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PubMed1982

Hypoxanthine levels in amniotic fluid: an indicator of fetal hypoxia?

During hypoxia there is an increased formation of hypoxanthine from the consumption of ATP; simultaneously the oxidation into uric acid is decreased. The purpose of this study was to determine possible correlations between hypoxanthine concentrations in the amniotic fluid and states of fetal hypoxia. We obtained 83 amniotic fluid samples from 68 patients during pregnancy or delivery. Hypoxanthine was assayed fluorimetrically according to GARDINER [4]. In the course of pregnancy, hypoxanthine levels in the amniotic fluid rise slightly. A marked increase occurs during delivery (without labor mean = 3.4 +/- 0.9 mumol/l, with labor mean = 7.0 +/- 5.4 mumol/l, p less than 0.02). There is no significant difference in the levels obtained from the first and second stages of labor. In intrauterine fetal death (Fig. 1) and in depressed newborns (Tab. I) there were increased hypoxanthine levels in the amniotic fluid, this was not seen in other complications of pregnancy. Independently from the fetal state increased hypoxanthine concentrations may occur in the amniotic fluid evidently as a consequence of labor activity. Thus the determination of hypoxanthine levels in the amniotic fluid cannot be used for the diagnosis of fetal hypoxia.

Adenosine Triphosphate↗
PubMed1994

Regulation of flagellar motility of fowl spermatozoa: evidence for the involvement of intracellular free Ca2+ and calmodulin.

The possible role of intracellular free Ca2+ and calmodulin in the regulation of fowl sperm motility was investigated using an intracellular Ca2+ chelator, 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid, tetraacetoxymethyl ester (BAPTA/AM) and calmodulin antagonists such as N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7), N-(6-aminohexyl)-1-naphthalenesulfonamide hydrochloride (W-5) and trifluoperazine. Intact fowl spermatozoa maintained vigorous movement in a Ca(2+)-free medium at 30 degrees C. In contrast, the motility of spermatozoa loaded with BAPTA/AM was negligible at 30 degrees C, but could be instantly restored by the addition of 2 mmol CaCl2 l-1. At this time, the intracellular free Ca2+ concentrations increased from 0 to about 100 nmol l-1, as measured by the fluorescent Ca2+ indicator fura-2. At 40 degrees C, neither control nor BAPTA/AM-treated spermatozoa were motile, but the motility of both kinds of spermatozoa was restored by the subsequent addition of 2 mmol CaCl2 l-1. Even in the presence of 2 mmol CaCl2 l-1, the addition of W-7 and trifluoperazine inhibited the motility of intact spermatozoa at 30 degrees C and 40 degrees C, and induced a concomitant decrease in the rate of oxygen consumption and ATP concentration, suggesting that energy depletion might be involved in the inhibition of motility. In contrast, the motility of demembranated spermatozoa was not inhibited by the addition of W-7 and trifluoperazine at 30 degrees C. The addition of W-5, a weaker antagonist, did not appreciably affect the motility of either intact or demembranated spermatozoa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Ca2+ sensitivity of contractile machinery and Ca2+ handling energy. Simulation.

Myocardial Ca2+ handling during excitation-contraction coupling has been modelled mathematically to gain a better insight into the expectation that Ca2+ sensitization of contractile machinery may save myocardial energy utilization for Ca2+ handling. The basic model of myocardial Ca2+ kinetics and mechanoenergetics involved the sarcoplasmic reticulum (SR), sarcoplasm, troponin C (Tn) and crossbridges (CB). The relations among the released Ca2+ ions from the SR, peak concentrations of sarcoplasmic free Ca2+ ([Ca2+]i) and Ca(2+)-bound troponin ([TnCa]) and peak contractile force were computed, based upon the assumptions that the released Ca2+ ions diffuse as free Ca2+ in sarcoplasm, bind kinetically with Tn with an association rate constant of k1, dissociate from TnCa with a dissociation rate constant of k2, and are sequestered into the SR with consumption of ATP. TnCa was associated with CB cycling to develop force with a set of given on and off rate constants. The association constant Ka (= k1/k2) of TnCa as an index of Ca2+ sensitivity of Tn was varied 32-fold from 0.25 to 8/microM. Results showed that Ca2+ sensitization from a lower Ka level could most sharply decrease the total Ca2+ release required to develop the same contractile force. Thus, it would reduce the total Ca2+ handling energy that the SR uses to maintain the same contractility.

