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Showing 1-15 of 15 results for "SAB4200691" within Papers
Covalent histone modifications underlie the developmental regulation of insulin gene transcription in pancreatic beta cells
Swarup K Chakrabarti
The Journal of Biological Chemistry (2003)
Proinsulin misfolding and diabetes: mutant INS gene-induced diabetes of youth
Trends in Endocrinology and Metabolism, 21 (2010)
Cedric S Asensio
Methods in molecular biology (Clifton, N.J.), 2473, 23-28 (2022-07-13)
The retention using selective hook (RUSH) system enables us to synchronize and visualize the movement of cargoes along the secretory pathway. A fluorescently tagged cargo of interest is retained in the endoplasmic reticulum and released in a biotin-dependent manner. Here
Tao Liang et al.
JCI insight, 5(3) (2020-02-14)
SNAP23 is the ubiquitous SNAP25 isoform that mediates secretion in non-neuronal cells, similar to SNAP25 in neurons. However, some secretory cells like pancreatic islet β cells contain an abundance of both SNAP25 and SNAP23, where SNAP23 is believed to play
Inhibition of Insulin-Degrading Enzyme Does Not Increase Islet Amyloid Deposition in Vitro
Meghan F
Endocrinology (2016)
Role of insulin resistance in human disease
G M Reaven
Diabetes, 37 (1988)
Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis
Intza Garin
Proceedings of the National Academy of Sciences of the USA, 107 (2010)
Blake H Hummer et al.
Molecular biology of the cell, 31(3), 157-166 (2019-12-12)
Regulated secretion of neuropeptides and peptide hormones by secretory granules (SGs) is central to physiology. Formation of SGs occurs at the trans-Golgi network (TGN) where their soluble cargo aggregates to form a dense core, but the mechanisms controlling the sorting
Meghan F Hogan et al.
Endocrinology, 157(9), 3462-3468 (2016-07-13)
Islet amyloid deposition in human type 2 diabetes results in β-cell loss. These amyloid deposits contain the unique amyloidogenic peptide human islet amyloid polypeptide (hIAPP), which is also a known substrate of the protease insulin-degrading enzyme (IDE). Whereas IDE inhibition
Insulin production by human embryonic stem cells
S Assady
Diabetes, 50 (2001)
Zhen Zhang et al.
Journal of diabetes research, 2019, 2583047-2583047 (2019-04-20)
Recent studies showed that alpha cells, especially immature cells and proalpha cells, might be the precursors of beta cells. Exposure to glucagon-like peptide 1 (GLP1) can ameliorate hyperglycemia in diabetic mice and restore the beta cell mass. In the present
Cristina M Fernández-Díaz et al.
American journal of physiology. Endocrinology and metabolism, 317(5), E805-E819 (2019-09-04)
Inhibition of insulin-degrading enzyme (IDE) has been proposed as a possible therapeutic target for type 2 diabetes treatment. However, many aspects of IDE's role in glucose homeostasis need to be clarified. In light of this, new preclinical models are required
Mutant INS-gene induced diabetes of youth: proinsulin cysteine residues impose dominant-negative inhibition on wild-type proinsulin transport
Ming Liu
PLoS ONE, 5(5) (2010)
Jeffrey Viviano et al.
PloS one, 15(5), e0233502-e0233502 (2020-05-21)
The environment within the Endoplasmic Reticulum (ER) influences Insulin biogenesis. In particular, ER stress may contribute to the development of Type 2 Diabetes (T2D) and Cystic Fibrosis Related Diabetes (CFRD), where evidence of impaired Insulin processing, including elevated secreted Proinsulin/Insulin
Insulin: understanding its action in health and disease
P Sonksen
British Journal of Anaesthesia, 85 (2000)
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