Amino Acid Transport Systems
Amino Acid Transport System L
Amino Acid Transport Systems, Basic
Amino Acid Transport System A
Amino Acid Transport Systems, Neutral
Biological Transport, Active
Amino Acid Transport System ASC
Antigens, CD98 Heavy Chain
Membrane Transport Proteins
Fatty Acid Transport Proteins
Vesicular Glutamate Transport Proteins
Amino Acid Sequence
Molecular Sequence Data
Amino Acid Transport Systems, Acidic
Sequence Homology, Amino Acid
Rats, Inbred Strains
Large Neutral Amino Acid-Transporter 1
Antigens, CD98 Light Chains
Amino Acid Substitution
Amino Acid Transport System X-AG
Monosaccharide Transport Proteins
Amino Acid Transport Disorders, Inborn
Amino Acids, Essential
Cationic Amino Acid Transporter 1
Amino Acid Motifs
ATP-Binding Cassette Transporters
Organic Anion Transporters
Anion Transport Proteins
Genetic Complementation Test
Radioisotope Dilution Technique
Protein Structure, Tertiary
Sequence Homology, Nucleic Acid
Recombinant Fusion Proteins
Organic Anion Transporters, Sodium-Dependent
Bile Acids and Salts
Carcinoma, Ehrlich Tumor
Glutamate Plasma Membrane Transport Proteins
Electrophoresis, Polyacrylamide Gel
Periplasmic Binding Proteins
Sequence Analysis, DNA
Dose-Response Relationship, Drug
Cell Membrane Permeability
Gene Expression Regulation
Evidence for a novel glutamate-mediated signaling pathway in keratinocytes. (1/509)Phenotypic alterations in keratinocyte behavior are essential for maintaining epidermal integrity during growth and wound repair and rely on co-ordinated cell signaling events. Numerous growth factors and cytokines have been shown to be instrumental in guiding such changes in keratinocyte activity; here we provide evidence which proposes a novel epidermal signaling pathway mediated by the excitatory amino acid glutamate. Glutamate is the major excitatory neurotransmitter at synaptic junctions within the central nervous system; however, we have identified expression in vivo of several regulatory molecules associated with glutamate signaling in keratinocytes. In resting rat skin epidermis, different classes of glutamate receptors, transporters, and a recently described clustering protein were shown to display distinct distribution patterns, supportive of a multifunctional cellular communication pathway. Immunoreactive N-methyl-D-aspartate-type, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate-type, and metabotropic-type glutamate receptors were colocalized with the specific glutamate transporter EAAC1 in basal layer keratinocytes, and GLT-1, a related transporter, was expressed suprabasally. In full-thickness rat skin wounds, marked modifications in the distribution of N-methyl-D-aspartate receptors and EAAC1 were observed during re-epithelialization, and alterations in N-methyl-D-aspartate receptor expression accompanied embryonic epidermal development, implicating glutamate signaling in these important biologic events. Furthermore, we provide evidence that these receptors are functional in vitro. These data provide strong evidence to support a role for glutamate in the control of epidermal renewal, and therefore suggest potentially novel therapeutic targets for the treatment of skin disease and enhancement of wound healing. (+info)
Optical detection of synaptically induced glutamate transport in hippocampal slices. (2/509)Although it has long been believed that glial cells play a major role in transmitter uptake at synapses in the CNS, the relative contribution of glial and neuronal cells to reuptake of synaptically released glutamate has been unclear. Recent identification of the diverse glutamate transporter subtypes provides an opportunity to examine this issue. To monitor glutamate transporter activity, we optically detected synaptically induced changes of membrane potential from hippocampal CA1 field in slice preparations using a voltage-sensitive dye, RH155. In the presence of ionotropic glutamate-receptor blockers, synaptic inputs gave rise to a slow depolarizing response (SDR) in the dendritic field. The amplitude of SDR correlated well with presynaptic activities, suggesting that it was related to transmitter release. The SDR was found to be caused by the activities of glutamate transporters because it was not affected by blockers for GABAA, nACh, 5-HT3, P2X, or metabotropic glutamate receptors but was greatly reduced by dihydrokainate (DHK), a specific blocker for GLT-1 transporter, and by D, L-threo-beta-hydroxyaspartate (THA), a blocker for EAAC, GLAST, and GLT-1 transporters. When SDR was detected with RH482 dye, which stains both glial and neuronal cells, 1 mM DHK and 1 mM THA were equally effective in suppressing SDR. The SDR was very small in GLT-1 knockout mice but was maintained in gerbil hippocampi in which postsynaptic neurons were absent because of ischemia. Because GLT-1 transporters are exclusively expressed in astrocytes, our results provide direct evidence that astrocytes play the dominant role in sequestering synaptically released glutamate. (+info)