Calcium↗
PubMed2002

Metabolic oscillations in beta-cells.

Whereas the mechanisms underlying oscillatory insulin secretion remain unknown, several models have been advanced to explain if they involve generation of metabolic oscillations in beta-cells. Evidence, including measurements of oxygen consumption, glucose consumption, NADH, and ATP/ADP ratio, has accumulated to support the hypothesis that energy metabolism in beta-cells can oscillate. Where simultaneous measurements have been made, these oscillations are well correlated with oscillations in intracellular [Ca(2+)] and insulin secretion. Considerable evidence has been accumulated to suggest that entry of Ca(2+) into cells can modulate metabolism both positively and negatively. The main positive effect of Ca(2+) is an increase in oxygen consumption, believed to involve activation of mitochondrial dehydrogenases. Negative feedback by Ca(2+) includes decreases in glucose consumption and decreases in the mitochondrial membrane potential. Ca(2+) also provides negative feedback by increasing consumption of ATP. The negative feedback provided by Ca(2+) provides a mechanism for generating oscillations based on a model in which glucose stimulates a rise in ATP/ADP ratio that closes ATP-sensitive K(+) (K(ATP)) channels, thus depolarizing the cell membrane and allowing Ca(2+) entry through voltage-sensitive channels. Ca(2+) entry reduces the ATP/ADP ratio and allows reopening of the K(ATP) channel.

Animals↗
PubMed2026

Beyond NAD Depletion: SARM1-Induced ATP Collapse Involves Direct ATP Degradation and Mitochondrial Dysfunction and Is Pharmacologically Reversible.

Sterile alpha and Toll/interleukin-1 receptor motif-containing protein 1 (SARM1) is an inducible NAD-consuming enzyme and execution factor in axon degeneration. Rapid ATP collapse after SARM1 activation, however, is not fully explained by NAD depletion alone. We used SARM1-overexpressing HEK293 cells and the cell-permeant activator CZ-48 to examine SARM1-induced non-apoptotic cell death, termed sarmoptosis. CZ-48 induced cell death that was suppressed by HSP90/70-annotated ATP-competitive compounds, especially geldanamycin and VER-155008 (VER), without reducing SARM1 abundance. VER preserved NAD and ATP during SARM1 activation but failed to rescue FK866-mediated NAD starvation, thereby distinguishing CZ-48/SARM1-driven cytotoxicity from generic NAD depletion. In cell-free assays, purified SARM1 reduced ATP levels; this effect was enhanced by SARM1's activator NMN and attenuated by its pharmacological inhibitors, although the in vitro activity was modest and the reaction products remain to be identified. ATPase-related perturbations, including thapsigargin and bafilomycin A1, also protected cells from CZ-48-induced death, further supporting a central role for ATP collapse in sarmoptosis. iTRAQ proteomics, MitoSOX Red staining, and DiOC6(3) staining revealed that CZ-48 treatment was associated with mitochondrial and metabolic remodeling, mitochondrial ROS accumulation, and mitochondrial depolarization, all of which were mitigated by VER. Collectively, these findings support a convergent ATP-collapse model in which SARM1 activation promotes NAD depletion, directly consumes ATP, and is associated with mitochondrial dysfunction that may amplify ATP-production failure.

ATP collapse↗
PubMed2005

Hypothermic maintenance of hepatocyte spheroids.

Primary hepatocytes form spheroids under some culture conditions. These spheroids exhibit many tissue-like ultrastructures and retain many liver-specific functions over a long period of time. They are attractive for many applications employing liver cells. The ability to maintain their viability and functions at a reduced temperature to allow for transportation to the site of their application will facilitate their use. Furthermore, with their structural and functional similarity, they could possibly be used as a model system for studying various liver ischemias. The effect of hypothermic treatment was assessed by oxygen consumption rate, ATP, H2O2, and caspase 8 content, as well as albumin and urea synthesis, during and posttreatment. No single outcome variable gives a superlative quantification of hypothermic damage. Taken together, the hypothermic treatment can be seen as increasingly damaging as the temperature decreases from 21 degrees C to 15 degrees C and 4 degrees C. The addition of the chemical protectants glutathione, N-acetyl-L-cystein (NAC), and tauroursodeoxycholic acid (TUDCA) decreased the damaging effect of hypothermic treatment. This protection effect was even more profound when spheroids were preincubated with the protectant for 24 h, and was most prominent at 4 degrees C. The viability of the hypothermically treated hepatocyte spheroids was confirmed by laser scanning confocal microscopy. The method reported provides a means of maintaining spheroids' viability and may allow for their distribution to application sites at a distance.

