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2. Preferential cleavage of des-31,32-proinsulin over intact proinsulin by the insulin secretory granule type II endopeptidase. Implication of a favored route for prohormone processing. Rhodes CJ, Lincoln B, Shoelson SE. J Biol Chem; 1992 Nov 15; 267(32):22719-27. PubMed ID: 1429623 [Abstract] [Full Text] [Related]
3. Predicted structural alterations in proinsulin during its interactions with prohormone convertases. Lipkind G, Steiner DF. Biochemistry; 1999 Jan 19; 38(3):890-6. PubMed ID: 9893983 [Abstract] [Full Text] [Related]
5. Biochemical and clinical implications of proinsulin conversion intermediates. Given BD, Cohen RM, Shoelson SE, Frank BH, Rubenstein AH, Tager HS. J Clin Invest; 1985 Oct 19; 76(4):1398-405. PubMed ID: 3902891 [Abstract] [Full Text] [Related]
6. What beta-cell defect could lead to hyperproinsulinemia in NIDDM? Some clues from recent advances made in understanding the proinsulin-processing mechanism. Rhodes CJ, Alarcón C. Diabetes; 1994 Apr 19; 43(4):511-7. PubMed ID: 8138054 [Abstract] [Full Text] [Related]
7. Processing of proinsulin by furin, PC2, and PC3 in (co) transfected COS (monkey kidney) cells. Vollenweider F, Kaufmann J, Irminger JC, Halban PA. Diabetes; 1995 Sep 19; 44(9):1075-80. PubMed ID: 7657031 [Abstract] [Full Text] [Related]
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18. Processing of mutated proinsulin with tetrabasic cleavage sites to mature insulin reflects the expression of furin in nonendocrine cell lines. Yanagita M, Hoshino H, Nakayama K, Takeuchi T. Endocrinology; 1993 Aug 05; 133(2):639-44. PubMed ID: 8344203 [Abstract] [Full Text] [Related]