Cationic Amino Acid Transporter 1
Cationic Amino Acid Transporter 2
Amino Acid Transport Systems, Basic
Amino Acid Transport Systems
Large Neutral Amino Acid-Transporter 1
Antigens, CD98 Heavy Chain
Amino Acid Transport Systems, Neutral
Antigens, CD98 Light Chains
Excitatory Amino Acid Transporter 1
Amino Acid Transport System ASC
Excitatory Amino Acid Transporter 3
Amino Acid Transport System A
Excitatory Amino Acid Transporter 2
Excitatory Amino Acid Transporter 4
Amino Acid Sequence
Molecular Sequence Data
Nitric Oxide Synthase
Glutamate Plasma Membrane Transport Proteins
Nitric Oxide Synthase Type II
Amino Acid Transport System L
Excitatory Amino Acid Transporter 5
Amino Acid Transport System X-AG
Sequence Homology, Amino Acid
Membrane Transport Proteins
Gene Expression Regulation
Organic Anion Transporters, Sodium-Dependent
Organic Anion Transporters
Biological Transport, Active
ATP-Binding Cassette Transporters
GABA Plasma Membrane Transport Proteins
Amino Acids, Essential
Amino Acid Substitution
Reverse Transcriptase Polymerase Chain Reaction
Monocarboxylic Acid Transporters
Vesicular Inhibitory Amino Acid Transport Proteins
Amino Acid Metabolism, Inborn Errors
Nucleotide Transport Proteins
Amino Acid Transport Disorders, Inborn
Excitatory Amino Acids
Leukemia Virus, Murine
Cytokine treatment increases arginine metabolism and uptake in bovine pulmonary arterial endothelial cells. (1/44)L-Arginine (L-Arg) is metabolized to nitric oxide (NO) by NO synthase (NOS) or to urea by arginase (AR). L-Arg is transported into bovine pulmonary arterial endothelial cells (BPAECs) by cationic amino acid transporter-2 (CAT-2). We hypothesized that cytokine treatment would increase L-Arg metabolism and increase CAT-2 mRNA expression. BPAECs were incubated for 24 h in medium (control) or medium with lipopolysaccharide and tumor necrosis factor-alpha (L-T). L-T increased nitrite production (3.1 +/- 0.4 nmol/24 h vs. 1.8 +/- 0.1 nmol/24 h for control; P < 0.01) and urea production (83.5 +/- 29.5 nmol/24 h vs. 17.8 +/- 8.6 nmol/24 h for control; P < 0.05). L-T-treated BPAECs had greater endothelial and inducible NOS mRNA expression compared with control cells. Increasing the medium L-Arg concentration resulted in increased nitrite and urea production in both the control and the L-T-treated BPAECs. L-T treatment resulted in measurable CAT-2 mRNA. L-T increased L-[(3)H]Arg uptake (5.78 +/- 0.41 pmol vs. 4.45 +/- 0.10 pmol for control; P < 0.05). In summary, L-T treatment increased L-Arg metabolism to both NO and urea in BPAECs and resulted in increased levels of CAT-2 mRNA. This suggests that induction of NOS and/or AR is linked to induction of CAT-2 in BPAECs and may represent a mechanism for maintaining L-Arg availability to NOS and/or AR. (+info)
Two-way arginine transport in human endothelial cells: TNF-alpha stimulation is restricted to system y(+). (2/44)Human umbilical vein endothelial cells transport arginine through two Na(+)-independent systems. System y(+)L is insensitive to N-ethylmaleimide (NEM), inhibited by L-leucine in the presence of Na(+), and referable to the expression of SLC7A6/y(+)LAT2, SLC7A7/y(+)LAT1, and SLC3A2/4F2hc. System y(+) is referable to the expression of SLC7A1/CAT1 and SLC7A2/CAT2B. Tumor necrosis factor-alpha (TNF-alpha) and bacterial lipopolysaccharide induce a transient stimulation of arginine influx and efflux through system y(+). Increased expression of SLC7A2/CAT2B is detectable from 3 h of treatment, while SLC7A1 expression is inhibited at later times of incubation. System y(+)L activity and expression remain unaltered. Nitric oxide synthase type 2 mRNA is not detected in the absence or presence of TNF-alpha, while the latter condition lowers nitric oxide synthase type 3 expression at the mRNA and the protein level. Nitrite accumulation is comparable in cytokine-treated and control cells up to 48 h of treatment. It is concluded that modulation of endothelial arginine transport by TNF-alpha or lipopolysaccharide occurs exclusively through changes in CAT2B and CAT1 expression and is dissociated from stimulation of nitric oxide production. (+info)