Animals↗
PubMed1977

Effects of ventricular fibrillation on coronary blood flow and myocardial metabolism.

Ventricular fibrillation is frequently induced during cardiac surgery to quiet the operative field. The reported effects of fibrillation on the myocardium vary considerably. In an attempt to better define these effects, we subjected 28 dogs to one hour of total normothermic bypass. Myocardial blood flow, lactate, adenosine triphosphate (ATP), oxygen consumption, and left ventricular fibrillation was induced in 5 dogs and continuous electrical fibrillation in 7 dogs. These groups were compared to two respective control groups with beating hearts of 8 animals each. Coronary sinus flow, total coronary blood flow, left ventricular flow, myocardial oxygen consumption, and myocardial tissue lactate increased significantly in the fibrillating hearts. Left ventricular dp/dt decreased with fibrillation, but not significantly. It is concluded that the metabolic demands of ventricular fibrillation exceed the increase in coronary blood flow, when compared to demands of the beating heart, and that decreased left ventricular performance may result.

Adenosine Triphosphate↗
PubMed1975

Incubation studies on human red cells utilizing glucose or inosine under various conditions.

Human red cells were incubated at pH 8.2 and 30 mM phosphate concentration with glucose, glucose plus methylene blue, or inosine. In 16 normal subjects, the lactate production rate (LPR) from glucose alone was 92.2 +/- 7.5 mumoles per minute per liter red blood cell. With methylene blue added, the mean LPR was 118.5 +/- 7.4 per cent of control glucose values. With inosine as substrate the mean LPR was 68.5 +/- 6.0 per cent of that from glucose. Lactate/glucose ratios averaged 1.36, presumably because of accumulation of intermediates under conditions of high pH and Pi. Patients with various kinds of anemias had LPR's from glucose that were usually markedly higher than normal, but the LPR's from inosine were generally about 2/3 of those from glucose. The LPR's of the anemic patients correlated with their degree of reticulocytosis and several patients with pyruvate kinase (PK) deficiency showed normal LPR if the red cell population age was ignored, byt marked depression when compared to expected LPR for degree of reticulocytosis. The LPR from glucose of red cells of G6PD-deficient subjects was decreased (not increased) by methylene blue. Methylene blue, while stimulating the pentose phosphate pathway, also mediated some oxidation of NADH, thus complicating the stoichiometry of the overall system. In addition, the results suggested that the dye may have attacked -SH groups on some enzymes. In normal red cells, the lower LPR from inosine than from glucose was explained as due to consumption of ATP for hexose utilization (thus generating more ADP for the triose reactions). In confirmation, when red cells were incubated without substrate to deplete their ATP-, and enhance their ADP-, levels, the LPR from inosine exceeded that from glucose. Fluoride and iodoacetate affected LPR from glucose more than from inosine, suggesting the necessity of adequate ATP levels in hexose utilization. Overall glycolysis in the red cell is seen as the resultant of a network of metabolic reactions in which ADP and ATP levels are important control parameters.

Adenosine Diphosphate↗
PubMed1989

Changes in the nucleotide metabolism of Ehrlich ascites tumour cells during their growth in vivo.

During the transition of Ehrlich mouse ascites tumour cells from the proliferating into the resting phase of growth a tremendous loss of purine and pyrimidine compounds was quantitated by ion-pair reversed-phase high performance liquid chromatography. This change is accompanied by a distinct decline in the incorporation rates of adenine, hypoxanthine, and adenosine. Inorganic phosphate stimulates the low rate of hypoxanthine incorporation of cells in the plateau phase, but lacks any effect on the high rate during proliferation. The mitochondria suffer structural deteriorations and decrease in their cellular content in the course of the plateau phase; however, other changes were not seen by morphometric analysis. The interrelations between nucleotide metabolism, mitochondrial content and the rates of formation and consumption of ATP are discussed.