Identification of truncated human glutamate transporter. (3/509)Excitatory amino-acid carrier 1 (EAAC1) is a high affinity Na+-dependent L-glutamate/D, L-Aspartate transporter protein. A truncated form of EAAC1 (tEAAC1) was identified by reverse transcription and polymerase chain reaction in the human cell line, ACHN, in which EAAC1 mRNA was highly expressed. The deduced amino acid sequence of tEAAC1 lacks 31-77 amino acids including the first extracellular domain. The mRNA encoding tEAAC1 was detected in various cells of human origin but not in cells of rat or mouse origin. The expression of tEAAC1 mRNA was proportional to that of full-length EAAC1 (fEAAC1) mRNA, suggesting common transcriptional regulation between tEAAC1 and fEAAC1. In addition, the expression of EAAC1 mRNA was relatively low or non-existent in non-adherent cells. (+info)
Expression of the GLT-1 subtype of Na+-dependent glutamate transporter: pharmacological characterization and lack of regulation by protein kinase C. (4/509)Several subtypes of Na+-dependent glutamate transporters have been pharmacologically differentiated in brain tissues. Five distinct cDNA clones that express Na+-dependent glutamate transport activity have been isolated. One goal of the current study was to compare the pharmacological properties of the rat GLT-1 subtype of transporter to those identified previously using rat brain tissues. To accomplish this goal, GLT-1 was stably transfected into two different cell lines that express low levels of endogenous transport activity (MCB and L-M (TK-)). Several clones stably transfected with GLT-1 were isolated. In each cell line, Na+-dependent glutamate transport activity was saturable with similar Km values (19 and 37 microM). The pharmacological properties of GLT-1-mediated transport in these cell lines paralleled those observed for the predominant pharmacology observed in cortical crude synaptosomes. These data are consistent with other lines of evidence that suggest that GLT-1 may be sufficient to explain most of the Na+-dependent glutamate transport activity in cortical synaptosomes. Although recent studies using HeLa cells have suggested that GLT-1 can be rapidly up-regulated by activation of protein kinase C (PKC), modulation of PKC or phosphatase activity had no effect on GLT-1-mediated activity in these transfected cell lines. To determine if GLT-1 regulation by PKC is cell-specific, HeLa cells, which endogenously express the EAAC1 subtype of transporter, were stably transfected with GLT-1. Although EAAC1-mediated activity was increased by activation of PKC, we found no evidence for regulation of GLT-1. Despite the present findings, GLT-1 activity may be regulated by PKC under certain conditions. (+info)
Nontransportable inhibitors attenuate reversal of glutamate uptake in synaptosomes following a metabolic insult. (5/509)Na+-dependent, high-affinity glutamate transporters in the central nervous system are generally credited with regulating extracellular levels of L-glutamate and maintaining concentrations below those that would induce excitotoxic injury. Under pathological conditions, however, it has been suggested that these same transporters may contribute to excitotoxic injury by serving as sites of efflux for cellular L-glutamate. In this study, we examine the efflux of [3H]D-aspartate from synaptosomes in response to both alternative substrates (i.e., heteroexchange), such as L-glutamate, and a metabolic insult (5 mM potassium cyanide and 1 mM iodoacetate). Exposure of synaptosomes containing [3H]D-aspartate to either L-glutamate or metabolic inhibitors increased the efflux of the radiolabeled substrate to over 200% of control values. Two previously identified competitive transport inhibitors (L-trans-2, 3-pyrrolidine dicarboxylate and dihydrokainate) failed to stimulate [3H]D-aspartate efflux but did inhibit glutamate-mediated heteroexchange, consistent with the action of nontransportable inhibitors. These compounds also attenuated the efflux of [3H]D-aspartate from synaptosomes exposed to the metabolic inhibitors. These results add further strength to the model of central nervous system injury-induced efflux of L-glutamate through its high-affinity transporters and identify a novel strategy to attenuate this process. (+info)