Garlic attenuates nitric oxide production in rat cardiac myocytes through inhibition of inducible nitric oxide synthase and the arginine transporter CAT-2 (cationic amino acid transporter-2). (3/44)It is now accepted that allicin, the main biologically active compound in garlic, exhibits antioxidant activity. The present study was designed to test the hypothesis that the antioxidant activity of garlic can be partially attributed to the inhibition of nitric oxide (NO) production by cytokine-induced NO synthase (iNOS). Cardiac myocytes cultured from neonatal Wistar rats were stimulated by lipopolysaccharide (LPS) and incubated for 24 h with various concentrations of allicin. This resulted in marked inhibition of nitrite production. Interestingly, a low concentration of allicin (10 microM) was significantly more potent in abrogating the effect of LPS on nitrite production than a higher concentration (40 microM). Allicin decreased steady-state iNOS mRNA levels, and this effect was maximal when a lower concentration was used (10 microM compared with 40 microM). In order to explore additional effects of allicin on NO generation that might counteract the effect on iNOS, we assessed the effects of higher allicin concentrations on arginine transport. Allicin inhibited the uptake of 1 mM extracellular arginine in a concentration-dependent manner. The expression of the two arginine transporters that are expressed in cardiac myocytes [CAT-1 (cationic amino acid transporter-1) and CAT-2] was studied using reverse transcription-PCR. A concentration of 200 microM allicin abolished the expression of CAT-2 mRNA, 100 microM significantly attenuated it, whereas 50 microM had no effect. Allicin had no effect on steady-state CAT-1 mRNA levels. Our results suggest that allicin inhibits iNOS activity through two different mechanisms: at lower concentrations it decreases iNOS mRNA levels, whereas at higher concentrations it inhibits arginine transport through down-regulation of CAT-2 mRNA. (+info)
Intrauterine growth retardation is associated with reduced activity and expression of the cationic amino acid transport systems y+/hCAT-1 and y+/hCAT-2B and lower activity of nitric oxide synthase in human umbilical vein endothelial cells. (4/44)Intrauterine growth retardation (IUGR) is associated with vascular complications leading to hypoxia and abnormal fetal development. The effect of IUGR on L-arginine transport and nitric oxide (NO) synthesis was investigated in cultures of human umbilical vein endothelial cells (HUVECs). IUGR was associated with membrane depolarization and reduced L-arginine transport (V(max)= 5.8+/-0.2 versus 3.3+/-0.1 pmol/microg protein per minute), with no significant changes in transport affinity (K(m)=159+/-15 versus 137+/-14 micromol/L). L-Arginine transport was trans-stimulated (8- to 9-fold) in cells from normal and IUGR pregnancies. IUGR was associated with reduced production of L-[3H]citrulline from L-[3H] arginine, lower nitrite and intracellular L-arginine, L-citrulline, and cGMP. IUGR decreased hCAT-1 and hCAT-2B mRNA, and increased eNOS mRNA and protein levels. IUGR-associated inhibition of L-arginine transport and NO synthesis, and membrane depolarization were reversed by the NO donor S-nitroso-N-acetyl-L,D-penicillamine. In summary, endothelium from fetuses with IUGR exhibit altered L-arginine transport and NO synthesis (L-arginine/NO pathway), reduced expression and activity of hCAT-1 and hCAT-2B and reduced eNOS activity. Alterations in L-arginine/NO pathway could be critical for the physiological processes involved in the etiology of IUGR in human pregnancies. (+info)