Adenine↗
PubMed1988

Toxicity of H2-receptor antagonists to isolated rat hepatocytes: structure-activity relationships.

Oxmetidine is a potent and specific antagonist of the histamine H2-receptor. Oxmetidine is also cytotoxic to isolated rat hepatocytes through inhibition of mitochondrial oxidative phosphorylation. The purpose of this investigation was to test a variety of H2-receptor antagonists that are structural analogs of oxmetidine in an attempt to identify a critical structural component or a physicochemical property of the molecule which may be responsible for cytotoxicity. Six histamine receptor H2-antagonists were tested. The minimum drug concentrations that caused 100% cell death (leakage of intracellular lactate dehydrogenase and loss of intracellular potassium) ranged from 0.87 to 22.50 mM for the analogs tested. At toxic concentrations, two of the least potent analogs, SK&F 92909 and SK&F 9205A both caused a rapid decrease in hepatocyte O2 consumption and ATP content which occurred before any evidence of cell injury. The potency of these molecules as cytotoxicants to isolated hepatocytes did not correlate with their potency as histamine H2-receptor antagonists whereas there was a significant correlation between increasing potency and increasing octanol/water partition coefficients. These data suggest that lipid solubility may be a key factor in the cytotoxicity of this class of drugs to isolated rat hepatocytes.

Animals↗
PubMed1988

Seven-day storage of single donor platelets in polyolefin bags: clinical, biochemical, morphological and microbiological evaluation.

We compared the in vitro and in vivo function of fresh and stored platelet concentrates (PCs) collected by an automated continuous-flow blood cell separator (CS 3000 Fenwal) in a closed-system apheresis kit in order to evaluate the possibility of extending the storage time to seven days with the polyolefin container (PL-732). The initial 220 ml platelet volume (5.14 +/- 1.23 x 10(11) was divided into two parts. Half was transfused and the other half was stored for 7 days. All cultured units were negative for bacterial contamination. Mean counts for fresh and stored platelets were respectively 2.34 +/- 0.59 and 2.17 +/- 0.50 X 10(11)/100 ml of PCs (mean recovery 88.7 +/- 11.9%). The pO2 levels were maintained during storage (179.9 +/- 30.5 mmHg) but pCO2, pH, LDH, osmolality, glucose consumption, bicarbonates, ATP, and osmotic stress values changed significantly after 7 days storage. From a clinical point of view, in 14 patients receiving a total of 38 PC transfusions no statistically significant change in corrected post-transfusional levels was observed between fresh and stored PC. Biochemical and morphological data and clinical results suggest that PCs collected with CS-3000 blood cell separator in a closed system and stored for 7 days in polyolefin bags (PL-732) can be satisfactorily employed in clinical practice.

Blood Platelets↗
PubMed1981

Voltage modulation of Na+/K+ transport in human erythrocytes.

For a cell to perform certain functions it presumably must maintain a steady-state transmembrane potential. This potential differential can take several forms, e.g. a proton gradient, an ionic concentration gradient, or an asymmetric distribution of charges in membraneous proteins and lipids. We report here a study which indicates that an externally applied electric field can induce opening/closing of membrane channels, including Na+/K+ ATPase channels. The method utilizes a continuous AC stimulation of cell suspensions. Reversible channel opening/closing of human erythrocytes in an isotonic suspension can be demonstrated by directly measuring the conductivity of the bulk suspension. Channel opening occurs at a field intensity of 10 V/cm, which corresponds to a maximum transmembrane potential of about 6 mV, when the frequency of AC field is maintained below 1 kHZ. The apparent half-time of the channel opening decreases with an increase in the stimulating voltage, and reaches a plateau value of 2 sec beyond 24 V/cm (15 mV of transmembrane potential). When the AC field is removed, these channels close with a half-time of 10.2 sec. Of the channels opened, roughly 20% belongs to the Na+/K+ ATPase, as this fraction of conductance signals can be quantitatively blocked by a specific inhibitor ouabain in a low ionic medium. The AC field appears to stimulate active Na+/K+ transport against a concentration gradient in erythrocytes. At a field strength of 24 V/cm, the net transport against a controlled sample is about 1 mM 42K+ ion per hour under our experimental condition. This translates into a rate of 60 K+ ions per channel per second. The AC field also increases the K+/Na+ ratio of cytoplasmic concentration in the stimulated sample, indicating an active extrusion of Na+ ion from the cells. Higher consumption of ATP is not detected in the stimulated cells as compared with unstimulated cells. As expected, an addition of ouabain in the external medium abolishes the above effects. Experiments described here would demonstrate that the phenomena observed are due to the effect of the field-induced transmembrane potential. The significance of these observations are discussed in the light of the recent discovery that transmembrane potential is an important driving force for certain cellular functions.