Structural features of the glutamate transporter family. (6/509)Neuronal and glial glutamate transporters remove the excitatory neurotransmitter glutamate from the synaptic cleft and thus prevent neurotoxicity. The proteins belong to a large and widespread family of secondary transporters, including bacterial glutamate, serine, and C4-dicarboxylate transporters; mammalian neutral-amino-acid transporters; and an increasing number of bacterial, archaeal, and eukaryotic proteins that have not yet been functionally characterized. Sixty members of the glutamate transporter family were found in the databases on the basis of sequence homology. The amino acid sequences of the carriers have diverged enormously. Homology between the members of the family is most apparent in a stretch of approximately 150 residues in the C-terminal part of the proteins. This region contains four reasonably well-conserved sequence motifs, all of which have been suggested to be part of the translocation pore or substrate binding site. Phylogenetic analysis of the C-terminal stretch revealed the presence of five subfamilies with characterized members: (i) the eukaryotic glutamate transporters, (ii) the bacterial glutamate transporters, (iii) the eukaryotic neutral-amino-acid transporters, (iv) the bacterial C4-dicarboxylate transporters, and (v) the bacterial serine transporters. A number of other subfamilies that do not contain characterized members have been defined. In contrast to their amino acid sequences, the hydropathy profiles of the members of the family are extremely well conserved. Analysis of the hydropathy profiles has suggested that the glutamate transporters have a global structure that is unique among secondary transporters. Experimentally, the unique structure of the transporters was recently confirmed by membrane topology studies. Although there is still controversy about part of the topology, the most likely model predicts the presence of eight membrane-spanning alpha-helices and a loop-pore structure which is unique among secondary transporters but may resemble loop-pores found in ion channels. A second distinctive structural feature is the presence of a highly amphipathic membrane-spanning helix that provides a hydrophilic path through the membrane. Recent data from analysis of site-directed mutants and studies on the mechanism and pharmacology of the transporters are discussed in relation to the structural model. (+info)
Differential expressions of glycine transporter 1 and three glutamate transporter mRNA in the hippocampus of gerbils with transient forebrain ischemia. (7/509)The extracellular concentrations of glutamate and its co-agonist for the N-methyl-d-aspartate (NMDA) receptor, glycine, may be under the control of amino acid transporters in the ischemic brain. However, there is little information on changes in glycine and glutamate transporters in the hippocampal CA1 field of gerbils with transient forebrain ischemia. This study investigated the spatial and temporal expressions of glycine transporter 1 (GLYT1) and three glutamate transporter (excitatory amino acid carrier 1, EAAC1; glutamate/aspartate transporter, GLAST; glutamate transporter 1, GLT1) mRNA in the gerbil hippocampus after 3 minutes of ischemia. The GLYT1 mRNA was transiently upregulated by the second day after ischemia in astrocytelike cells in close vicinity to hippocampal CA1 pyramidal neurons, possibly to reduce glycine concentration in the local extracellular spaces. The EAAC1 mRNA was abundantly expressed in almost all pyramidal neurons and dentate granule cells in the control gerbil hippocampus, whereas the expression level in CA1 pyramidal neurons started to decrease by the fourth day after ischemia in synchrony with degeneration of the CA1 neurons. The GLAST and GLT1 mRNA were rather intensely expressed in the dentate gyrus and CA3 field of the control hippocampus, respectively, but they were weakly expressed in the CA1 field before and after ischemia. As GLAST and GLT1 play a major role in the control of extracellular glutamate concentration, the paucity of these transporters in the CA1 field may account for the vulnerability of CA1 neurons to ischemia, provided that the functional GLAST and GLT1 proteins are also less in the CA1 field than in the CA3 field. This study suggests that the amino acid transporters play pivotal roles in the process of delayed neuronal death in the hippocampal CA1 field. (+info)
