuss the latest updates regarding metabotropic glutamate receptors and their role in Alzheimer's disease, as well as promising metabotropic glutamate receptor ligands that have been investigated in preclinical models of Alzheimer's disease.
    Keywords: Pharmacy, Therapeutics, & Pharmacology
    ISSN: 1471-4892
    E-ISSN: 1471-4973
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Language: English
    In: BBA - Molecular Cell Research, December 2016, Vol.1863(12), pp.2942-2976
    Description: Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple signaling pathways such as: PI3K/PTEN/Akt/mTOR, Ras/Raf/MEK/ERK, Wnt/beta-catenin, hedgehog, Notch and TP53. Mutations that occur in these and other pathways can alter the effects that natural GSK-3 activity has on regulating these signaling circuits that can lead to cancer as well as other diseases. The novel roles that microRNAs play in regulation of the effects of GSK-3 will also be evaluated. Targeting GSK-3 and these other pathways may improve therapy and overcome therapeutic resistance.
    Keywords: Gsk-3 ; Wnt/Beta-Catenin ; Pi3k ; Akt ; Mtor ; Hedgehog ; Notch ; Targeted Therapy ; Therapy Resistance ; Biology ; Chemistry
    ISSN: 0167-4889
    E-ISSN: 1879-2596
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Language: English
    In: Trends in Pharmacological Sciences, 2010, Vol.31(4), pp.153-160
    Description: Activation of metabotropic glutamate 2 (mGlu2) receptors inhibits pain transmission at the synapses between primary afferent fibers and neurons in the dorsal horn of the spinal cord. In addition, mGlu2 receptors are found in peripheral nociceptors, and in pain-regulatory centers of the brain stem and forebrain. mGlu2 receptor agonists produce analgesia in models of inflammatory and neuropathic pain, but their use is limited by the development of tolerance. A new therapeutic strategy could be based on the transcriptional regulation of mGlu2 receptors via the acetylation-promoted activation of the p65/RelA transcription factor. “Epigenetic” drugs that increase mGlu2 receptor expression, including -acetylcarnitine and inhibitors of histone deacetylases, have a different analgesic profile with no tolerance to the therapeutic effect after repeated dosing.
    Keywords: Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0165-6147
    E-ISSN: 1873-3735
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    Language: English
    In: Molecular Neurobiology, 2012, Vol.46(3), pp.605-613
    Description: Alzheimer's disease is the most common form of dementia among older people and is still untreatable. While β-amyloid protein is recognized as the disease determinant with a pivotal role in inducing neuronal loss and dementia, an impaired brain insulin signaling seems to account in part for the cognitive deficit associated with the disease. The origin of this defective signaling is uncertain. Accumulating toxic species of β-amyloid, the so-called oligomers, has been proposed to be responsible for downregulation of neuronal insulin receptors. We have found that the nontoxic form of β-amyloid, the monomer, is able to activate insulin/insulin-like growth factor-1 (IGF-1) receptor signaling and thus behaves as a neuroprotectant agent. Our suggestion is that depletion of β-amyloid monomers, occurring in the preclinical phase of Alzheimer's disease, might be the cause of early insulin/IGF-1 signaling disturbances that anticipate cognitive decline.
    Keywords: β-Amyloid ; Insulin ; Insulin-like growth factor 1 ; Alzheimer's disease
    ISSN: 0893-7648
    E-ISSN: 1559-1182
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Language: English
    In: Neuropharmacology, March 2013, Vol.66, pp.143-150
    Description: Synaptic transmission is essential for early development of the central nervous system. However, the mechanisms that regulate early synaptic transmission in the cerebral cortex are unclear. PKMζ is a kinase essential for the maintenance of LTP. We show for the first time that inhibition of PKMζ produces a profound depression of basal synaptic transmission in neonatal, but not adult, rat perirhinal cortex. This suggests that synapses in early development are in a constitutive LTP-like state. Furthermore, basal synaptic transmission in immature, but not mature, perirhinal cortex relies on persistent activity of metabotropic glutamate (mGlu) receptor, PI3Kinase and mammalian target of rapamycin (mTOR). Thus early in development, cortical synapses exist in an LTP-like state maintained by tonically active mGlu receptor-, mTOR- and PKMζ- dependent cascades. These results provide new understanding of the molecular mechanisms that control synapses during development and may aid our understanding of developmental disorders such as autism and schizophrenia. This article is part of a Special Issue entitled ‘Metabotropic Glutamate Receptors’. ► Synapses are in a constitutive LTP-like state in the developing perirhinal cortex. ► PKMζ inhibition reduces synaptic transmission in the developing perirhinal cortex. ► Group-I mGlu receptors support the LTP-like state in the perirhinal cortex. ► PKMζ, PI3Kinase and mTOR are down stream of group-I mGlu receptors.
    Keywords: Ltp ; Pkmζ ; Group I Mglu Receptor ; Cerebral Cortex ; Development ; Mtor ; Protein Translation ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages