Search Results - "ONAY, TUNCER"

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    Cellular crosstalk regulates the aqueous humor outflow pathway and provides new targets for glaucoma therapies by Thomson, Benjamin R., Liu, Pan, Onay, Tuncer, Du, Jing, Tompson, Stuart W., Misener, Sol, Purohit, Raj R., Young, Terri L., Jin, Jing, Quaggin, Susan E.

    Published in Nature communications (18-10-2021)
    “…Primary congenital glaucoma (PCG) is a severe disease characterized by developmental defects in the trabecular meshwork (TM) and Schlemm’s canal (SC),…”
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    Journal Article
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    Inhibition of MTOR Disrupts Autophagic Flux in Podocytes by CINA, Davide P, ONAY, Tuncer, PALTOO, Aarti, CHENGJIN LI, MAEZAWA, Yoshiro, DE ARTEAGA, Javier, JURISICOVA, Andrea, QUAGGIN, Susan E

    “…Inhibitors of the mammalian target of rapamycin (MTOR) belong to a family of drugs with potent immunosuppressive, antiangiogenic, and antiproliferative…”
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    Duplication of GTF2I Results in Separation Anxiety in Mice and Humans by Mervis, Carolyn B., Dida, Joana, Lam, Emily, Crawford-Zelli, Nicole A., Young, Edwin J., Henderson, Danielle R., Onay, Tuncer, Morris, Colleen A., Woodruff-Borden, Janet, Yeomans, John, Osborne, Lucy R.

    Published in American journal of human genetics (08-06-2012)
    “…Duplication (dup7q11.23) and deletion (Williams syndrome) of chromosomal region 7q11.23 cause neurodevelopmental disorders with contrasting anxiety phenotypes…”
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    Ectopic Notch Activation in Developing Podocytes Causes Glomerulosclerosis by WATERS, Aoife M, WU, Megan Y. J, ONAY, Tuncer, SCUTARU, Jacob, JU LIU, LOBE, Corrinne G, QUAGGIN, Susan E, PISCIONE, Tino D

    “…Genetic evidence supports an early role for Notch signaling in the fate of podocytes during glomerular development. Decreased expression of Notch…”
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    Genetic Deletion of Emp2 Does Not Cause Proteinuric Kidney Disease in Mice by Donnan, Michael D, Scott, Rizaldy P, Onay, Tuncer, Tarjus, Antoine, Onay, Ummiye Venus, Quaggin, Susan E

    Published in Frontiers in medicine (27-08-2019)
    “…Nephrotic syndrome is one of the most common glomerular diseases in children and can be classified on the basis of steroid responsiveness. While multiple…”
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    MTOR regulates autophagic flux in the glomerulus by Cinà, Davide P., Onay, Tuncer, Paltoo, Aarti, Li, Chengjin, Maezawa, Yoshiro, De Arteaga, Javier, Jurisicova, Andrea, Quaggin, Susan E.

    Published in Autophagy (01-04-2012)
    “…Sirolimus (rapamycin), an inhibitor of the mechanistic target of rapamycin (MTOR), was originally proposed as an immunosuppressant to prevent rejection of…”
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    Endothelial Tyrosine Kinase Tie1 Is Required for Normal Schlemm’s Canal Development—Brief Report by Du, Jing, Thomson, Benjamin R., Onay, Tuncer, Quaggin, Susan E.

    “…Schlemm's canal (SC) is a large vessel residing in the iridocorneal angle and is required to regulate aqueous humor outflow. Normal SC structure and function…”
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    Glaucoma-Protective Human Single-Nucleotide Polymorphism in the Angpt2 Locus Increased ANGPT2 Expression and Schlemm Canal Area in Mice-Brief Report by Kiyota, Naoki, Onay, Tuncer, Leeaw, Phoebe, Liu, Pan, Deb, Dilip K, Thomson, Benjamin R, Segrè, Ayellet V, Wiggs, Janey L, Quaggin, Susan E

    “…The ANGPT (angiopoietin)-TEK (tyrosine kinase, endothelial) vascular signaling pathway plays a key role in the formation of Schlemm canal, and loss-of-function…”
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    A lymphatic defect causes ocular hypertension and glaucoma in mice by Thomson, Benjamin R, Heinen, Stefan, Jeansson, Marie, Ghosh, Asish K, Fatima, Anees, Sung, Hoon-Ki, Onay, Tuncer, Chen, Hui, Yamaguchi, Shinji, Economides, Aris N, Flenniken, Ann, Gale, Nicholas W, Hong, Young-Kwon, Fawzi, Amani, Liu, Xiaorong, Kume, Tsutomu, Quaggin, Susan E

    Published in The Journal of clinical investigation (01-10-2014)
    “…Glaucoma is a leading cause of blindness, afflicting more than 60 million people worldwide. Increased intraocular pressure (IOP) due to impaired aqueous humor…”
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    Primary cilia TRP channel regulates hippocampal excitability by Vien, Thuy N, Ta, My C, Kimura, Louise F, Onay, Tuncer, DeCaen, Paul G

    “…Polycystins (PKD2, PKD2L1, and PKD2L2) are members of the transient receptor potential family, which form ciliary ion channels. Most notably, PKD2…”
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