Effects of inhibiting glutamine synthetase and blocking glutamate uptake on b-wave generation in the isolated rat retina. (8/509)The purpose of the present experiments was to evaluate the contribution of the glutamate-glutamine cycle in retinal glial (Muller) cells to photoreceptor cell synaptic transmission. Dark-adapted isolated rat retinas were superfused with oxygenated bicarbonate-buffered media. Recordings were made of the b-wave of the electroretinogram as a measure of light-induced photoreceptor to ON-bipolar neuron transmission. L-methionine sulfoximine (1-10 mM) was added to superfusion media to inhibit glutamine synthetase, a Muller cell specific enzyme, by more than 99% within 5-10 min, thereby disrupting the conversion of glutamate to glutamine in the Muller cells. Threo-hydroxyaspartic acid and D-aspartate were used to block glutamate transporters. The amplitude of the b-wave was well maintained for 1-2 h provided 0.25 mM glutamate or 0.25 mM glutamine was included in the media. Without exogenous glutamate or glutamine the amplitude of the b-wave declined by about 70% within 1 h. Inhibition of glutamate transporters led to a rapid (2-5 min) reversible loss of the b-wave in the presence and absence of the amino acids. In contrast, inhibition of glutamine synthetase did not alter significantly either the amplitude of the b-wave in the presence of glutamate or glutamine or the rate of decline of the b-wave found in the absence of these amino acids. Excellent recovery of the b-wave was found when 0.25 mM glutamate was resupplied to L-methionine sulfoximine-treated retinas. The results suggest that in the isolated rat retina uptake of released glutamate into photoreceptors plays a more important role in transmitter recycling than does uptake of glutamate into Muller cells and its subsequent conversion to glutamine. (+info)
Cystinuria is caused by mutations in the SLC7A9 gene, which codes for a protein involved in the transport of cystine across the brush border membrane of renal tubular cells. The disorder is inherited in an autosomal recessive pattern, meaning that affected individuals must inherit two copies of the mutated gene (one from each parent) to develop symptoms.
There is no cure for cystinuria, but various treatments can help manage its symptoms. These may include medications to reduce the acidity of the urine and prevent infection, as well as surgical procedures to remove stones or repair damaged kidneys. In some cases, a kidney transplant may be necessary.
It's important for individuals with cystinuria to drink plenty of water and maintain good hydration to help flush out the urinary tract and prevent stone formation. They should also avoid certain foods that may increase the risk of stone formation, such as oxalate-rich foods like spinach and rhubarb.
Overall, while there is no cure for cystinuria, with proper management and care, individuals with this disorder can lead relatively normal lives and minimize the complications associated with it.
Hartnup disease is a rare genetic disorder that affects the body's ability to absorb vitamin B12 (cobalamin) and other nutrients. It is caused by a mutation in the HCN1 gene, which codes for a protein involved in the transport of cobalamin into the cells.
Symptoms of Hartnup Disease:
The symptoms of Hartnup disease can vary in severity and may include:
* Pale skin
* Shortness of breath
* Numbness or tingling in the hands and feet
* Poor appetite
Complications of Hartnup Disease:
If left untreated, Hartnup disease can lead to complications such as:
* Anemia (low red blood cell count)
* Nerve damage
* Skin problems
* Eye problems
* Hearing loss
* Increased risk of infections
Treatment of Hartnup Disease:
The treatment of Hartnup disease typically involves a combination of dietary changes and supplements. Patients with the condition may need to follow a strict diet that includes foods high in vitamin B12, such as meat, fish, and dairy products. They may also need to take supplements to ensure they are getting enough of this important nutrient. In some cases, medication may be prescribed to help manage symptoms.
Prognosis of Hartnup Disease:
The prognosis for Hartnup disease is generally good if the condition is diagnosed and treated early. With proper management, most patients with Hartnup disease can lead active and healthy lives. However, if left untreated, the condition can have serious complications that can be difficult to reverse.
Inheritance Pattern of Hartnup Disease:
Hartnup disease is an autosomal recessive disorder, which means that a person must inherit two copies of the mutated HCN1 gene (one from each parent) in order to develop the condition. If a person inherits only one copy of the mutated gene, they will be a carrier of the condition but are unlikely to develop symptoms themselves. Carriers of Hartnup disease can pass the mutated gene on to their children, who have a 25% chance of inheriting two copies of the gene and developing the condition.
