Glutamate leakage from a compartmentalized intracellular metabolic pool and activation of the lipoxygenase pathway mediate oxidative astrocyte death by reversed glutamate transport

Glia ◽  
2006 ◽  
Vol 54 (1) ◽  
pp. 47-57 ◽  
Author(s):  
Diane B. Re ◽  
Imane Nafia ◽  
Christophe Melon ◽  
Keiko Shimamoto ◽  
Lydia Kerkerian-Le Goff ◽  
...  
Keyword(s):  
Glutamate Transport ◽  
Lipoxygenase Pathway ◽  
Metabolic Pool

Neurochemistry of L-Glutamate Transport in the CNS: A Review of Thirty Years of Progress

2001 ◽  
Vol 66 (9) ◽  
pp. 1315-1340 ◽  
Author(s):  
Vladimir J. Balcar ◽  
Akiko Takamoto ◽  
Yukio Yoneda
Keyword(s):  
Molecular Biology ◽  
Glutamate Transport ◽  
Mammalian Brain ◽  
Activity Data ◽  
System A ◽  
Recent Developments ◽  
The Central Nervous System ◽  
Health And Disease ◽  
Disease Analysis

The review highlights the landmark studies leading from the discovery and initial characterization of the Na+-dependent "high affinity" uptake in the mammalian brain to the cloning of individual transporters and the subsequent expansion of the field into the realm of molecular biology. When the data and hypotheses from 1970's are confronted with the recent developments in the field, we can conclude that the suggestions made nearly thirty years ago were essentially correct: the uptake, mediated by an active transport into neurons and glial cells, serves to control the extracellular concentrations of L-glutamate and prevents the neurotoxicity. The modern techniques of molecular biology may have provided additional data on the nature and location of the transporters but the classical neurochemical approach, using structural analogues of glutamate designed as specific inhibitors or substrates for glutamate transport, has been crucial for the investigations of particular roles that glutamate transport might play in health and disease. Analysis of recent structure/activity data presented in this review has yielded a novel insight into the pharmacological characteristics of L-glutamate transport, suggesting existence of additional heterogeneity in the system, beyond that so far discovered by molecular genetics. More compounds that specifically interact with individual glutamate transporters are urgently needed for more detailed investigations of neurochemical characteristics of glutamatergic transport and its integration into the glutamatergic synapses in the central nervous system. A review with 162 references.

scholarly journals dl-β-Aminobutyric Acid–Induced Resistance of Potato Against Phytophthora infestans Requires Salicylic Acid but Not Oxylipins

2010 ◽  
Vol 23 (5) ◽  
pp. 585-592 ◽  
Author(s):  
Lennart Eschen-Lippold ◽  
Simone Altmann ◽  
Sabine Rosahl
Keyword(s):  
Salicylic Acid ◽  
Phytophthora Infestans ◽  
Induced Resistance ◽  
Crop Plants ◽  
Aminobutyric Acid ◽  
Systemic Resistance ◽  
Lipoxygenase Pathway ◽  
Promising Alternative ◽  
Functional Analyses ◽  
Late Blight Pathogen

Inducing systemic resistance responses in crop plants is a promising alternative way of disease management. To understand the underlying signaling events leading to induced resistance, functional analyses of plants defective in defined signaling pathway steps are required. We used potato, one of the economically most-important crop plants worldwide, to examine systemic resistance against the devastating late blight pathogen Phytophthora infestans, induced by treatment with dl-β-aminobutyric acid (BABA). Transgenic plants impaired in either the 9-lipoxygenase pathway, which produces defense-related compounds, or the 13-lipoxygenase pathway, which generates jasmonic acid–derived signals, expressed wild-type levels of BABA-induced resistance. Plants incapable of accumulating salicylic acid (SA), on the other hand, failed to mount this type of induced resistance. Consistently, treatment of these plants with the SA analog 2,6-dichloroisonicotinic acid restored BABA-induced resistance. Together, these results demonstrate the indispensability of a functional SA pathway for systemic resistance in potato induced by BABA.

