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Results for “RNA Aggregation”

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At least 91 records · Page 5Linked to original sources

PubMed2006

Localization and characterization of a novel secreted protein SCUBE1 in human platelets.

OBJECTIVE: The aim of the study was to investigate the protein expression and function of a novel secreted protein in the vascular system, named SCUBE1 for signal peptide, CUB (Complement proteins C1r/C1s, Uegf, and Bmp1) and epidermal growth factor-like (EGF)-like domain containing protein 1. METHODS AND RESULTS: Immunohistochemical analysis demonstrated that the SCUBE1 staining is mainly confined to the intravascular platelet-rich thrombus in vascular tissue samples. While quantitative real-time RT-PCR verified that the SCUBE1 mRNA is expressed in human platelets, numerous immunolocalization techniques revealed that the preformed SCUBE1 protein is stored in the alpha-granules and translocated to the surface upon platelet stimulation. A smaller SCUBE1 fragment, possibly formed by limited proteolysis after being released from the storage granules, was detected in thrombus lysate by Western blot analysis. Interestingly, deposition of SCUBE1 into the subendothelial matrix of the atherosclerotic plaques was evidenced by immunohistochemistry. In addition, studies of platelet adhesion and ristocetin-induced platelet agglutination showed that fragments containing the amino-terminal EGF-like repeats were able to support platelet adhesion and enhance the ristocetin-induced platelet agglutination, respectively. CONCLUSION: These data suggest that platelet-derived SCUBE1 could function as a novel adhesive molecule and its matrix-bound and soluble fragments may play critical (patho)physiological roles in cardiovascular biology.

Animals↗

PubMed2006

Gene silencing in mosquito salivary glands by RNAi.

Salivary glands are the ultimate site of development in the insect of mosquito born pathogens such as Plasmodium. Mosquito salivary glands also secrete components involved in anti-haemostatic activities and allergic reactions. We investigated the feasibility of RNAi as a tool for functional analysis of genes expressed in Anopheles gambiae salivary glands. We show that specific gene silencing in salivary glands requires the use of large amounts of dsRNA, condition that differs from those for efficient RNAi in other mosquito tissues. Using this protocol, we demonstrated the role of AgApy, which encodes an apyrase, in the probing behaviour of An. gambiae.

Animals↗

PubMed2005

Genomic structure, organization and promoter analysis of the human F11R/F11 receptor/junctional adhesion molecule-1/JAM-A.

The F11-receptor (F11R) (a.k.a. JAM-1, JAM-A, CD321) is a cell adhesion molecule of the immunoglobulin superfamily involved in platelet adhesion, secretion and aggregation. In addition, the F11R plays a critical role in the function of endothelial cells and in platelet adhesion to inflamed endothelium. In the present study, we used partial sequences of the human F11R gene, F11R cDNAs, and information in unannotated human genome databases, to delineate the F11R gene. We found that the F11R gene is composed of 13 exons (E1a, 1b, 1c, E1-E10) encoding two groups of mRNAs differing in length and sequence at their 5' UTRs, referred to as type 1 and type 2 messages. Type 1 cDNAs are shorter at the 5' end and contain a region not found within type 2 messages. Type 1 mRNAs are present in endothelial cells (EC), platelets, white blood cells and in the cell lines CMK, HeLa, K562, HOG and A549, while type 2 messages are limited to EC. Type 1 messages contain exons E1-E10 whereas type 2 messages usually contain exons E1a, 1c, part of E1 and E2-E10. The translation start site is localized in the 3' end of E1, common for both type 1 and type 2 messages. Expression of these messages is regulated by two alternative promoters, P1 and P2. P1 is a TATA-less promoter containing an initiator element, multiple transcription start sites, several GC and CCAAT boxes, and GATA, NF-kappaB and ets consensus sequences. The cloned P1 drives efficient expression of the luciferase reporter gene. A high level of similarity between human P1 and its rat and mouse counterparts was observed. Promoter P2, located upstream of P1, contains a TATA box, GC boxes, a CCAAT box and GATA and ets consensus sequences. 3' RACE provided evidence for variability in the 3' UTR due to the presence of two polyadenylation signals. The finding of multiple regulatory sites in the promoters supplements the biochemical evidence that the F11R has several different roles in the functional repertoire of endothelial cells, platelets and other cells. In particular, the presence of NF-kappaB provides additional evidence to the significance of the F11R function in the initiation of inflammatory thrombosis.