Prevention of Hartnup Disease:
There is no known prevention for Hartnup disease. However, if a person knows they are a carrier of the condition, they can work with their healthcare provider to ensure they are getting enough vitamin B12 and monitoring their diet to prevent any complications.
In conclusion, Hartnup disease is a rare genetic disorder that affects the absorption of vitamin B12 in the small intestine. It can cause a range of symptoms, including diarrhea, abdominal pain, and fatigue. Treatment typically involves a combination of dietary changes and supplements, and early diagnosis and management can lead to a good prognosis. However, if left untreated, the condition can have serious complications. If you suspect you or someone you know may be experiencing symptoms of Hartnup disease, it is important to speak with a healthcare provider for proper diagnosis and treatment.
Also known as: aminoacyl-tRNA synthetase deficiency, aminoacyl-tRNA synthetase/tRNA synthetase deficiency, and amino acid transporter defects.
The signs and symptoms of CE can vary depending on the location of the tumor, but they may include:
* Lumps or swelling in the neck, underarm, or groin area
* Weight loss
* Night sweats
* Swollen lymph nodes
* Pain in the affected area
CE is caused by a genetic mutation that leads to uncontrolled cell growth and division. The exact cause of the mutation is not fully understood, but it is believed to be linked to exposure to certain viruses or chemicals.
Diagnosis of CE typically involves a combination of physical examination, imaging tests such as CT scans or PET scans, and biopsy to confirm the presence of cancer cells. Treatment options for CE depend on the stage and location of the tumor, but may include:
* Chemotherapy to kill cancer cells
* Radiation therapy to shrink the tumor
* Surgery to remove the tumor
* Immunotherapy to boost the immune system's ability to fight the cancer
Overall, CE is a rare and aggressive form of cancer that requires prompt diagnosis and treatment to improve outcomes.
There are several types of inborn errors of amino acid metabolism, including:
1. Phenylketonuria (PKU): This is the most common inborn error of amino acid metabolism and is caused by a deficiency of the enzyme phenylalanine hydroxylase. This enzyme is needed to break down the amino acid phenylalanine, which is found in many protein-containing foods. If phenylalanine is not properly broken down, it can build up in the blood and brain and cause serious health problems.
2. Maple syrup urine disease (MSUD): This is a rare genetic disorder that affects the breakdown of the amino acids leucine, isoleucine, and valine. These amino acids are important for growth and development, but if they are not properly broken down, they can build up in the blood and cause serious health problems.
3. Homocystinuria: This is a rare genetic disorder that affects the breakdown of the amino acid methionine. Methionine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
4. Arginase deficiency: This is a rare genetic disorder that affects the breakdown of the amino acid arginine. Arginine is important for the body's production of nitric oxide, a compound that helps to relax blood vessels and improve blood flow.
5. Citrullinemia: This is a rare genetic disorder that affects the breakdown of the amino acid citrulline. Citrulline is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
6. Tyrosinemia: This is a rare genetic disorder that affects the breakdown of the amino acid tyrosine. Tyrosine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
7. Maple syrup urine disease (MSUD): This is a rare genetic disorder that affects the breakdown of the amino acids leucine, isoleucine, and valine. These amino acids are important for growth and development, but if they are not properly broken down, they can build up in the blood and cause serious health problems.
8. PKU (phenylketonuria): This is a rare genetic disorder that affects the breakdown of the amino acid phenylalanine. Phenylalanine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
9. Methionine adenosyltransferase (MAT) deficiency: This is a rare genetic disorder that affects the breakdown of the amino acid methionine. Methionine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
10. Homocystinuria: This is a rare genetic disorder that affects the breakdown of the amino acid homocysteine. Homocysteine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
It is important to note that these disorders are rare and affect a small percentage of the population. However, they can be serious and potentially life-threatening, so it is important to be aware of them and seek medical attention if symptoms persist or worsen over time.
Examples of experimental liver neoplasms include:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.
The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.
List of MeSH codes (D12.776.157)
List of MeSH codes (D12.776.543)
PTS Mannose-Fructose-Sorbose Family
Max Planck Institute of Molecular Plant Physiology
Tartrate-resistant acid phosphatase
Plastid terminal oxidase
Importin subunit alpha-4
Mason-Pfizer monkey virus
Jebsen & Jessen (SEA)
Trimeric autotransporter adhesin
Liver support system
African swine fever virus
Zinc in biology
GABA transporter type 1
Cystic fibrosis transmembrane conductance regulator
Epigenetics of neurodegenerative diseases
MH DELETED MN ADDED MN
Hyaluronan synthesis supports glutamate transporter activity<...