Glutamine and Glutamate Transport inCyanophora paradoxa

Botanica Acta ◽  
1993 ◽  
Vol 106 (5) ◽  
pp. 435-440 ◽  
Author(s):  
K. Kloos ◽  
R. Schlichting ◽  
W. Zimmer ◽  
H. Bothe
Keyword(s):  
Glutamate Transport

scholarly journals Report of a Novel ALOX12B Mutation in Self-Improving Collodion Ichthyosis with an Overview of the Genetic Background of the Collodion Baby Phenotype

Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 624
Author(s):  
Pálma Anker ◽  
Norbert Kiss ◽  
István Kocsis ◽  
Éva Czemmel ◽  
Krisztina Becker ◽  
...  
Keyword(s):  
Genetic Diseases ◽  
Severity Index ◽  
Severe Form ◽  
Heterozygous Mutation ◽  
Lipoxygenase Pathway ◽  
Severe Condition ◽  
Skin Changes ◽  
Congenital Ichthyosis ◽  
Autosomal Recessive Congenital Ichthyosis ◽  
Collodion Baby

Collodion baby is a congenital, transient phenotype encountered in approximately 70–90% of autosomal recessive congenital ichthyosis and is an important entity of neonatal erythroderma. The clinical outcome after this severe condition is variable. Genetic mutations of components of the epidermal lipoxygenase pathway have been implicated in the majority of self-improving collodion ichthyosis (SICI). In SICI, the shedding of the collodion membrane reveals clear skin or only mild residual manifestation of ichthyosis. Here we report the case of a girl born with a severe form of collodion baby phenotype, whose skin almost completely cleared within the first month of life. At the age of 3 years, only mild symptoms of a keratinization disorder remained. However, the severity of erythema and scaling showed mild fluctuations over time. To objectively evaluate the skin changes of the patient, we assessed the ichthyosis severity index. Upon sequencing of the ALOX12B gene, we identified a previously unreported heterozygous nonsense mutation, c.1607G>A (p.Trp536Ter) with the recurrent, heterozygous mutation c.1562A>G (p.Tyr521Cys). Thereby, our findings expand the genotypic spectrum of SICI. In addition, we summarize the spectrum of further genetic diseases that can present at birth as collodion baby, in particular the SICI.

Candidate Genes of the 5-Lipoxygenase Pathway in Acute Coronary Syndrome: A Pilot Study

2008 ◽  
Vol 9 (4) ◽  
pp. 280-292 ◽  
Author(s):  
Shu-Fen Wung ◽  
Bradley E. Aouizerat
Keyword(s):  
Acute Coronary Syndrome ◽  
Pilot Study ◽  
Nucleotide Polymorphisms ◽  
Common Allele ◽  
Lipoxygenase Pathway ◽  
Single Nucleotide ◽  
Coronary Syndrome ◽  
Increased Risk ◽  
Caucasian Patients ◽  
Alox5ap Gene

Purpose. The purpose of this pilot study was to examine arachidonate 5-lipoxygenase (ALOX5) and ALOX5-activating protein (ALOX5AP) gene variations in patients with and without acute coronary syndrome (ACS). Methodology. Four and six single nucleotide polymorphisms spanning the ALOX5 and ALOX5AP genes, respectively, were genotyped in 19 non-Hispanic Caucasian patients with ACS and 27 controls. Results. Presence of the common allele of rs9508835 (ALOX5AP) and the minor allele of rs2029253 (ALOX5) were associated with ACS. After adjustment for age, being a carrier of the rs9508835 common allele was associated with an increased risk of ACS (odds ratio = 2.86). Relevance for nursing practice. Through the inhibition of the ALOX5AP gene by downregulation of the leukotriene pathway, the risk of ACS may be decreased in individuals that carry susceptibility allele(s). Knowledge of the genetic basis of treatments that downregulate the leukotriene pathway may prove essential to the care of individuals with ACS.

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