Adult↗
PubMed1983

Protons and glucose metabolism in shock.

When oxygen is limiting, animals can ferment glucose via several metabolic pathways varying in energetic efficiency and leading to various end products (such as lactate, succinate, or propionate). Because the pH dependence of H+ production by fermentation is opposite to that by hydrolysis of adenosine triphosphate formed in the fermentation, the total number of moles of protons generated is always two per mole of fermentable substrate. However, two and three times more adenosine triphosphate can be turned over per mole of protons produced in succinate and propionate fermentations, respectively, than in lactate fermentation. At its limit, this advantage would achieve the same balance between H+ production and H+ consumption during ATP cycling that is observed in aerobic metabolism, a situation observed in certain alcohol fermentations. Since proton balance during anaerobiosis is clearly adaptable, we consider possible impact and functions of net H+ accumulation during carbohydrate metabolism in endotoxin shock.

Adenosine Diphosphate↗
PubMed1984

Inhibition of glutathione efflux from isolated rat hepatocytes by methionine.

A substantial inhibition (50-70%) of GSH efflux by methionine was demonstrated in hepatocytes isolated from fed rats. Concurrent measurements of intracellular GSH revealed maintenance of a higher concentration in methionine-supplemented cells over the 1-h incubation. Analysis of total GSH suggested that maintenance of higher intracellular GSH by methionine could be quantitatively accounted for by inhibition of GSH efflux rather than by net GSH synthesis. This conclusion was supported by studies with propargylglycine, a potent inhibitor of cysteine synthesis from methionine. Identical results were obtained in incubations containing either propargylglycine and methionine or methionine alone, thereby suggesting that net synthesis of GSH from methionine was minimal under the assay conditions. Similar decreases (40-60%) in the rate of extracellular accumulation of GSH were observed with ethionine and buthionine, two higher homologs of methionine, but not with a wide range of other naturally occurring and synthetic amino acids. The inhibition of GSH efflux by methionine was not dependent on the presence of sodium in the medium and did not correlate with metabolic consumption of ATP.

Alkynes↗
PubMed1984

[Homologous plasma cross-circulation on galactosamine induced hepatic failure rats].

Plasma cross-circulation which resembles plasma exchange clinically was carried out in between galactosamine (GalN) treated hepatic failure rats and normal rats. Twenty-four hours after the injection of GalN, plasma cross-circulation was performed at a plasma flow rate of 0.1 ml/min for 6 hours. In eighteen hours after the completion of a procedure, survival rate was 75% (6 out of 8 survived) in GalN injected rats treated with plasma cross-circulation, as compared to 40% (4 out of 10 survived) in GalN injected rats treated with sham-circulation. State 3 oxygen consumption and ATP synthesis in the liver mitochondrial respiratory function, and ATP and total adenine nucleotide contents in the liver in the former group were significantly higher than those in the latter group at the time of sacrifice of the survived animals. These appear to suggest that plasma cross-circulation enhances mitochondrial phosphorylative activity in the liver and may contribute higher survival rate of the rats. Plasma exchange using a large amount of fresh plasma, therefore, would be effective for the treatment of acute liver failure in its early stage.

Animals↗
PubMed1995

Role of endogenous acid in gastric mucosal injury induced by local ischemia-reperfusion in the rat.