Amitriptyline pretreatment preserves the antinociceptive effect of morphine in pertussis toxin-treated rats by lowering CSF...
Glioma; Glial Cell Tumors
Francis Valiyaveetil - Publications - Oregon Health & Science University
Expression of mutant huntingtin in mouse brain astrocytes causes age-dependent neurological symptoms<...
Reduced plasma membrane surface expression of GLAST mediates decreased glutamate regulation in the aged striatum - HSC
NEW (2002) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 8/27/2001
MH DELETED MN ADDED MN
IJMS | Free Full-Text | Recent Developments in Peptide-Based Nucleic Acid Delivery
Frontiers | Coupling of HIV-1 Antigen to the Selective Autophagy Receptor SQSTM1/p62 Promotes T-Cell-Mediated Immunity
NDF-RT Code NDF-RT Name
Proteomic interrogation of androgen action in prostate cancer cells reveals roles of aminoacyl tRNA synthetases - PubMed
PRICKLE1 gene: MedlinePlus Genetics
Pesquisa | Biblioteca Virtual em Saúde - BRASIL
Ministry of Education, Science and Technological Development, Republic of Serbia, Grant no. 451-03-68/2020-14/200026 ...
Victam Asia grows in professionalism - All About Feed
Report of the NIH Consensus Development Conference on Phenylketonuria (PKU): Screening & Management: Chapter I | NICHD - Eunice...
Defining the role of Parasutterella, a previously uncharacterized member of the core gut microbiota | The ISME Journal
Sodium chloride decreases cadmium accumulation and changes the response of metabolites to cadmium stress in the halophyte...
American Journal of PharmTech Research
- 1980. Selective depression of excitatory amino-acid induced depolarizations by magnesium ions in isolated spinal cord preparations. (cdc.gov)
- There, peptides are loaded on MHC class I before transport of the peptide/MHC complex to the cell surface ( 10 ). (frontiersin.org)
- CPPs are capable of mediating the cellular uptake of hydrophilic macromolecules like peptides and nucleic acids (e.g. siRNAs, aptamers and antisense-oligonucleotides), which are internalised by cells at a very low rate when applied alone. (mdpi.com)
- Plant growth and Cd uptake were measured, and the accumulation of peptides, and organic and amino acids in plant tissues were assessed. (deepdyve.com)
- The present study also supports the important role of peptides and organic acids, particular of phytochelatins, in Cd tolerance and accumulation although the changes of those metabolites was not the main reason for the decreased Cd accumulation. (deepdyve.com)
- A family of POTASSIUM and SODIUM-dependent acidic amino acid transporters that demonstrate a high affinity for GLUTAMIC ACID and ASPARTIC ACID . (nih.gov)
- Both astrocytes and neurons used Na(+)-dependent systems as the major route for cysteine uptake (80-90% of total), while Na(+)-independent uptake represented a minor component of total transport (10-20% of total). (nih.gov)
- 80-90%) for cysteine uptake in both neurons and astrocytes, with a minor contribution from the ASC transport system (Na(+)-dependent neutral amino acid transport system for alanine, serine, and cysteine). (nih.gov)
- In the Na(+)-independent transport systems (10-20% of total cysteine transport), multifunctional ectoenzyme/amino acid transporter gamma-glutamyltranspeptidase (GGT), and the neutral amino acid L-system contributed approximately equally towards cysteine uptake, in both neurons and astrocytes. (nih.gov)
- The present studies demonstrate that astrocytes and neurons accumulate cysteine by both Na(+)-dependent and Na(+)-independent uptake systems, with major uptake occurring through the X(AG(-)) system and minor uptake via the ASC, GGT and L-systems. (nih.gov)
- Amino acids, Cd uptake, Cd translocation, glutathione, organic acids, phytochelatins, phytoremediation, phytoextraction, salinity INTRODUCTION Cadmium (Cd) is one of the most serious pollutants in the landscape because it can accumulate readily in plants to levels that are harmful in animal and human diets without being toxic to the plant itself. (deepdyve.com)
- Organic anion transporting polypeptides (OATPs) mediate hepatic drug uptake and serve as the loci of drug-drug interactions (DDIs). (aspetjournals.org)
- The complement control protein (CCP) modules (also known as short consensus repeats SCRs or SUSHI repeats) contain approximately 60 amino acid residues and have been identified in several proteins of the complement system. (embl.de)
