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Titlebook: Membrane Transporter Diseases; Stefan Br?er,Carsten A. Wagner Book 2003 Springer Science+Business Media New York 2003 ATP.Amino acid.Aspar

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發(fā)表于 2025-3-21 16:04:56 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Membrane Transporter Diseases
編輯Stefan Br?er,Carsten A. Wagner
視頻videohttp://file.papertrans.cn/631/630413/630413.mp4
圖書封面Titlebook: Membrane Transporter Diseases;  Stefan Br?er,Carsten A. Wagner Book 2003 Springer Science+Business Media New York 2003 ATP.Amino acid.Aspar
描述Every cell and organism faces the problem of spaces, made up of the two leaflets of the lipid generating a confined space in which metabolic bilayer. The importance of traffic and signaling across membranes is reflected by the estimate and anabolic reactions take place and at the same time allowing entry and exit of metabo- that 20% of all genes in the human genome encode membrane proteins. A failure of any of lites, ions, proteins, and signals across its bor- der. Evolution has solved the problem by these proteins may have dramatic con se- generating lipid membranes that contain trans- quences for ceH function. In recent years much porters, ion channels, and receptors. In eukary- attention has been paid to diseases resulting otic cells, this problem is exacerbated by the from nonfunctional ion channels ("chan- presence of multiple organelles, which are con- nelopathies"). Not surprisingly, many of these fined spaces in their own right. Even the lipid diseases affect the excitability of cells. membrane consists of two relatively separate Transporter diseases (perhaps coined "carrier vi PREFACE diseases") are more related to metabolic dis- Each chapter is concluded by a summary, and
出版日期Book 2003
關鍵詞ATP; Amino acid; Aspartat; Glutamat; Glycogen; Oxidation; dopamine; pathophysiology; physiology; Tree Biology
版次1
doihttps://doi.org/10.1007/978-1-4419-9023-5
isbn_softcover978-1-4613-4761-3
isbn_ebook978-1-4419-9023-5
copyrightSpringer Science+Business Media New York 2003
The information of publication is updating

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Electrogenic Na+/HCO 3 ? cotransporter NBC1 (SLC4A4): proximal renal tubular acidosis and ocular patBlood and cellular pH are tightly controlled. Normal blood pH is 7.35–7.45, that is,[H. of 36–45nM. In fact, humans with blood pH below 7.2 or above 7.6 are quite sick. Chronic blood pH below 7.0 ([H.=100nM) or above 7.8 (H. ~ 15nM) is incompatible with life.
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Introductione taken up from the food in only small quantities but are essential components of enzymes, hormones, energy substrates, and nucleic acids, or for the formation of extracellular matrix in bone (phosphate) or cartilage (sulfate). The absolute requirement for these substrates and their often low concen
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Anion exchangers DTDST (SLC26A2), DRA (SLC26A3), and pendrin (SLC26A4)ns in the body arising from defect s in cell surface (plasma membrane) anion transport. This famil y of proteins, designated /ldsulfate transporters” based on their function, belongs to the Human Genome Nomenclature Committee (HGNC) designated Solute Linked Carrier (SLC) family 26, of which presentl
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Divalent metal transporter DMT1 (SLC11A2); we will describe the existing mutants representing specific transporter diseases in rodents. In addition, the chapter will further describe the potential contribution of DMT1 to diseases where . is not the gene mutated. Lastly, we will present insights derived from or to be gained from in vitro mu
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