5' Untranslated Regions↗

PubMed2000

Identification of lysophospholipid receptors in human platelets: the relation of two agonists, lysophosphatidic acid and sphingosine 1-phosphate.

Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (Sph-1-P) are known as structurally related bio-active lipids activating platelets through their respective receptors. Although the receptors for LPA and Sph-1-P have been recently identified in various cells, the identification and characterization of ones in platelets have been reported only preliminarily. In this report, we first investigated the distinct modes of LPA and Sph-1-P actions in platelet activation and found that LPA functioned as a much stronger agonist than Sph-1-P, and high concentrations of Sph-1-P specifically desensitized LPA-induced intracellular Ca(2+) mobilization. In order to identify the responsible receptors underlying these observations, we analyzed the LPA and Sph-1-P receptors which might be expressed in human platelets, by RT-PCR. We found for the first time that Edg2, 4, 6 and 7 mRNA are expressed in human platelets.

Blood Platelets↗

PubMed2002

Effects of amrinone on hepatic ischemia-reperfusion injury in rats.

BACKGROUND/AIMS: The present study was designed to investigate the effect of amrinone, a phosphodiesterase III inhibitor, on hepatic ischemia-reperfusion injury in rats. METHODS: Amrinone was infused at a rate of 20 or 100 microg/kg/min, and 60-min partial ischemia was induced. The effects of amrinone on hemodynamic status, hepatic tissue cyclic adenosine 5'-monophosphate (cAMP), hepatic tissue blood flow, platelet aggregation and plasma levels of transaminase were examined. The expression of intercellular adhesion molecule-1 (ICAM-1) and myeloperoxidase activity were analyzed and histological examination was performed in the injured liver. The cumulative survival rates for 14 days were also examined. RESULTS: Hemodynamic status was not affected by amrinone. The levels of cAMP during reperfusion were significantly higher in rats with amrinone. Hepatic tissue blood flow during reperfusion was increased and platelet aggregation was inhibited by amrinone. The expression of ICAM-1 mRNA and protein in the injured liver was suppressed in rats with amrinone. The levels of transaminase, necrotic changes and myeloperoxidase activity were suppressed after reperfusion and higher survival was achieved in the rats treated with amrinone. CONCLUSIONS: Amrinone protected against ischemia-reperfusion injury of the liver in the present model.

Alanine Transaminase↗

PubMed2004

Possible involvement of MIP-1alpha in the recruitment of osteoclast progenitors to the distal tibia in rats with adjuvant-induced arthritis.

In the rat model of rheumatoid arthritis, a marked formation of osteoclasts is found in the distal tibia and the metatarsal bone. It was therefore postulated that osteoclast progenitors would be increased in the bone marrow cavities of rats with adjuvant-induced arthritis (AA rats). Bone marrow cells obtained from tibia of AA rats were cultured to form cells in the osteoclast lineage to access the number of osteoclast progenitors. Unexpectedly, only a suppressed level of osteoclast progenitors was detected in the diaphyseal bone marrow of tibia in AA rats. Distribution of osteoclast progenitors in the bone marrow cavity was examined, and it was shown that osteoclast progenitors accumulated in the distal tibia. Macrophage inflammatory protein (MIP)-1alpha, an osteoclastogenic CC chemokine, was expressed in ED-1-positive macrophages localizing in the distal tibia with marked bone destruction. Chemotaxis studies showed that MIP-1alpha expressed significant activity towards bone marrow cells. The suppressed level of osteoclastogenesis in bone marrow cells of AA rats was restored to a normal level by the addition of MIP-1alpha. It was suggested that MIP-1alpha is involved in the migration of osteoclast progenitors to the distal tibia as well as in osteoclastogenesis in AA rats. In these rats, in situ hybridization of the distal tibia with a high level of bone destruction showed significant expression of Receptor activator nuclear factor kappaB ligand (RANKL) messenger RNA in aggregates of multinucleated osteoclast-like cells present in the bone marrow cavity, a unique pathological feature for these rats. Migrated osteoclast progenitors are thought to be efficiently differentiated into osteoclasts in response to RANKL expressed by the aggregates of osteoclast-like cells under the influence of the MIP-1alpha. Such positive-feedback regulation of osteoclastogenesis could result in the highest recruitment of active osteoclasts in the area of marked bone destruction.