L-Arginine transport is augmented through up-regulation of tubular CAT-2 mRNA in ischemic acute renal failure in rats. (5/44)BACKGROUND: Ischemic acute renal failure (iARF) is associated with increased nitric oxide (NO) production during the reperfusion period, as endothelial nitric oxide synthase (eNOS) is maximally activated, and renal tubular inducible NOS (iNOS) is stimulated. Increased NO production leads to augmented tubular injury, probably through the formation of peroxynitrite. l-Arginine (l-Arg), the only precursor for NO, is transported into cells by cationic amino acid transporters, CAT-1 and CAT-2. We hypothesized that the increased NO production observed in iARF may result from increased l-Arg uptake, which would be reflected in the augmented expression of l-Arg transporter(s). METHODS: Ischemic acute renal failure was induced in rats by right nephrectomy + left renal artery clamping for 60 minutes. l-Arg uptake was examined in freshly harvested glomeruli and tubuli from control, sham operated, and animals subjected to 15, 30, and 60 minutes, and 24 hours of reperfusion, following 60 minutes of ischemia. Using RT-PCR, renal tissues were examined further for the expression of iNOS, CAT-1, CAT-2, arginase I and arginase II. RESULTS: Tubular expression of iNOS mRNA was initiated by ischemia, continued to increase after 60 minutes of reperfusion, and decreased after 24 hours. l-Arg transport into glomeruli was similar in all experimental groups. l-Arg uptake into tubuli was markedly augmented following the 60-minute reperfusion, while it moderately increased after 24 hours of reperfusion. This was accompanied by a parallel, preferential increase in tubular CAT-2 mRNA expression at 60 minutes of reperfusion. CAT-1 mRNA expression was unchanged, as detected by RT-PCR. In addition, the expression of arginase II and arginase I mRNA was attenuated by 30 minutes and one hour of reperfusion, and returned to baseline values after 24 hours of reperfusion. CONCLUSIONS: Ischemic ARF is associated with augmented tubular CAT-2 mRNA expression, which leads to enhanced l-Arg transport and increased NO production. This may contribute to the renal injury exhibited in iARF. (+info)
Regulation of the S100B gene by alpha 1-adrenergic stimulation in cardiac myocytes. (6/44)We previously reported that S100B, a 20-kDa Ca(2+)-binding homodimer, inhibited the postinfarct myocardial hypertrophic response mediated by alpha(1)-adrenergic stimulation through the protein kinase C (PKC) signaling pathway. In the present study, we examined whether the same pathway induced the S100B gene, supporting the hypothesis that S100B is a feedback negative regulator of this pathway. We transfected cultured neonatal rat cardiac myocytes with a luciferase reporter gene driven by the maximal human S100B promoter and progressively shorter segments of this promoter sequentially deleted from the 5' end. We identified a basic promoter essential for transcription spanning 162 bp upstream of the transcription initiation site and positive (at -782/-162 and -6,689/-4,463) and negative (at -4,463/-782) myocyte-selective regulatory elements. We showed that the basic and maximal S100B promoters were activated specifically by alpha(1)-adrenergic agonists through the alpha(1A)-adrenergic receptor, but not by any other trophic hormonal stimuli. The activation of the S100B promoter was mediated through the PKC signaling pathway. Transcription enhancer factor-1 (TEF-1) and related to TEF-1 (RTEF-1) influenced transcription from the maximal, but not the basic, promoter implicating active MCAT elements upstream from the basic promoter. Acting in opposing fashions, TEF-1 transrepressed the S100B promoter and RTEF-1 transactivated the promoter. Our results suggest that alpha(1)-adrenergic stimulation induces the S100B gene after myocardial infarction through the PKC signaling pathway and that this induction is modulated by TEF-1 and RTEF-1. (+info)