- These modules have been identified more than 140 times in over 20 proteins, including 12 proteins of the complement system. (embl.de)
- Nitrogen (N) is a component of many macromolecules including nucleic acids and proteins. (biomedcentral.com)
- Globulins are a diverse group of proteins that transport various substances in the blood. (cdc.gov)
- Besides mitochondrial fatty acid oxidation, the liver is also a central organ for carbohydrate metabolism and for a vast array of further metabolic pathways, such as the synthesis of glutathione via amino acid metabolism, driving antioxidant defense mechanisms [ 13 ]. (biomedcentral.com)
- Liver samples were subjected to a targeted metabolomics analysis using the AbsoluteIDQ p180 Kit (Biocrates Life Sciences AG, Innsbruck, Austria). (biomedcentral.com)
- The impacted bile acid profile was consistent with altered expression of ileal bile acid transporter genes and hepatic bile acid synthesis genes, supporting the potential role of Parasutterella in bile acid maintenance and cholesterol metabolism. (nature.com)
- In comparison, Cd inhibited the synthesis of organic acids in shoots and roots in the absence of NaCl, but increased it in shoots in the presence of NaCl. (deepdyve.com)
- While Cd increased the concentrations of amino acids in plant shoots, the effect of NaCl on the synthesis of amino acids was inconsistent. (deepdyve.com)
- These studies demonstrate that a Cys430-Phe mutation does not prevent the de novo synthesis of the b subunit, but alters the conformation of the mutant protein sufficiently to impair its intracellular transport, resulting in its deficiency in this patient. (embl.de)
- At LN, Socaire plants showed an increased root biomass (including a higher number and total length of lateral roots), a differential regulation of a nitrate transporter (a NPF6.3 -like homologue) belonging to the Low Affinity Transport System (LATS), and an upregulation of a nitrate transporter (a NRT2.1 -like homologue) belonging to the High Affinity nitrate Transport System (HATS) compared to Faro. (biomedcentral.com)
- Several variants of this system are found in neuronal tissue. (nih.gov)
- Researchers believe that prickle homolog 1 controls REST by transporting it out of the nucleus, which prevents it from binding to DNA and suppressing gene activity. (medlineplus.gov)
- It remains unclear how the interaction between prickle homolog 1 and REST contributes to the normal development of the nervous system. (medlineplus.gov)
- Each mutation changes a single protein building block (amino acid) in the prickle homolog 1 protein. (medlineplus.gov)
- One of the known mutations appears to disrupt the interaction between prickle homolog 1 and REST, blocking the transport of REST out of the nucleus. (medlineplus.gov)
- The latter represent an assortment of fairly unrelated sequences essentially characterised by a high content of basic amino acids and a length of 10-30 residues. (mdpi.com)
- The complement control protein (CCP) modules (also known as short consensus repeats) are defined by a consensus sequence within a stretch of about 60 amino acid residues. (embl.de)
- Carnitine facilitates the flux of long-chain fatty acids for hepatic mitochondrial beta-oxidation, which acts to ameliorate the negative energy balance commonly affecting high-yielding dairy cows. (biomedcentral.com)
- Notable changes in microbial-derived metabolites were aromatic amino acid, bilirubin, purine, and bile acid derivatives. (nature.com)
- The amino acid, cysteine, is the key rate-limiting substrate for the biosynthesis of GSH, and the maintenance of adequate intracellular GSH levels is dependent upon the extracellular availability and transport of cysteine into cells. (nih.gov)
- The amino acid biosynthesis pathways in MED/Q genome are partitioned among the host and endosymbiont genomes in a manner distinct from other hemipterans. (biomedcentral.com)
- Outside the central nervous system they function as signal mediators and regulators of glutamate metabolism. (bvsalud.org)
- Comparing the metabolite profiles on 100 d, carnitine increased the concentration of short- and long-chain acyl-carnitines, which may be explained by an enhanced mitochondrial fatty acid shuttle and hence greater energy availability. (biomedcentral.com)
- Niacinamide builds complex compounds out of fatty acids and cholesterol. (ulprospector.com)