Animals↗

PubMed1979

Kinetics and mechanism of tobacco mosaic virus assembly: direct measurement of relative rates of incorporation of 4S and 20S protein.

The mechanism of assembly of tobacco mosaic virus has been investigated under conditions in which the rates of incorporation of the 4S and 20S proteins can each be directly measured by analytical centfrifugation. Under these conditions, pH 6.5, 6.5 degrees C, 0.10 M ionic strength potassium orthophosphate, the protein can be made to exist as a metastable 20S aggregate that is necessary for efficient reconstitution. The overall assembly process consists of an initiation (nucleation) reaction that requires two to three 20S disk aggregates per RNA molecule and is followed by an elongation (growth) reaction. In the elongation phase of assembly the 4S protein is incorporated 50 to 70 times faster than the 20S disk, calculated on the basis of a steady-state kinetic analysis. Therefore, under these conditions, in which the rate of assembly is about 0.06 of that at pH 7, 20 degrees C, 0.10 M ionic strength orthophosphate, the 4S protein preferentially participates in the elongation phase. At this slow reconstitution rate intermediate assembly states (about 70-168 S) can be observed. The kinetics of both protein incorporation and nucleoprotein formation suggest that the elongation process is composed of at least two different, possibly sequential, rate-limiting reactions.

Kinetics↗

PubMed1985

Regulated expression of ras gene constructs in Dictyostelium transformants.

Constructs were made in which approximately equal to 500 base pairs of the 5' flanking region of the ras gene of Dictyostelium discoideum and variable amounts of the coding region were linked to a ras cDNA in a transformation vector. These constructs then were used to transform Dictyostelium cells and their regulation was examined. In Dictyostelium transformants, transcripts from the ras gene constructs were found at high levels in cells in fast-shaking cultures containing cAMP, whereas transcripts were either not detectable or present at very low levels in cultures lacking exogenous cAMP. In slow-shaking culture, a significantly lower level of ras RNA was detected. When normal developing aggregates were dissociated, RNA from the ras constructs decreased rapidly but then reaccumulated in the presence of cAMP. These results show that the sequences necessary for the response to external cAMP are present within an approximately equal to 650-base-pair region upstream from the ATG start codon and/or within portions of the protein-coding region. Moreover, the proper regulation of ras gene expression in high-copy-number transformants suggests that trans-acting factors which may control transcription are not limiting. Vector constructs were also examined in which the cDNA was present in the opposite orientation compared to the gene fragment (antisense orientation). When these were transfected into cells, no transformants were obtained, suggesting that expression of the ras gene is essential for vegetative growth.

Base Composition↗

PubMed2003

Molecular identification of Aggrus/T1alpha as a platelet aggregation-inducing factor expressed in colorectal tumors.

Platelets play an important role in hemostasis, thrombosis, and antimicrobial host defense and are also involved in the induction of inflammation, tissue repair, and tumor metastasis. We have previously characterized the platelet aggregation-inducing sialoglycoprotein (Aggrus/gp44) overexpressed on the surface of tumor cells. Because a platelet aggregation-neutralizing 8F11 monoclonal antibody that could specifically recognize Aggrus suppressed tumor-induced platelet aggregation, we have previously purified Aggrus by 8F11-affinity chromatography and found that purified Aggrus possessed the ability to induce aggregation of platelets. Here we show that Aggrus is identical to the T1alpha/gp38P/OTS-8 antigen, the function of which in tumors is unknown. Expression of mouse Aggrus and its human homologue (also known as T1alpha-2/gp36) induced platelet aggregation without requiring plasma components. Using the 8F11 antibody, we identified the highly conserved platelet aggregation-stimulating domain with putative O-glycosylated threonine residues as the critical determinant for exhibiting platelet aggregation-inducing capabilities. We compared the expression level of human aggrus mRNA using an array containing 160 cDNA pair samples derived from multiple human tumorigenic and corresponding normal tissues from individual patients. We found that expression level of aggrus was enhanced in most colorectal tumor patients. To confirm the protein expression, we generated anti-human Aggrus polyclonal antibodies. Immunohistochemical analysis revealed that Aggrus expression was frequently up-regulated in colorectal tumors. These results suggest that Aggrus/T1alpha is a newly identified, platelet aggregation-inducing factor expressed in colorectal tumors.

