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21دورية أكاديمية
المؤلفون: Jiang, C., Kawabe, H., Rotin, D.
المصدر: The Journal of Biological Chemistry
وصف الملف: application/pdf
العلاقة: http://hdl.handle.net/11858/00-001M-0000-002D-709F-4Test; http://hdl.handle.net/11858/00-001M-0000-002D-70A1Test-D
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22دورية أكاديمية
المؤلفون: Hsia, H., Kumar, R, Luca, R, Takeda, M, Courchet, J, Nakashima, J, Wu, S, Goebbels, S, An, W, Eickholt, Bj, Polleux, F, Rotin, D, Wu, H, Rossner, Mj, BAGNI, CLAUDIA, Rhee, J., Brose, N, Kawabe, H.
المساهمون: Hsia, H, Kumar, R, Luca, R, Takeda, M, Courchet, J, Nakashima, J, Wu, S, Goebbels, S, An, W, Eickholt, B, Polleux, F, Rotin, D, Wu, H, Rossner, M, Bagni, C, Rhee, J, Brose, N, Kawabe, H
مصطلحات موضوعية: Animal, Axon, Cerebral Cortex, Endosomal Sorting Complexes Required for Transport, Hippocampu, Mice, Knockout, Models, Biological, Morphogenesi, Multiprotein Complexe, Neurite, PTEN Phosphohydrolase, Phosphatidylinositol 3-Kinase, Polyubiquitin, Protein Biosynthesi, TOR Serine-Threonine Kinase, Ubiquitin-Protein Ligase, Ubiquitination, Signal Transduction, Settore BIO/13 - BIOLOGIA APPLICATA
الوصف: Protein ubiquitination is a core regulatory determinant of neural development. Previous studies have indicated that the Nedd4-family E3 ubiquitin ligases Nedd4-1 and Nedd4-2 may ubiquitinate phosphatase and tensin homolog (PTEN) and thereby regulate axonal growth in neurons. Using conditional knockout mice, we show here that Nedd4-1 and Nedd4-2 are indeed required for axonal growth in murine central nervous system neurons. However, in contrast to previously published data, we demonstrate that PTEN is not a substrate of Nedd4-1 and Nedd4-2, and that aberrant PTEN ubiquitination is not involved in the impaired axon growth upon deletion of Nedd4-1 and Nedd4-2. Rather, PTEN limits Nedd4-1 protein levels by modulating the activity of mTORC1, a protein complex that controls protein synthesis and cell growth. Our data demonstrate that Nedd4-family E3 ligases promote axonal growth and branching in the developing mammalian brain, where PTEN is not a relevant substrate. Instead, PTEN controls neurite growth by regulating Nedd4-1 expression.
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/25157163; volume:111; issue:36; firstpage:13205; lastpage:13210; numberofpages:6; journal:PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA; http://hdl.handle.net/2108/244785Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84906968893
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23دورية أكاديمية
المؤلفون: VECCHIONE, ANDREA, MARCHESE A, HENRY P, ROTIN D, MORRIONE A.
المساهمون: Vecchione, Andrea, Marchese, A, Henry, P, Rotin, D, Morrione, A.
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/12697834; info:eu-repo/semantics/altIdentifier/wos/WOS:000182325500029; volume:23; firstpage:3363; lastpage:3372; journal:MOLECULAR AND CELLULAR BIOLOGY; http://hdl.handle.net/11573/125670Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-0345381737; http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=000182325500029&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=0c7ff228ccbaaa74236f48834a34396aTest; http://www.scopus.com/inward/record.url?eid=2-s2.0-0345381737&partnerID=65&md5=c3979af7aeaa8666bbd307fdebc69677Test
الإتاحة: https://doi.org/10.1128/MCB.23.9.3363-3372.2003Test
http://hdl.handle.net/11573/125670Test
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=000182325500029&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=0c7ff228ccbaaa74236f48834a34396aTest
http://www.scopus.com/inward/record.url?eid=2-s2.0-0345381737&partnerID=65&md5=c3979af7aeaa8666bbd307fdebc69677Test -
24دورية أكاديمية
المؤلفون: Kimura, T., Kawabe, H., Jiang, C., Zhang, W., Xiang, Y., Lu, C., Salter, M., Brose, N., Lu, W., Rotin, D.
