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Download Exchangers by Mark O. Bevensee (Eds.) PDF

By Mark O. Bevensee (Eds.)

Current themes in Membranes is precise towards scientists and researchers in biochemistry and molecular and mobile biology, offering the required membrane study to aid them in knowing the present kingdom and destiny clients of a selected box.

This quantity on exchangers, at the side of a prior quantity on cotransporters (volume 70), represents an updated, systematic, and accomplished assessment of the entire significant secondary energetic provider proteins chargeable for the absorption, secretion, and basic delivery of ions and solutes in mammalian organ structures and extra species. each one bankruptcy is dedicated to a selected transporter or a grouping of comparable transporters in keeping with the well-recognized nomenclature of the SoLute service (SLC) gene relatives. This e-book presents readers with the newest mechanistic details at the functionality and constitution of particular transporters, in addition to their heritage and physiological value.

  • Comprehensive assessment of the entire significant exchangers
  • Emphasis on protein mechanism with the newest findings from sensible and structural work
  • Authoritative paintings from specialists within the field

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Jin, X. , & Hamasaki, N. (2004). Mass spectrometric analyses of transmembrane proteins in human erythrocyte membrane. Journal of Biochemistry, 136, 97–106. , et al. (2011). Genetic polymorphisms in CTLA4 and SLC4A2 are differentially associated with the pathogenesis of primary biliary cirrhosis in Japanese patients. Journal of Gastroenterology, 46, 1203–1212. , et al. (1996). The cisternae decorating the red blood cell membrane in congenital dyserythropoietic anemia (type II) originate from the endoplasmic reticulum.

Interestingly, castanospermine treatment of cells resulted in movement of some dominant but not recessive dRTA kAE1 mutants to the BLM (Patterson & Reithmeier, 2010). Mutation of the N-glycosylation site (N642D) that precludes an interaction with the lectin calnexin had the same effect. The severely misfolded SAO mutant, however, was not rescued. Thus, some dominant dRTA mutants are retained in the ER of polarized MDCK by SLC4 and SLC26 Anion Transporters 33 their interaction with calnexin. It has been shown (Chu, King, Berrini, Alexander, & Cordat, 2013) that it is possible to rescue the trafficking and partially the function of the recessive G701D mutant to the BLM of MDCK cells using a chemical chaperone, while the dominant R589H or C479W mutants were not rescued.

2004). The association of these two proteins stimulates their mutual transport activities. 2. 3). Mutations in SLC26A2 cause chrondrodysplasias, mutations in SLC26A3 cause chronic chloride diarrhea, and mutations in SLC26A4 cause enlargement of the vestibular aqueduct in the inner ear and deafness. Mouse knockout models have revealed the physiological consequences of losing Slc26 family members including Slc26a1, 5, 6, 7, 8, 9. No (or only a few in the case of SLC26A8) human mutations associated with these genes have been clearly linked to disease to date.

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