scholarly journals Dysregulation of signal transduction pathways as a potential mechanism of nervous system alterations in HIV-1 gp120 transgenic mice and humans with HIV-1 encephalitis.

1996 ◽  
Vol 97 (3) ◽  
pp. 789-798 ◽  
Author(s):  
T Wyss-Coray ◽  
E Masliah ◽  
S M Toggas ◽  
E M Rockenstein ◽  
M J Brooker ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Nervous System ◽  
Transgenic Mice ◽  
Signal Transduction Pathways ◽  
Potential Mechanism ◽  
Hiv 1

scholarly journals Signal Transduction Pathways of Acupuncture for Treating Some Nervous System Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-37 ◽  
Author(s):  
Hsiang-Chun Lai ◽  
Qwang-Yuen Chang ◽  
Ching-Liang Hsieh
Keyword(s):  
Signal Transduction ◽  
Nervous System ◽  
Cochrane Library ◽  
Signal Transduction Pathways ◽  
Signal Pathways ◽  
Nervous System Diseases ◽  
China National Knowledge Infrastructure ◽  
Knowledge Infrastructure ◽  
Cerebral Ischemic ◽  
The Cochrane Library

In this article, we review signal transduction pathways through which acupuncture treats nervous system diseases. We electronically searched the databases, including PubMed, MEDLINE, clinical Key, the Cochrane Library, and the China National Knowledge Infrastructure from their inception to December 2018 using the following MeSH headings and keywords alone or in varied combination: acupuncture, molecular, signal transduction, genetic, cerebral ischemic injury, cerebral hemorrhagic injury, stroke, epilepsy, seizure, depression, Alzheimer’s disease, dementia, vascular dementia, and Parkinson’s disease. Acupuncture treats nervous system diseases by increasing the brain-derived neurotrophic factor level and involves multiple signal pathways, including p38 MAPKs, Raf/MAPK/ERK 1/2, TLR4/ERK, PI3K/AKT, AC/cAMP/PKA, ASK1-JNK/p38, and downstream CREB, JNK, m-TOR, NF-κB, and Bcl-2/Bax balance. Acupuncture affects synaptic plasticity, causes an increase in neurotrophic factors, and results in neuroprotection, cell proliferation, antiapoptosis, antioxidant activity, anti-inflammation, and maintenance of the blood-brain barrier.

scholarly journals Visual Cortex Plasticity: A Complex Interplay of Genetic and Environmental Influences

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
José Fernando Maya-Vetencourt ◽  
Nicola Origlia
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Nervous System ◽  
Sensory Deprivation ◽  
Environmental Influences ◽  
Signal Transduction Pathways ◽  
Gene Promoters ◽  
Complex Interplay ◽  
Intracellular Signal Transduction ◽  
Intracellular Signal

The central nervous system architecture is highly dynamic and continuously modified by sensory experience through processes of neuronal plasticity. Plasticity is achieved by a complex interplay of environmental influences and physiological mechanisms that ultimately activate intracellular signal transduction pathways regulating gene expression. In addition to the remarkable variety of transcription factors and their combinatorial interaction at specific gene promoters, epigenetic mechanisms that regulate transcription have emerged as conserved processes by which the nervous system accomplishes the induction of plasticity. Experience-dependent changes of DNA methylation patterns and histone posttranslational modifications are, in fact, recruited as targets of plasticity-associated signal transduction mechanisms. Here, we shall concentrate on structural and functional consequences of early sensory deprivation in the visual system and discuss how intracellular signal transduction pathways associated with experience regulate changes of chromatin structure and gene expression patterns that underlie these plastic phenomena. Recent experimental evidence for mechanisms of cross-modal plasticity following congenital or acquired sensory deprivation both in human and animal models will be considered as well. We shall also review different experimental strategies that can be used to achieve the recovery of sensory functions after long-term deprivation in humans.

scholarly journals FoxO Proteins in the Nervous System

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Kenneth Maiese
Keyword(s):  
Signal Transduction ◽  
Nervous System ◽  
Transcription Factors ◽  
Protein Kinase ◽  
The Body ◽  
Signal Transduction Pathways ◽  
Forkhead Transcription Factors ◽  
Cell Death Pathways ◽  
Neuronal Disease ◽  
Inducible Protein

Acute as well as chronic disorders of the nervous system lead to significant morbidity and mortality for millions of individuals globally. Given the ability to govern stem cell proliferation and differentiated cell survival, mammalian forkhead transcription factors of the forkhead box class O (FoxO) are increasingly being identified as potential targets for disorders of the nervous system, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and auditory neuronal disease. FoxO proteins are present throughout the body, but they are selectively expressed in the nervous system and have diverse biological functions. The forkhead O class transcription factors interface with an array of signal transduction pathways that include protein kinase B (Akt), serum- and glucocorticoid-inducible protein kinase (SgK), IκB kinase (IKK), silent mating type information regulation 2 homolog 1 (S. cerevisiae) (SIRT1), growth factors, and Wnt signaling that can determine the activity and integrity of FoxO proteins. Ultimately, there exists a complex interplay between FoxO proteins and their signal transduction pathways that can significantly impact programmed cell death pathways of apoptosis and autophagy as well as the development of clinical strategies for the treatment of neurodegenerative disorders.

Central nervous system damage produced by expression of the HIV-1 coat protein gpl20 in transgenic mice

Nature ◽  
1994 ◽  
Vol 367 (6459) ◽  
pp. 188-193 ◽  
Author(s):  
Stephanie M. Toggas ◽  
Eliezer Masliah ◽  
Edward M. Rockenstein ◽  
Glenn F. Rail ◽  
Carmela R. Abraham ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Coat Protein ◽  
Transgenic Mice ◽  
Central Nervous System Damage ◽  
Hiv 1

scholarly journals Interactions and Signal Transduction Pathways Involved during Central Nervous System Entry by Neisseria meningitidis across the Blood–Brain Barriers

2020 ◽  
Vol 21 (22) ◽  
pp. 8788
Author(s):  
Julia Borkowski ◽  
Horst Schroten ◽  
Christian Schwerk
Keyword(s):  
Signal Transduction ◽  
Central Nervous System ◽  
Nervous System ◽  
Neisseria Meningitidis ◽  
Severe Disease ◽  
Blood Stream ◽  
Brain Parenchyma ◽  
Host Cells ◽  
Signal Transduction Pathways ◽  
Blood Brain

The Gram-negative diplococcus Neisseria meningitidis, also called meningococcus, exclusively infects humans and can cause meningitis, a severe disease that can lead to the death of the afflicted individuals. To cause meningitis, the bacteria have to enter the central nervous system (CNS) by crossing one of the barriers protecting the CNS from entry by pathogens. These barriers are represented by the blood–brain barrier separating the blood from the brain parenchyma and the blood–cerebrospinal fluid (CSF) barriers at the choroid plexus and the meninges. During the course of meningococcal disease resulting in meningitis, the bacteria undergo several interactions with host cells, including the pharyngeal epithelium and the cells constituting the barriers between the blood and the CSF. These interactions are required to initiate signal transduction pathways that are involved during the crossing of the meningococci into the blood stream and CNS entry, as well as in the host cell response to infection. In this review we summarize the interactions and pathways involved in these processes, whose understanding could help to better understand the pathogenesis of meningococcal meningitis.

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