Hypothermia attenuates iNOS, CAT-1, CAT-2, and nitric oxide expression in lungs of endotoxemic rats. (7/44)Endotoxemia stimulates endogenous nitric oxide formation, induces transcription of arginine transporters, and causes lung injury. Hypothermia inhibits nitric oxide formation and is used as a means of organ preservation. We hypothesized that hypothermia inhibits endotoxin-induced intrapulmonary nitric oxide formation and that this inhibition is associated with attenuated transcription of enzymes that regulate nitric oxide formation, such as inducible nitric oxide synthase (iNOS) and the cationic amino acid transporters 1 (CAT-1) and 2 (CAT-2). Rats were anesthetized and randomized to treatment with hypothermia (18-24 degrees C) or normothermia (36-38 degrees C). Endotoxin was administered intravascularly. Concentrations of iNOS, CAT-1, CAT-2 mRNA, iNOS protein, and nitrosylated proteins were measured in lung tissue homogenates. We found that hypothermia abrogated the endotoxin-induced increase in exhaled nitric oxide and lung tissue nitrotyrosine concentrations. Western blot analyses revealed that hypothermia inhibited iNOS, but not endothelial nitric oxide synthase, protein expression in lung tissues. CAT-1, CAT-2, and iNOS mRNA concentrations were lower in the lungs of hypothermic animals. These findings suggest that hypothermia protects against intrapulmonary nitric oxide overproduction and nitric oxide-mediated lung injury by inhibiting transcription of iNOS, CAT-1, and CAT-2. (+info)
Differential regulation of glomerular arginine transporters (CAT-1 and CAT-2) in lipopolysaccharide-treated rats. (8/44)The decrease in glomerular filtration rate (GFR) that is characteristic of sepsis has been shown to result from inhibition of glomerular endothelial nitric oxide synthase (eNOS) by nitric oxide (NO) generated from the inducible isoform of NOS (iNOS). Although l-arginine is the sole precursor for NO biosynthesis, its intracellular availability in glomeruli from septic animals has never been investigated. Arginine uptake was measured in freshly harvested glomeruli from the following experimental groups: 1) untreated rats; 2) rats pretreated with LPS (4 mg/kg body wt, 4 h before experiments); 3) rats treated with LPS as above with either l-N(6)-(1-iminoethyl)lysine hydrochloride (l-NIL), a selective iNOS antagonist, or 7-nitroindazole, a selective neuronal NOS antagonist; and 4) rats treated with l-NIL only. Both glomeular and mesangial arginine transport characteristics were found compatible with a y(+) system. Arginine uptake was augmented in glomeruli from LPS-treated rats. Treatment with l-NIL completely abolished this effect whereas l-NIL alone had no effect. Similar results were obtained when primary cultures of rat mesangial cells were preincubated with LPS (10 microg/ml for 24 h) with or without l-NIL. Using RT-PCR, we found that in vivo administration of LPS resulted in a significant increase in glomerular cationic amino acid transporter-2 (CAT-2) mRNA expression whereas CAT-1 mRNA was undetected. Northern blotting further confirmed a significant increase in glomerular CAT-2 by LPS. In mesangial cells, the expression of both CAT-1 and CAT-2 mRNA was augmented after incubation with LPS. In conclusion, in vivo administration of LPS augments glomerular arginine transport through upregulation of steady-state CAT-2 mRNA while downregulating CAT-1 mRNA. These results may correspond to the changes in glomerular iNOS and eNOS activity in sepsis. (+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.
There are two forms of cystinosis: neonatal and adult. Neonatal cystinosis is present at birth and can cause a range of symptoms including failure to gain weight, diarrhea, and difficulty feeding. Adult cystinosis typically develops in adulthood and may cause symptoms such as kidney damage, blindness, and skin rashes.