Animals↗

PubMed2005

Glucose uptake via glucose transporter 3 by human platelets is regulated by protein kinase B.

In insulin-responsive tissues, insulin is a potent activator of protein kinase B (PKB)-mediated glucose uptake through the facilitative glucose transporter GLUT4. In platelets, glucose uptake is mediated through GLUT3, which is present in plasma (15%) and intracellular alpha-granule (85%) membranes. Here we report the PKB-mediated glucose uptake by platelets by agents that do (thrombin) or do not (insulin) induce alpha-granule translocation to the plasma membrane. Both thrombin and insulin activate PKB and induce glucose uptake albeit with different kinetics. Inhibition of PKB by the pharmacological inhibitor ML-9 decreases thrombin-induced alpha-granule release and thrombin- and insulin-induced glucose uptake. At low glucose (0.1 mm), both agents stimulate glucose uptake by lowering the Km for glucose (thrombin and insulin) and increasing Vmax (thrombin). At high glucose (5 mm), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. We conclude that in platelets glucose transport through GLUT3 is regulated by changes in surface expression and affinity modulation, which are both under control of PKB.

Azepines↗

PubMed2003

Molecular and biochemical evidence for the presence of type III adenylyl cyclase in human platelets.

The isoform(s) of adenylyl cyclase (AC) present in human platelets has not been identified, and evidence supporting a role for AC in platelet aggregation is equivocal. We recently characterized deaggregation as an active component of the platelet aggregation response that may be an important determinant of the extent and duration of aggregation. G(i)-coupled receptors are linked to the inhibition of AC and are targets of antiplatelet drugs. They also affect platelet aggregation by modulating deaggregation, suggesting a role for AC in modulating this response. The purpose of this study was to identify the AC isoform(s) present in human platelets and to identify its physiological modulators. RT-PCR screening of platelet, buffy coat layer cell and bone marrow megakaryocyte cDNA, and Western blot analysis with AC type III (AC-III) antibodies identified AC-III in platelets and in megakaryocytes. Human platelet AC-III was cloned and expressed in HEK293 cells and its characteristics compared to native platelet AC. Both platelet AC and cloned AC-III required Mg(2+) for activity, were insensitive to Ca(2+) and were G(s)- and G(i)-coupled. Zn(2+) and SQ22536 inhibited platelet AC activity. The affinity of SQ22536 was increased with Mg(2+)-related stimulation of AC, while that of Zn(2+) was unchanged, which is consistent with a non-competitive interaction between the two metal ions on AC. The Zn(2+) chelator TPEN reversed the inhibitory effects of Zn(2+). This study identified AC-III as the predominant AC isoform in human platelets, the activity of which may affect the extent and duration of the net aggregation response by modulating deaggregation.

Adenylyl Cyclases↗

PubMed2005

Platelet characteristics change with aging: role of estrogen receptor beta.

Estrogen receptor beta (betaER) is the predominant estrogen receptor in platelets. Experiments were designed to define phenotypic changes in platelets with aging following deletion of betaER (betaERKO). Blood was collected from wild-type and betaERKO female mice at 4-7 (young) and 24-25 (aged) months of age. In young animals, total number of platelets, number of platelets containing RNA (reticulated platelets), aggregation, dense body adenosine triphosphate secretion, and alpha granular secretion were the same in both groups. With aging, total number of platelets decreased but reticulated platelets increased in betaERKO mice; aggregation and dense granule adenosine triphosphate secretion decreased whereas basal expression of fibrinogen receptors increased with age in wild-type and betaERKO mice. Basal expression of P-selectin and annexin V binding increased with aging only in betaERKO mice; thrombin did not increase expression in these mice. Therefore, deletion of betaER is associated with specific platelet functions, which are expressed only with age-associated reproductive senescence.

Adenosine Triphosphate↗

PubMed2002

Endothelial nitric oxide synthase pathophysiology after nonocclusive common carotid artery thrombosis in rats.