The role of endogenous acid was evaluated in a rat model of gastric epithelial damage induced by local ischemia-reperfusion (IR). Because no gross lesion was induced in this model, the damage was quantified by measuring the blood-to-lumen [51Cr]EDTA clearance. A proton pump inhibitor (omeprazole) or an H2-receptor antagonist (T-593) was used to suppress luminal acidity from pH 5 to pH 6.3-7.0. Both drugs significantly attenuated the increase in clearance induced by IR, indicating an important role for endogenous acid. A second series of experiments was performed to confirm whether the change in pH from around 5 to 7 was sufficient to reduce IR-induced gastric mucosal damage. Phosphate-buffered saline was perfused into the gastric lumen to neutralize the endogenous luminal acid. Although the luminal acid was completely neutralized, no reduction in clearance was observed. These data indicate that endogenous luminal acid does not play an important role in gastric injury induced by local IR stress and that a proton pump inhibitor or H2-receptor antagonist may suppress IR injury by a mechanism other than reducing luminal acidity, i.e., reducing consumption of ATP needed for acid secretion, thereby improving gastric mucosal energy metabolism.

Animals↗
PubMed1996

[Alcohol ingestion and hyperuricemia].

Purine nucleotide degradation during ethanol catabolism, inhibition of renal excretion of urate by lactic acid, and high purine content of certain kinds of beverage are responsible for the elevation of serum uric acid level following alcohol drinking. It is well documented that rapid consumption of ATP produces uric acid via purine nucleotide degradation. Since individuals with ALDH2*1 can catalyze ethanol readily, they consume large amount of ATP, and thus produce more hypoxanthine than those with ALDH2*2. Thus, daily drinker and heavy drinker tend to readily induce hyperuricemia after alcohol ingestion. A high purine content in beer may contribute to the increasing frequency of hyperuricemia. Restriction of any kind of alcohol beverages, especially beer, is necessary in the medical control of patients with gout or hyperuricemia.

Adenosine Triphosphate↗
PubMed1997

[Multidrug resistance (MDR) in oncology].

Multidrug resistance or mdr is a frequent phenomenon for which tumor cells can develop, in only one step, cross-resistance to a different anticancer drugs such as antibiotics, vinca alkaloids and podophylotoxins. This is due to an extrusion of drugs out of the cells, since it is interrelated with the decrease of the intracellular concentration of the drug, compared to sensitive cells. This phenomeno of multidrug resistance (mdr) is considered one of the principal causes of failure in quimiotherapic treatment of cancer, and is associated in many cases to an hyperexpression of mdr-I gene, that codifies for a high molecular weight glycoprotein (p-170) (170-180 Kdaltons), also called p-glycoprotein (pgp). Locadet it in the cellular membrane extracts, like a pump, the quimiotherapic drugs with consumption of ATP. In humans, there are two principal genes that codify for pgp: mdr-I and mdr2/3; being the most important the mdr-I gene. The structure of p-glycoprotein consists in two symmetrical halves anchored in the cellular membrane that includes three extracellular dominances each one, and on intracellular portion with the ATP binding site. Also, has got an for extracellular carbohydrates chain. It is specially important to find drugs that reverse the multidrug resistance. Chemicals such as verapamil, nifedine, quinidine and calmodulin inhibitors are joined to pgp inhibiting it. A Cyclosporine and its non-immunosuppressors derivateds such as SDZ 280-125 and SDZ PSC 833 reverse mdr. At present it is being advancing in clinical trials, but the results are not satisfactory. Most useful chemicals are verapamil, better R-verapamil and A-cyclosporine or its non-immunosuppressors derivates. Futures possibilities are grateful. From diagnostic point of view the mains are: 1. Detection of mdr-I gene. 2. Recognition of the presence of mRNA for pgp. 3. Detection of pgp by flow cytometry or western blot. 4. Immunohistochemistry with monoclonal antibodies to pgp. 5. Rhodamine 123 to study mdr phenotype. 6. Multidrug resistance modulators in vitro. 7. pgp in vivo as a tumor marker. From therapeutic point of view: 1. To assay mdr modulators with higher power and better tolerated. 2. Reversing of mdr with in vivo MoAbs and/or immunotoxins. 3. Gene therapy. 4. New chemicals that joined to tubulin do not be extrused by pgp. 5. Drugs joined to liposomes. 6. Interpheron to increase the efficacy of MoAbs in mdr reversion. 7. Photodynamic therapy. Other possibilities can be the use of MoAbs in diagnostic (immunodetection) by PET and SPECT: and the MoAbs joined to drugs and radioisotopes.

ATP Binding Cassette Transporter, Subfamily B, Mem↗