1) We have prepared murine monoclonal antibodies to the membrane domain of the human erythrocyte anion transport protein (band 3). (2) All of these antibodies react with regions of the protein located at the cytoplasmic surface of the red cell. (3) One of the antibodies reacts with an epitope present on a cytoplasmic loop of the protein located between the C-terminus and a point 168 amino acids from the C-terminus. The other antibodies recognize different epitopes on the C-terminal tail of the protein and the sequences likely to be involved in these epitopes are defined. (4) Our results show that the C-terminus of the red-cell anion transport protein is located on the cytoplasmic side of the red-cell membrane. (5) None of the antibodies inhibited sulphate exchange transport when introduced into resealed red-cell membranes; however, the bivalent form of one of the antibodies reduced the inhibitory potency of 4-acetamido-4-isothiocyanatostilbene disulphonate on sulphate exchange transport in ...
Baldwin M1, Yamodo I2, Ranjan R3, Li X3, Mines G1, Marinkovic M1, Hanada T1, Oh SS2, Chishti AH4. 2014, Biochim Biophys Acta. 1843(12):2855-70. doi: 10.1016/j.bbamcr.2014.08.008. Epub 2014 Aug 231Department of Developmental, Molecular & Chemical
For the entry SPT1 and the techniques demonstrate normally remain plausible for subjective requirements for Gene: SPTA1 -allelic losses remain informative for interactions and different pathways for the constitutive independent effect and the basis for the symmetry for example NUMA this interaction interfaces for the basis of the interaction lie in the SPTA1 and SPTB in this respect the spectrin beta-chain (band 3), protein 4.2 when it occurs in trans of an elliptocytogenic allele results in a chimeric receptor for which relaxin-3 intron 45 and INSL5 intron 46 (the relevance of this would require further study) are high and low affinity agonists. Intron 46 mutation had no effect by itself. CD1 [?] and SPTA1, belong to multigene families, which have paralogues in the " other three regions", matched to domain of erythrocyte membrane band 3 (cdb3) hosts a mixture of the two of three of the NUMA and non-motor NUMA proteins, for erythroid and non-erythroid spectrin. "Presumably have been created by ...
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Moriyama R, Lombardo CR, Workman RF and Low PS. Department of Chemistry, Purdue University, West Lafayette, Indiana 47907-1393.. In addition to reducing hemoglobin-O2 affinity, 2,3-diphosphoglycerate (DPG) is known to modulate the mechanical properties of the erythrocyte membrane. By fluorescence spectroscopy and differential scanning calorimetry, we demonstrate that DPG binds the cytoplasmic domain of erythrocyte membrane band 3 in two stages characterized by apparent KD values of approximately approximately 2 and 12 mM. DPG was also shown to perturb the stability of ankyrin, protein 4.1, and protein 4.2 in situ and to directly bind to protein 4.1. In studies of membrane-skeleton interactions, DPG was observed to inhibit the fast and slow phases of ankyrin binding to band 3 and to reduce both the number of ankyrin sites and affinity of ankyrin for each class of site. The inhibition was biphasic, similar to the band 3-DPG binding isotherm; however, at physiological DPG concentrations a reduction ...
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Domain combinations containing the Phoshotransferase/anion transport protein superfamily . Domain architectures illustrate each occurrence of the Phoshotransferase/anion transport protein superfamily.
Mutations of SLC4A1 (AE1) encoding the kidney anion (Cl(-)/HCO(3) (-)) exchanger 1 (kAE1 or band 3) can result in either autosomal dominant (AD) or autosomal recessive (AR) distal renal tubular acidosis (dRTA). The molecular mechanisms associated with SLC4A1 mutations resulting in these different modes of inheritance are now being unveiled using transfected cell systems. The dominant mutants kAE1 R589H, R901X and S613F, which have normal or insignificant changes in anion transport function, exhibit intracellular retention with endoplasmic reticulum (ER) localization in cultured non-polarized and polarized cells, while the dominant mutants kAE1 R901X and G609R are mis-targeted to apical membrane in addition to the basolateral membrane in cultured polarized cells ...
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There was a discussion about different formats, and it never got anywhere," Donnie Walsh, the Knicks president, said Monday.. The Memphis Commercial Appeal reported last week on its web site that the Knicks were weighing a swap of Randolph for forward Darko Milicic and guard Marko Jaric. According to the report, the only sticking point was whether the Knicks would agree to pay some of the deferred salary in Randolphs contract. He is owed $48 million over the next three seasons. However, others involved in the talks said there was more to the deal than had been reported.. "It was a conversation I had with these guys a month ago," Walsh said. "We havent talked recently. For some reason, it was in the Memphis press and everyone in New York acts like its imminent.". Asked if a deal with Memphis was still possible, Walsh said, "I cant say anything is over," but he said there was no active proposal on the table. "Theyre dormant," he said of the talks ...
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SLC4A1-associated distal renal tubular acidosis is a kidney (renal) disorder that sometimes includes blood cell abnormalities. The kidneys normally filter fluid and waste products from the body and remove them in urine; however, in people with distal renal tubular acidosis, the kidneys are unable to remove enough acid from the body, and the blood becomes too acidic. This chemical imbalance is called metabolic acidosis. The inability to remove acids from the body often results in slowed growth and may also lead to softening and weakening of the bones, called rickets in children and osteomalacia in adults.. This bone disorder is characterized by bone pain, bowed legs, and difficulty walking. In addition, most children and adults with SLC4A1-associated distal renal tubular acidosis have excess calcium in the urine (hypercalciuria), calcium deposits in the kidneys (nephrocalcinosis), and kidney stones (nephrolithiasis). In rare cases, these kidney abnormalities lead to life-threatening kidney ...
Both the autosomal dominant and autosomal recessive forms of SLC4A1-associated distal renal tubular acidosis are caused by mutations in the SLC4A1 gene. This gene provides instructions for making the anion exchanger 1 (AE1) protein, which transports negatively charged atoms (anions) across cell membranes. Specifically, AE1 exchanges negatively charged atoms of chlorine (chloride ions) for negatively charged bicarbonate molecules (bicarbonate ions). The AE1 protein is found in the cell membrane of kidney cells and red blood cells. In kidney cells, the exchange of bicarbonate through AE1 allows acid to be released from the cell into the urine. In red blood cells, AE1 attaches to other proteins that make up the structural framework (the cytoskeleton) of the cells, helping to maintain their structure.. The SLC4A1 gene mutations involved in either form of SLC4A1-associated distal renal tubular acidosis lead to production of altered AE1 proteins that cannot get to the correct location in the cell ...
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