Cystinosis is diagnosed through a combination of physical examination, medical history, and laboratory tests. Treatment for the disorder typically involves managing the symptoms and preventing complications. For neonatal cystinosis, this may involve feeding tubes and medication to help the baby gain weight. For adult cystinosis, treatment may include medication to lower cystine levels in the body and manage any associated complications such as kidney damage or blindness.
In some cases, a stem cell transplant may be recommended to treat cystinosis. This involves replacing the affected cells with healthy ones from a donor. The procedure is typically performed in children with neonatal cystinosis and can help improve their quality of life and prevent complications.
Overall, cystinosis is a rare and debilitating genetic disorder that affects the kidneys and eyes. While there is currently no cure for the disorder, treatment options are available to manage the symptoms and prevent complications. With proper management and care, individuals with cystinosis can lead fulfilling lives.
The hallmark symptom of RA is an inability to reabsorb these amino acids, leading to their excessive excretion in the urine. This can cause a range of health problems, including:
1. Cystinuria: excessive excretion of cystine in the urine, which can form stones and damage the kidneys.
2. Glutaric aciduria type 1 (GA1): excessive excretion of glutaric acid and other branched-chain amino acids in the urine, which can lead to developmental delays, intellectual disability, and seizures.
3. Aminoaciduria: excessive excretion of various amino acids in the urine, including alanine, glycine, and proline.
4. Kidney damage: chronic exposure to high levels of certain amino acids in the urine can cause damage to the kidneys, leading to chronic kidney disease and potentially end-stage renal disease (ESRD).
5. Other complications: RA can also lead to other health problems, such as electrolyte imbalances, bone disease, and metabolic acidosis.
RA is diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment typically involves a combination of dietary restrictions, medications, and kidney transplantation in severe cases.
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.
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.
Also known as: aminoacyl-tRNA synthetase deficiency, aminoacyl-tRNA synthetase/tRNA synthetase deficiency, and amino acid transporter defects.
Cationic amino acid transporter 2
Cationic amino acid transporter 4
Cationic amino acid transporter 3
Y+L amino acid transporter 2
High affinity cationic amino acid transporter 1
Large neutral amino acids transporter small subunit 2
Neutral and basic amino acid transport protein rBAT
Large neutral amino acids transporter small subunit 1
Amino acid transporter
List of MeSH codes (D12.776.157)
List of MeSH codes (D12.776.543)
Solute carrier family
ATP-binding cassette transporter
Y+L amino acid transporter 1
Lambda holin family
Organo anion transporter family
Niche (protein structural motif)
Prostaglandin-endoperoxide synthase 2
Ligand-gated ion channel
Runx1t1 (Runt-related transcription factor 1; translocated to, 1) epigenetically regulates the proliferation and nitric oxide...
NIOSHTIC-2 Search Results - Full View
MH DELETED MN ADDED MN
Coordinated Action of Multiple Transporters in the Acquisition of Essential Cationic Amino Acids by the Intracellular Parasite...
Pharos : Target Details - SLC7A2
Pharos : Target Details - SLC7A2
po:0000014 pato:0001272 - RIKEN Arabidopsis Genome Encyclopedia
Pesquisa | Prevenção e Controle de Câncer
Carlos Alberto Flores Infante - Science Portal | Universidad de La Laguna
SLC7A9 gene: MedlinePlus Genetics
GI numbers Protein Name Gene Symbol Amino Acid Number Species Sequence pI MW Tech
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
Rat GLRa2(Glycine Receptor Alpha 2) ELISA Kit - Isogem
Amino acids basic. Medical search
Mouse CACNa1S(Calcium Channel, Voltage Dependent, L-Type, Alpha 1S Subunit) ELISA Kit - Operatie Biotech Research Purchasing ...
