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Items: 1 to 20 of 84

1.

Proinsulin maturation, misfolding, and proteotoxicity.

Liu M, Hodish I, Rhodes CJ, Arvan P.

Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15841-6.

2.

Misfolded proinsulin affects bystander proinsulin in neonatal diabetes.

Hodish I, Liu M, Rajpal G, Larkin D, Holz RW, Adams A, Liu L, Arvan P.

J Biol Chem. 2010 Jan 1;285(1):685-94. doi: 10.1074/jbc.M109.038042.

3.

In vivo misfolding of proinsulin below the threshold of frank diabetes.

Hodish I, Absood A, Liu L, Liu M, Haataja L, Larkin D, Al-Khafaji A, Zaki A, Arvan P.

Diabetes. 2011 Aug;60(8):2092-101. doi: 10.2337/db10-1671.

4.

Dominant negative pathogenesis by mutant proinsulin in the Akita diabetic mouse.

Izumi T, Yokota-Hashimoto H, Zhao S, Wang J, Halban PA, Takeuchi T.

Diabetes. 2003 Feb;52(2):409-16.

5.

Endoplasmic reticulum stress response in an INS-1 pancreatic beta-cell line with inducible expression of a folding-deficient proinsulin.

Hartley T, Siva M, Lai E, Teodoro T, Zhang L, Volchuk A.

BMC Cell Biol. 2010 Jul 26;11:59. doi: 10.1186/1471-2121-11-59.

6.

Proinsulin intermolecular interactions during secretory trafficking in pancreatic β cells.

Haataja L, Snapp E, Wright J, Liu M, Hardy AB, Wheeler MB, Markwardt ML, Rizzo M, Arvan P.

J Biol Chem. 2013 Jan 18;288(3):1896-906. doi: 10.1074/jbc.M112.420018.

7.

Proinsulin misfolding and endoplasmic reticulum stress during the development and progression of diabetes.

Sun J, Cui J, He Q, Chen Z, Arvan P, Liu M.

Mol Aspects Med. 2015 Apr;42:105-18. doi: 10.1016/j.mam.2015.01.001. Review.

8.

Insulin gene mutations resulting in early-onset diabetes: marked differences in clinical presentation, metabolic status, and pathogenic effect through endoplasmic reticulum retention.

Meur G, Simon A, Harun N, Virally M, Dechaume A, Bonnefond A, Fetita S, Tarasov AI, Guillausseau PJ, Boesgaard TW, Pedersen O, Hansen T, Polak M, Gautier JF, Froguel P, Rutter GA, Vaxillaire M.

Diabetes. 2010 Mar;59(3):653-61. doi: 10.2337/db09-1091.

9.

Proinsulin disulfide maturation and misfolding in the endoplasmic reticulum.

Liu M, Li Y, Cavener D, Arvan P.

J Biol Chem. 2005 Apr 8;280(14):13209-12.

10.

Role of clathrin in the regulated secretory pathway of pancreatic beta-cells.

Molinete M, Dupuis S, Brodsky FM, Halban PA.

J Cell Sci. 2001 Aug;114(Pt 16):3059-66.

11.

Insulin targeting to the regulated secretory pathway after fusion with green fluorescent protein and firefly luciferase.

Pouli AE, Kennedy HJ, Schofield JG, Rutter GA.

Biochem J. 1998 Apr 15;331 ( Pt 2):669-75.

13.

INS-gene mutations: from genetics and beta cell biology to clinical disease.

Liu M, Sun J, Cui J, Chen W, Guo H, Barbetti F, Arvan P.

Mol Aspects Med. 2015 Apr;42:3-18. doi: 10.1016/j.mam.2014.12.001. Review.

14.

Imaging secretory vesicles by fluorescent protein insertion in propeptide rather than mature secreted peptide.

Watkins S, Geng X, Li L, Papworth G, Robbins PD, Drain P.

Traffic. 2002 Jul;3(7):461-71.

15.

Proinsulin misfolding and diabetes: mutant INS gene-induced diabetes of youth.

Liu M, Hodish I, Haataja L, Lara-Lemus R, Rajpal G, Wright J, Arvan P.

Trends Endocrinol Metab. 2010 Nov;21(11):652-9. doi: 10.1016/j.tem.2010.07.001. Review.

16.

Diabetes mellitus due to the toxic misfolding of proinsulin variants.

Weiss MA.

FEBS Lett. 2013 Jun 27;587(13):1942-50. doi: 10.1016/j.febslet.2013.04.044. Review.

17.

Proinsulin maturation disorder is a contributor to the defect of subsequent conversion to insulin in β-cells.

Wang J, Osei K.

Biochem Biophys Res Commun. 2011 Jul 22;411(1):150-5. doi: 10.1016/j.bbrc.2011.06.119.

PMID:
21723250
18.

Proinsulin atypical maturation and disposal induces extensive defects in mouse Ins2+/Akita β-cells.

Yuan Q, Tang W, Zhang X, Hinson JA, Liu C, Osei K, Wang J.

PLoS One. 2012;7(4):e35098. doi: 10.1371/journal.pone.0035098.

19.

Stimulation of autophagy improves endoplasmic reticulum stress-induced diabetes.

Bachar-Wikstrom E, Wikstrom JD, Ariav Y, Tirosh B, Kaiser N, Cerasi E, Leibowitz G.

Diabetes. 2013 Apr;62(4):1227-37. doi: 10.2337/db12-1474.

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