التفاصيل البيبلوغرافية
| العنوان: |
SLC26A4-AP-2 mu2 interaction regulates SLC26A4 plasma membrane abundance in the endolymphatic sac. |
| المؤلفون: |
Hyun Jae Lee1, Fenollar-Ferrer, Cristina1,2, Isgrig, Kevin3, Ya-Xian Wang4, Valente, Kerstin1,2, Eide, Juleh1, Keiji Honda5, Chien, Wade W.3,6, Petralia, Ronald S.4, Lijin Dong7, Friedman, Thomas B.2, Bonifacino, Juan S.8, Griffith, Andrew J.1,9, Roux, Isabelle1,2 isabelle.roux@nih.gov |
| المصدر: |
Science Advances. 10/11/2024, Vol. 10 Issue 41, p1-16. 16p. |
| مصطلحات موضوعية: |
*CELL membranes, *ADAPTOR proteins, *INNER ear, *ATOMIC interactions, *MICROVILLI, *COATED vesicles |
| مستخلص: |
Decreased presence or activity of human SLC26A4 at the plasma membrane is a common cause of hearing loss. SLC26A4 (Pendrin) is necessary for normal reabsorption of endolymph, the fluid bathing the inner ear. We identified the μ2 subunit of adaptor protein 2 (AP-2) complex required for clathrin-mediated endocytosis as a protein-partner of SLC26A4 involved in regulating its plasma membrane abundance. We showed that, in the endolymphatic sac, where fluid reabsorption occurs, SLC26A4 is localized along the apical microvilli of mitochondria-rich cells, in contact with the endolymph, and associated with clathrin-coated pits where μ2 and AP-2 are present. Based on SLC26A4 structure, the elements involved in SLC26A4-μ2 interaction were identified and validated experimentally, allowing modeling of this interaction at the atomic level. Pharmacological inhibition of clathrin-mediated endocytosis led to an increased plasma membrane abundance of hemagglutinin-tagged SLC26A4 virally or endogenously expressed in mitochondria-rich cells. These results indicate that the SLC26A4-μ2 interaction regulates SLC26A4 abundance at the apical surface of mitochondria-rich cells. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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