Mouse Retina SAGE Library
Human Genome Epidemiology Literature Finder|Home|PHGKB
ugt1a10 gene|ugt1a10 gene|C1421323|udp glucuronosyltransferase 1 family, polypeptide a10|gngm
NCIt Code SwissProt ID NCIt Preferred Name
Subject: 'copper' - PubAg Search Results
ugt1a10 gene|ugt1a10 gene|C1421323|udp glucuronosyltransferase 1 family, polypeptide a10|gngm
Pharmaceutics | Free Full-Text | Cell Penetrating Peptides, Novel Vectors for Gene Therapy
- 7. Transport of asymmetric dimethylarginine (ADMA) by cationic amino acid transporter 2 (CAT2), organic cation transporter 2 (OCT2) and multidrug and toxin extrusion protein 1 (MATE1). (nih.gov)
- The protein encoded by this gene is a cationic amino acid transporter and a member of the APC (amino acid-polyamine-organocation) family of transporters. (nih.gov)
- FUNCTIONS IN: P-P-bond-hydrolysis-driven protein transmembrane transporter. (riken.jp)
- This subunit joins with another protein subunit, produced from the SLC3A1 gene, to form a transporter protein complex. (medlineplus.gov)
- During the process of urine formation in the kidneys, this protein complex absorbs particular protein building blocks (amino acids) back into the blood. (medlineplus.gov)
- These changes lead to an abnormally functioning transporter protein complex, which causes certain amino acids to become concentrated in the urine. (medlineplus.gov)
- The naturally occurring or experimentally induced replacement of one or more AMINO ACIDS in a protein with another. (lookformedical.com)
- If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. (lookformedical.com)
- Cellular proteins and protein complexes that transport amino acids across biological membranes. (lookformedical.com)
- Cell penetrating peptides (CPPs), also known as protein transduction domains (PTDs), first identified ~25 years ago, are small, 6-30 amino acid long, synthetic, or naturally occurring peptides, able to carry variety of cargoes across the cellular membranes in an intact, functional form. (mdpi.com)
- In addition,the physical and chemical properties,protein interaction network and gene structure of MdVIT family were analyzed,the results showed that the main factors for VIT family amplification in apple were tandem duplication and segmental duplication,cationic co-transporters（XP_008372221.1 and XP_008383418.1）were mainly involved in the interaction of VIT proteins in apple. (ahs.ac.cn)
- Using a combination of parasite assays and heterologous characterisation of TgApiAT6-1 in Xenopus laevis oocytes, we demonstrate that TgApiAT6-1 is a general cationic amino acid transporter that mediates both the high-affinity uptake of lysine and the low-affinity uptake of arginine. (mendeley.com)
- TgApiAT6-1 is the primary lysine transporter in the disease-causing tachyzoite stage of T. gondii and is essential for parasite proliferation. (mendeley.com)
- Isoform 1 functions as permease that mediates the transport of the cationic amino acids (arginine, lysine and ornithine), and it has much higher affinity for arginine than isoform 2. (nih.gov)
- In particular, the amino acids cystine, ornithine, arginine, and lysine are absorbed back into the blood through this mechanism. (medlineplus.gov)
- The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. (lookformedical.com)
- The sequential correspondence of nucleotides in one nucleic acid molecule with those of another nucleic acid molecule. (lookformedical.com)
- The cargoes they can deliver range from other small peptides, full-length proteins, nucleic acids including RNA and DNA, liposomes, nanoparticles, and viral particles as well as radioisotopes and other fluorescent probes for imaging purposes. (mdpi.com)
- Condensates separation from the surrounding CYTOPLASM or nucleoplasm or by the concentration of proteins and nucleic acids into droplets as they aggregate on static cellular structures such as CELL MEMBRANES. (nih.gov)
- Schlessinger A, Khuri N, Giacomini KM, Sali A. Molecular modeling and ligand docking for solute carrier (SLC) transporters. (revistasad.com)
