By M. Sahay
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Dial. 1, (January 2010), pp. ; Levy, D. S. (2008). Overweight, obesity, and the development of stage 3 CKD: the Framingham Heart Study. 1, (July 2008), pp. K. K. (2009). Antiatherosclerotic and anti-insulin resistance effects of adiponectin: basic and clinical studies. 2, (September-October 2009), pp. Y. & Jin, W. (2010). Impact of non-alcoholic fatty liver disease on microalbuminuria in patients with prediabetes and diabetes. Intern. Med. 6, (June 2010), pp. ; Ohtake, T. & Kobayashi, S. (2008).
In the presence of bafilomycin-A1, the acidification was almost fully ablated by the knockdown of endogenous ClC-5 by siRNA. Contrasting previous assumption, these authors suggested that ClC-5 exchanges two Clions from the endosomal lumen for a proton from the cytoplasm. 2). V-ATPase; vacuolar ATPase. ClC-5; chloride channel 5 mutated in Dent 1 disease. NHE6; Na+/H+ exchanger 6. TRPML3; mucolipin 3. TPC; two poor channel. Fig. 2. Major classes of transporters in the early endosome; protons can enter endosome via V-ATPase, ClC-5 and NHE6.
15110-15118, ISSN 0021-9258 Scott CC, Gruenberg J. (2010). Ion flux and the function of endosomes and lysosomes: pH is just the start. Bioessays, 33, pp. 103-110, ISSN 0265-9247 Scott JW, Hawley SA, Green KA, Anis M, Stewart G, Scullion GA, Norman DG, Hardie DG. (2004). CBS domains form energy-sensing modules whose binding of adenosine ligands is disrupted by disease mutations. J Clin Invest, 113, pp. 274-284, ISSN 00219738 Smith AJ, Reed AA, Loh NY, Thakker RV, Lippiat JD. (2009). Characterization of Dent’s disease mutations of CLC-5 reveals a correlation between functional and cell biological consequences and protein structure.