المصدر: Proceedings of the National Academy of Sciences of the USA
وصف الملف: application/pdf
العلاقة: http://hdl.handle.net/11858/00-001M-0000-002A-369B-1Test; http://hdl.handle.net/11858/00-001M-0000-002A-369D-ETest; http://hdl.handle.net/11858/00-001M-0000-002A-369E-CTest
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25دورية أكاديمية
المؤلفون: Zelenkov, P., Shevelev, I., Potapov, A., Golbin, D., Konovalov, N., Saveljeva, T., Nazarenko, A., Kuszel, Y., Rotin, D., Kuzmin, S., Loshenov, V., Grachev, P.
المصدر: Photodiagnosis and Photodynamic Therapy ; volume 8, issue 2, page 163 ; ISSN 1572-1000
مصطلحات موضوعية: Pharmacology (medical), Dermatology, Oncology, Biophysics
الإتاحة: https://doi.org/10.1016/j.pdpdt.2011.03.133Test
https://api.elsevier.com/content/article/PII:S1572100011001591?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1572100011001591?httpAccept=text/plainTest -
26كتاب
المؤلفون: Staub, O, Plant, P, Ishikawa, T, Schild, L, Rotin, D
المصدر: Amiloride-sensitive sodium channels, Physiology and functional diversity, Current Topics in Membranes, pp. 65-87
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27دورية أكاديمية
المؤلفون: Robert, R, Carlile, GW, Liao, J, Balghi, H, Lesimple, P, Liu, Ningqing, Kus, B, Rotin, D, Wilke, Martina, de Jonge, Hugo, Scholte, Bob, Thomas, DY, Hanrahan, JW
المصدر: Robert , R , Carlile , GW , Liao , J , Balghi , H , Lesimple , P , Liu , N , Kus , B , Rotin , D , Wilke , M , de Jonge , H , Scholte , B , Thomas , DY & Hanrahan , JW 2010 , ' Correction of the Delta Phe508 Cystic Fibrosis Transmembrane Conductance Regulator Trafficking Defect by the Bioavailable Compound Glafenine ' , Molecular Pharmacology , vol. 77 , no. 6 , pp. 922-930 . https://doi.org/10.1124/mol.109.062679Test
الوصف: Cystic fibrosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, which encodes a cAMP-activated anion channel expressed in epithelial cells. The most common mutation Delta Phe508 leads to protein misfolding, retention by the endoplasmic reticulum, and degradation. One promising therapeutic approach is to identify drugs that have been developed for other indications but that also correct the CFTR trafficking defect, thereby exploiting their known safety and bioavailability in humans and reducing the time required for clinical development. We have screened approved, marketed, and off-patent drugs with known safety and bioavailability using a Delta Phe508-CFTR trafficking assay. Among the confirmed hits was glafenine, an anthranilic acid derivative with analgesic properties. Its ability to correct the misprocessing of CFTR was confirmed by in vitro and in vivo studies using a concentration that is achieved clinically in plasma (10 mu M). Glafenine increased the surface expression of Delta Phe508-CFTR in baby hamster kidney (BHK) cells to similar to 40% of that observed for wild-type CFTR, comparable with the known CFTR corrector 4-cyclohexyloxy-2-{1-[4-(4-methoxybenzensulfonyl)-piperazin-1-yl]-ethyl} -quinazoline (VRT-325). Partial correction was confirmed by the appearance of mature CFTR in Western blots and by two assays of halide permeability in unpolarized BHK and human embryonic kidney cells. Incubating polarized CFBE41o(-) monolayers and intestines isolated from Delta Phe508-CFTR mice (treated ex vivo) with glafenine increased the short-circuit current (I-sc) response to forskolin + genistein, and this effect was abolished by 10 mu M CFTRinh 172. In vivo treatment with glafenine also partially restored total salivary secretion. We conclude that the discovery of glafenine as a CFTR corrector validates the approach of investigating existing drugs for the treatment of CF, although localized delivery or further medicinal chemistry may be needed to reduce side effects.