- This gene encodes a member of a heteromeric, sodium-independent, anionic amino acid transport system that is highly specific for cysteine and glutamate. (huabio.com)
- Frontiers in molecular neuroscience 2023 2 16 1069375. (cdc.gov)
- Reyes N, Ginter C, Boudker O. Transport mechanism of a bacterial homologue of glutamate transporters. (revistasad.com)
- The uptake of these peptides by AMs may be mediated through an active peptide transport system similar to that of the pepT1 transporter. (cdc.gov)
- We previously identified a large family of apicomplexan-specific plasma membrane-localized amino acid transporters, the ApiATs, and showed that the Toxoplasma gondii transporter TgApiAT1 functions in the selective uptake of arginine. (mendeley.com)
- TgApiAT1 is essential for parasite virulence, but dispensable for parasite growth in medium containing high concentrations of arginine, indicating the presence of at least one other arginine transporter. (mendeley.com)
- Here we identify TgApiAT6-1 as the second arginine transporter. (mendeley.com)
- 5. Plasma Membrane Cholesterol Regulates the Allosteric Binding of 1-Methyl-4-Phenylpyridinium to Organic Cation Transporter 2 (SLC22A2). (nih.gov)
- Melanogenesis begins with the conversion of amino acid, tyrosine to dopa and subsequently to dopaquinone in the presence of tyrosinase. (hindawi.com)
- Identification and Expression Analysis of the Vacuolar Iron Transporter Gene Family in Apple[J]. Acta Horticulturae Sinica, 2021, 48(2): 205-218. (ahs.ac.cn)
- Intracellular parasites of the phylum Apicomplexa are dependent on the scavenging of essential amino acids from their hosts. (mendeley.com)
- Description: Quantitative sandwich ELISA for measuring Rat Glycine receptor subunit alpha-2 (GLRA2) in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids. (isogem.org)
- 6. Inhibitory Effect of Crizotinib on Creatinine Uptake by Renal Secretory Transporter OCT2. (nih.gov)
- The uptake of Arg-Lys* and Beta-Ala-Lys* at concentration of 10 uM was blocked (70 - 80%) by Gly-Sar (200 uM) through competitive inhibition, but not by L-Lys, which shares a common cationic amino acid transporter with L-Arg. (cdc.gov)
- This data set measures the change in intracellular oocyte metabolism over a time course of up to 54 hours, charting the uptake of Lys or Arg by the transporters in addition to fluctuations in endogenous oocyte metabolite levels. (mendeley.com)
- 1. Fluorocholine Transport Mediated by the Organic Cation Transporter 2 (OCT2, SLC22A2): Implication for Imaging of Kidney Tumors. (nih.gov)
- 3. Organic Cation Transporter 2 Overexpression May Confer an Increased Risk of Gentamicin-Induced Nephrotoxicity. (nih.gov)
- 9. Organic cation transporter 2 (SLC22A2), a low-affinity and high-capacity choline transporter, is preferentially enriched on synaptic vesicles in cholinergic neurons. (nih.gov)
- 10. Key role of organic cation transporter 2 for the nephrotoxicity effect of triptolide in rheumatoid arthritis. (nih.gov)
- 13. Functional characterization of the human organic cation transporter 2 variant p.270Ala>Ser. (nih.gov)
- 18. The role of cholesterol recognition (CARC/CRAC) mirror codes in the allosterism of the human organic cation transporter 2 (OCT2, SLC22A2). (nih.gov)
- 19. Structural determinants of inhibitor interaction with the human organic cation transporter OCT2 (SLC22A2). (nih.gov)
- Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. (lookformedical.com)
- Description: A sandwich ELISA kit for detection of Glycine Receptor Alpha 2 from Rat in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (isogem.org)
- The primary antibody (HA600097) at 1/500 dilution was used in 5% NFDM/TBST at room temperature for 2 hours. (huabio.com)
- Upon administration, C3-targeted complement inhibitor APL-2 selectively binds to C3 and blocks the cleavage of C3 into C3a and C3b by C3 convertase. (blogspot.com)
- Antibodies against terest in cells of the vaccinated animal, but is the viral influenza proteins nucleoprotein unable to replicate in this species (1,2). (who.int)