Although vascular dysregulation has been documented in patients with extracranial vascular disease, transient ischemic attacks, and stroke, the pathomechanisms are poorly understood. To model thromboembolic stroke in rats, photochemically induced nonocclusive common carotid artery thrombosis (CCAT) was used to generate a platelet thrombus in the carotid artery of anesthetized rats. After CCAT, platelet aggregates break off the thrombus, travel to the distal cerebral vasculature, damage blood vessels, and cause small infarctions. The authors hypothesized that deficits in the endothelial nitric oxide synthase (eNOS) pathway may be responsible for vascular dysfunction after embolic stroke. To examine the functional status of the eNOS system, they measured eNOS-dependent dilation after CCAT by applying acetylcholine through a cranial window over the middle cerebral artery. The authors also measured eNOS mRNA and protein in the middle cerebral artery to determine whether functional changes were caused by alterations in expression. eNOS-dependent dilation was reduced at 6 hours, elevated at 24 hours, and returned to baseline 72 hours after CCAT. Endothelial nitric oxide synthase mRNA increased at 2 hours and was followed by a rise in protein 24 hours after CCAT. Changes in the eNOS system may account for some of the observed vascular deficits in patients with cerebrovascular disease.

Acetylcholine↗

PubMed2004

Transcriptional down-regulation of the platelet ADP receptor P2Y(12) and clusterin in patients with systemic lupus erythematosus.

Cardiovascular complications are common in systemic lupus erythematosus (SLE) and myocardial infarctions are the leading cause of increased mortality. The ADP receptor P2Y(12) plays a central role in platelet activation and the P2Y(12) blocker clopidogrel reduces the incidence of cardiovascular events. Clusterin, a complement inhibitory protein suggested to be involved in the pathogenesis of SLE, has been found recently in a microarray study to be expressed at very high levels in platelets. Using a new protocol for mRNA quantification in platelets we set out to study if gene expression is altered in SLE patients compared with a healthy control group. Quantitative assay based on real-time PCR was used to measure mRNA expression, Western blot for P2 receptor protein expression and PFA-100 for platelet aggregation. The P2Y(12) receptor expression was decreased in SLE compared to the controls (P < 0.05), while expression of P2Y(1) and P2X(1) were unaltered. These findings were consistent at the protein level. The clusterin mRNA expression was very high. However, SLE patients had significantly lower levels than controls (P < 0.05). Platelet aggregation was similar in both groups. It may be suggested that a decreased level of P2Y(12) receptors could represent a protective response in SLE against thrombotic complications. Lowered clusterin levels could be involved in the pathogenesis of SLE due to decreased protective effects. These findings could help to achieve a better understanding of the platelet function in SLE and serve as a guide for further research and drug use.

Adolescent↗

PubMed2005

Shiga toxin 1 causes direct renal injury in rats.

Infection with Shiga toxin (Stx)-producing Escherichia coli has been implicated to cause hemolytic uremic syndrome, which is characterized by histological abnormalities such as microvascular thrombi and tubular cell damage in the kidney. Although Stx is known to be the major virulence factor of the pathogen, it is still unclear whether Stx directly impairs renal cells in vivo to cause such histological changes and deterioration of renal function. To assess the consequence of the direct action of Stx on renal cells, left kidneys of rats were perfused with Stx1 from the renal artery through the renal vein and then revascularized. Kidneys of control animals were perfused with the vehicle alone. On day 1, apoptosis and induction of tumor necrosis factor alpha gene expression were noticed to occur in the medulla of the Stx1-perfused kidneys. On day 3, extensive tubular injuries were observed by light microscopy: aggregated platelets and monocytic infiltrates in both glomeruli and the medullary interstitium were detected by immunostaining. Tubular changes were more extensive on day 9, with areas of infarction seen in the cortex and medulla. These changes were not found to occur in the sham-operated kidneys. No obvious glomerular changes were detected by light microscopy at any time point. When nonperfused right kidneys were removed after the Stx1 perfusion of the left kidneys, the serum creatinine and blood urea nitrogen levels were increased from day 2, and acute renal failure followed on day 3. These results indicate that Stx1 caused glomerular platelet aggregation, tubular damage, and acute deterioration of renal function by acting directly on renal cells.

Animals↗

PubMed1998

In vitro release of vascular endothelial growth factor during platelet aggregation.