- Extracellular l-glutamate poses a severe excitotoxic threat to neurons and glia when unregulated, therefore low synaptic levels of this neurotransmitter must be maintained via a rapid and robust transport system. (unthsc.edu)
- The effect of BaCl2 on intestinal sugar transport in the rat in vitro . (cdc.gov)
- Through stimulating the in vitro oxidation of palmitate to acid-soluble products and decreasing the generation of esterified palmitate, supplementary carnitine improved the fat-corrected milk yield [ 5 ] and milk fat content [ 6 ], which was explained by increased acetyl-CoA availability. (biomedcentral.com)
- Autophagy is an intracellular degradation system that delivers constituents to the lysosome. (frontiersin.org)
- The expansion of detoxification genes families, such as P450s, may contribute to the development of insecticide resistance traits and a broad host range in MED/Q and MEAM1/B, and facilitate species' invasions into intensively managed cropping systems. (biomedcentral.com)
- 1989. Cellular alterations and enhanced induction of cleft palate after coadministration of retinoic acid and TCDD. (cdc.gov)
- 6. Increased Expression of System xc- in Glioblastoma Confers an Altered Metabolic State and Temozolomide Resistance. (nih.gov)
- Inflammation triggered by lipopolysaccharide (LPS) load can however pose a challenge to the metabolic integrity via the expression of pro-inflammatory mediators, leading to immune system activation and respective metabolic alterations. (biomedcentral.com)
- Together with pH determination, bicarbonate measurements are used in the diagnosis and treatment of numerous potentially serious disorders associated with acid-base imbalance in the respiratory and metabolic systems. (cdc.gov)
- As a result, REST may inappropriately suppress certain genes in the developing nervous system. (medlineplus.gov)
- Purity's Advanced D™ goes beyond ordinary Vitamin D formulas to promote multiple areas of general wellbeing including immune system function, heart health, brain function, and bone & muscle strength. (purityproducts.com)
- In the CENTRAL NERVOUS SYSTEM they regulate neurotransmission through synaptic reuptake of the excitatory neurotransmitter glutamate. (bvsalud.org)
- However, the molecular targets of hyaluronan to regulate synaptic transmission in the central nervous system have not been fully identified. (elsevier.com)
- The function of this protein is unclear, although it appears to play an important role in the development of the nervous system. (medlineplus.gov)
- MAR: Well, I started out doing a little bit of both because the Institute of Neurological Sciences had the novel idea that if you were going to study the nervous system, you wouldn't be working in just one discipline. (nih.gov)
- Measurements of creatine kinase are used in the diagnosis and treatment of myocardial infarction, skeletal muscle diseases, and diseases of the central nervous system. (cdc.gov)
- The mutant b subunit was secreted from the cells much less effectively than the wild type and remained susceptible to endoglycosidase H, indicating that it was not transported from the endoplasmic reticulum to the Golgi apparatus where the processing of oligosaccharides occurs. (embl.de)
- Strong acids are those that are completely ionized in body fluids, and weak acids are those that are incompletely ionized in body fluids. (medscape.com)
- Hydrochloric acid (HCl) is considered a strong acid because it is present only in a completely ionized form in the body, whereas carbonic acid (H2 CO3) is a weak acid because it is ionized incompletely, and, at equilibrium, all three reactants are present in body fluids. (medscape.com)
- Advanced D™ provides a powerful dose of cholecalciferol (Vitamin D) backed by nutrients that work in tandem with this crucial vitamin to support the health of numerous systems within the body. (purityproducts.com)
- Early seed germination and a functional root system development during establishment are crucial attributes contributing to nutrient competence under marginal nutrient soil conditions. (biomedcentral.com)
- En el SISTEMA NERVIOSO CENTRAL regulan la neurotransmisión por medio de la recaptación sináptica del glutamato, un neurotransmisor excitador. (bvsalud.org)
- Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. (medscape.com)
- Among the Na(+)-dependent systems, X(AG(-)) was the major contributor (approx. (nih.gov)