- In order to secure human food supply, it is therefore important to ensure the health of honey bees, which is continuously threatened by the overuse of insecticides such as neonicotinoid 2 in agriculture and also by various viral, bacterial, and fungal pathogens as well as metazoan parasites 3 . (nature.com)
- Further, Runx1t1 and HDACs were shown to promote neurotoxic effect of microglia by repressing expression of LAT2, L-aminoacid transporter-2 (cationic amino acid transporter, y+ system), which normally inhibits NO production. (nih.gov)
- So on day one, Session 1 will focus on macrophages and the immune system during HIV and SARS-CoV-2 infection, Session 2 will focus on challenges to study HIV/SIV reservoirs, and Session 3 will really have the highlights from recent awardees of the NIMH/NINDS/NIDA Myeloid Reservoir RFA. (nih.gov)
- Using tandem mass spectrometry, nuclear magnetic resonance spectroscopy and synthetic diastereomers, we identified the N-terminal amino group of the agmatinamic acid as the N -acetylation site. (nature.com)
- The structural changes in activated CNFs were investigated using the following characterization techniques: N(2) adsorption isotherms at 77K, XRD, temperature-programmed desorption of hydrogen, TEM, TPO and elemental composition. (nih.gov)
- Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories. (lookformedical.com)
- The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. (lookformedical.com)
- A primary requirement though is that it should not adversely affect the organism and its components [2, 3]. (nanomedicine-rj.com)
- 2. The failure of DAC to induce OCT2 expression and its remission by hemoglobin-based nanocarriers under hypoxia in renal cell carcinoma. (nih.gov)
- The qRT-PCR analysis showed that the expression levels of MdVIT1 and MdVIT2 in leaves of'M26'apple rootstock seedlings treated with 2 000 μmol · L -1 FeSO 4 · 7H 2 O for 24 h were 6.6 and 12 times higher than those of the control. (ahs.ac.cn)
- After 6 h treatment with 2 000 μmol · L -1 FeSO 4 · 7H 2 O,the relative expression level of MdVIT4 showed in the stem was the highest,which was 237 times higher than that of the control. (ahs.ac.cn)
- The results showed that the surface area increased by a factor of 3.3, 2.0 and 1.8 referred to the parent CNFs after the treatment with KOH, K(2)CO(3) and KHCO(3), respectively. (nih.gov)
- Paenibacillus larvae , the causative agent of the devastating honey-bee disease American Foulbrood, produces the cationic polyketide-peptide hybrid paenilamicin that displays antibacterial and antifungal activity. (nature.com)
- Here we provide an LC-MS data set of Xenopus laevis oocytes expressing the TgApiAT6-1 transporter in the presence of Arg or Lys and the TgApiAT1 transporter in the presence of Arg. (mendeley.com)
- 2. A compressed (zipped) folder containing individual raw data files numbered with the same sample ID as in the summary spreadsheet. (mendeley.com)
- HA523 trade name] is indicated for the treatment of HIV-1 infection in infants and children weighing 2 to 14 kg. (who.int)
- The meeting will also highlight recent work on macrophage inflammation in the context of SARS-CoV-2 infection and work from recently-funded NIMH, NIDA, and NINDS investigators. (nih.gov)
- FUNCTIONS IN: amino acid transmembrane transporter acti. (riken.jp)
- Twenty alpha-amino acids are the subunits which are polymerized to form proteins. (lookformedical.com)
- The effects of different activations conditions, including type of protector gas (He, Ar and N(2)) and helium flow rate on the properties of activated carbon nanofibers were studied. (nih.gov)
- 0.1% v/v formic acid) at a flow rate of 300 µl/min, followed by a linear gradient to 20% mobile phase B over 18 min. (mendeley.com)
- Total 2 UniGene clusters found. (harvard.edu)
- For each condition 12 oocytes were washed × 3 with 1 × ND96 solution (96 mM NaCl, 2 mM KCl, 1 mM MgCl2, 5 mM HEPES, pH 7.4) and incubated in the same buffer containing 1 mM Lys or Arg substrate for 48 hrs. (mendeley.com)