الإتاحة: https://doi.org/10.1124/mol.109.062679Test
https://pure.eur.nl/en/publications/d83290f0-b0c8-4175-9ce9-6da88e4d1025Test
http://hdl.handle.net/1765/27413Test -
28دورية أكاديمية
المؤلفون: Fouladkou, F., Lu, C., Jiang, C., Zhou, L., She, Y., Walls, J., Kawabe, H., Brose, N., Henkelman, R., Huang, A., Bruneau, B., Rotin, D.
المصدر: Journal of Biological Chemistry
وصف الملف: application/pdf
العلاقة: http://hdl.handle.net/11858/00-001M-0000-002A-3276-6Test; http://hdl.handle.net/11858/00-001M-0000-002A-3278-2Test
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29
المصدر: Frontiers In Physiology, vol. 3, pp. 212
مصطلحات موضوعية: urogenital system, macromolecular substances, respiratory system
الوصف: Nedd4-2 is a ubiquitin ligase previously demonstrated to regulate endocytosis and lysosomal degradation of the epithelial Na(+) channel (ENaC) and other ion channels and transporters. Recent studies using Nedd4-2 knockout mice specifically in kidney or lung epithelia has revealed a critical role for this E3 ubiquitin ligase in regulating salt and fluid transport in these tissues/organs and in maintaining homeostasis of body blood pressure. Interestingly, the primary targets for Nedd4-2 may differ in these two organs: in the lung Nedd4-2 targets ENaC, and loss of Nedd4-2 leads to excessive ENaC function and to cystic fibrosis - like lung disease, whereas in the kidney, Nedd4-2 targets the Na(+)/Cl(-) cotransporter (NCC) in addition to targeting ENaC. In accord, loss of Nedd4-2 in the distal nephron leads to increased NCC abundance and function. The aldosterone-responsive kinase, Sgk1, appears to be involved in the regulation of NCC by Nedd4-2 in the kidney, similar to its regulation of ENaC. Collectively, these new findings underscore the physiological importance of Nedd4-2 in regulating epithelial salt and fluid transport and balance.
وصف الملف: application/pdf
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=od______1900::5fa208d3c29d9c63c41f1fb212102bc6Test
https://serval.unil.ch/notice/serval:BIB_CBB290F20218Test -
30دورية أكاديمية
مصطلحات موضوعية: Animals, Humans, Ubiquitin-Protein Ligases, Guanine Nucleotide Exchange Factors, Protein Isoforms, Ubiquitin, Signal Transduction, Protein Conformation, Models, Molecular, Ubiquitination, Endosomal Sorting Complexes Required for Transport, Nedd4 Ubiquitin Protein Ligases
الوصف: The ubiquitylation of proteins is carried out by E1, E2 and E3 (ubiquitin ligase) enzymes, and targets them for degradation or for other cellular fates. The HECT enzymes, including Nedd4 family members, are a major group of E3 enzymes that dictate the specificity of ubiquitylation. In addition to ubiquitylating proteins for degradation by the 26S proteasome, HECT E3 enzymes regulate the trafficking of many receptors, channels, transporters and viral proteins. The physiological functions of the yeast HECT E3 ligase Rsp5 are the best known, but the functions of HECT E3 enyzmes in metazoans are now becoming clearer from in vivo studies. ; Daniela Rotin & Sharad Kumar
العلاقة: ARC; Nature Reviews Molecular Cell Biology, 2009; 10(6):398-409; http://hdl.handle.net/2440/55019Test; Kumar, S. [0000-0001-7126-9814]