Platelet aggregation is a cardinal feature of both vascular repair and vascular disease. During aggregation platelets release a variety of vasoactive substances; some of these promote angiogenesis, endothelial permeability, and endothelial growth, actions shared by vascular endothelial growth factor (VEGF). This study was undertaken to investigate the hypothesis that VEGF is released by aggregating platelets. We found that VEGF was secreted during the in vitro aggregation of platelet-rich plasma induced by thrombin, collagen, epinephrine, and ADP (range 23-518 pg VEGF/ml). Furthermore, serum VEGF levels were elevated compared with plasma (230 +/- 63 vs. 38 +/- 8 pg VEGF/ml), indicative of VEGF release during whole blood coagulation. Lysates of apheresed, leukocyte-poor platelet units contained significant amounts of VEGF (2.4 +/- 0.8 pg VEGF/mg protein). VEGF message and protein were also present in a megakaryocytic cell line (Dami cell). These results suggest constitutive roles for platelet VEGF in the repair of intimal vessel injury and in the altered permeability and intimal proliferation seen at sites of platelet aggregation and thrombosis.

Adenosine Diphosphate↗

PubMed2003

Expression of human scavenger receptor B1 on and in human platelets.

OBJECTIVE: The abundance of HDL particles correlates inversely with the incidence of coronary heart disease. The human scavenger receptor B1 (hSR-B1/CLA-1) is a receptor for HDL. Expression of hSR-B1/CLA-1 mRNA and protein in human platelets was determined using reverse transcriptase-polymerase chain reaction and Western blot, respectively. Presence of the protein on the surface of platelets was shown using flow cytometry. METHODS AND RESULTS: Immunochemical staining for hSR-B1/CLA-1 showed that it was expressed in megakaryocytes, the platelet precursors of human bone marrow. These findings prompted us to ask whether hSR-B1/CLA-1 was differentially expressed on platelets obtained from patients with atherosclerotic disease compared with those in control subjects. Our findings showed that abundance of hSR-B1/CLA-1 was significantly reduced on the surface of platelets from patients with atherosclerotic disease. The reduced levels of hSR-B1/CLA-1 were associated with increased cholesterol ester content in platelets from patients with atherosclerotic disease compared with control subjects. A negative correlation existed between hSR-B1/CLA-1 expression and platelet aggregation. In summary, our studies show that the HDL receptor hSR-B1/CLA-1 is expressed in platelets and their precursor, the megakaryocyte. The levels of hSR-B1/CLA-1 expression correlate inversely with cholesterol ester content and platelet aggregation. CONCLUSIONS: These findings suggest that determining the level of hSR-B1/CLA-1 expression on the platelets may be a useful clinical marker for atherosclerotic diseases.

Adult↗

PubMed1994

Insulin-like growth factor I inhibits induction of nitric oxide synthase in vascular smooth muscle cells.

Experiments were designed to examine whether or not insulin-like growth factor I (IGF-I), which is produced by vascular cells in response to injury, affects the production of nitric oxide evoked by the inducible nitric oxide synthase in cultures of smooth muscle cells from the rat aorta. Nitric oxide production was assessed indirectly by the measurement of nitrite accumulation and nitric oxide synthase activity by determining the formation of L-citrulline from L-arginine. Nitric oxide synthase was induced in vascular smooth muscle cells that had been exposed to interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha). IGF-I inhibited, in a concentration-dependent manner, the production of nitrite and L-citrulline evoked by IL-1 beta or TNF-alpha. The inhibition caused by IGF-I required the presence of the growth factor during the induction of nitric oxide synthase. Two IGF-I-related proteins, IGF-II and insulin, also inhibited, but to a smaller extent, the release of nitrite and the formation of L-citrulline stimulated by IL-1 beta. Under bioassay conditions, the perfusates from columns containing IL-1 beta-treated smooth muscle cells relaxed rings of rat aorta without endothelium that had been contracted with phenylephrine; these relaxations were reversed by nitro-L-arginine. Addition of IL-1 beta-treated vascular smooth muscle cells to indomethacin-treated platelets inhibited their aggregation to thrombin; methylene blue prevented this inhibition. Control smooth muscle cells or cells exposed to IGF-I alone did not have such effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