insulinoma/protease

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[Effects of various HIV protease inhibitors on function of rat insulinoma cells].

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OBJECTIVE To investigate the effects of various HIV protease inhibitors on the function of pancreatic beta-cells. METHODS Rat insulinoma INS-1 cells were incubated with different concentrations of ritonavir or amprenavir for 48 h and stimulated with 20 mmol/L D-glucose for 30 min. The rate of

Berberine induces cell apoptosis through cytochrome C/apoptotic protease-activating factor 1/caspase-3 and apoptosis inducing factor pathway in mouse insulinoma cells.

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OBJECTIVE To investigate apoptotic effects of berberine, a significant alkaloids component existing in Rhizoma coptidis, and its possible acting mechanism in insulinoma cells. METHODS Different concentrations of berberine were used to treat mouse insulinoma (MIN6) cells for various period of time.

Identification of a human insulinoma cDNA encoding a novel mammalian protein structurally related to the yeast dibasic processing protease Kex2.

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We have identified a human insulinoma cDNA (PC2) that encodes a protein homologous to the precursor processing Kex2 endoprotease of yeast by using a polymerase chain reaction to detect and amplify conserved sequences within the catalytic site. The 638-residue amino acid sequence of PC2 begins with a

Insulin degradation in insulinoma: evidence for the occurrence of an inactive form of glutathione-insulin transhydrogenase and for the absence of insulin A and B chains degrading protease(s).

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Cathepsin B-related proteases in the insulin secretory granule.

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The distribution of proteases potentially reactive with peptide sequences containing pairs of basic amino acids or single basic amino acids was studied in subcellular fractions of a transplantable rat insulinoma using the affinity probes 125I-Tyr-Ala-Lys- ArgCH2Cl and 125I-Tyr-Ala-norleucine-

[Impairment of IRS-2 signaling in rat insulinoma INS-1 cells by nelfinavir].

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OBJECTIVE To investigate whether HIV-1 protease inhibitor nelfinavir alters the insulin stimulated phosphorylation of insulin signaling parameters in rat insulinoma INS-1 cells. METHODS INS-1 cells were incubated with nelfinavir for 48 h and stimulated with 100 nmol/L insulin for 2 min.

A novel form of gastric inhibitory polypeptide (GIP) isolated from bovine intestine using a radioreceptor assay. Fragmentation with staphylococcal protease results in GIP1-3 and GIP4-42, fragmentation with enterokinase in GIP1-16 and GIP17-42.

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A novel form of gastric inhibitory polypeptide (GIP), later also referred to as glucose-dependent insulinotropic polypeptide, has been isolated from bovine upper intestine. The purification was monitored by a recently developed radioreceptor assay, specific for GIP, using membrane preparations from

Isolation of two complementary deoxyribonucleic acid clones from a rat insulinoma cell line based on similarities to Kex2 and furin sequences and the specific localization of each transcript to endocrine and neuroendocrine tissues in rats.

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We have identified two rat insulinoma cDNAs that code for proteins homologous to the Kex2 dibasic protease of yeast and the mammalian furin gene product. A 5.0-kilobase (kb) cDNA, termed BDP, coding for a 752-amino acid protein and a 2.5-kb cDNA coding for a 636-amino acid protein, which was found

Serpin peptidase inhibitor clade A member 1 as a potential marker for malignancy in insulinomas.

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OBJECTIVE The biological behavior of insulinomas cannot be predicted based on histopathologic criteria in which the diagnosis of malignancy is confirmed by the presence of metastases. In this study, microarray and quantitative real-time reverse transcription-PCR were applied to identify

Differential expression of genes encoding proteins of the HGF/MET system in insulinomas.

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BACKGROUND Insulinomas are the most common functional pancreatic neuroendocrine tumors, whereas histopathological features do not predict their biological behaviour. In an attempt to better understand the molecular processes involved in the tumorigenesis of islet beta cells, the present study

Serine protease inhibitor Kazal type 1 and epidermal growth factor receptor are expressed in pancreatic tubular adenocarcinoma, intraductal papillary mucinous neoplasm, and pancreatic intraepithelial neoplasia.

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BACKGROUND Serine protease inhibitor Kazal type 1 (SPINK1) is expressed in normal human pancreatic acinar cells and in a variety of tumors, and binds to the epidermal growth factor receptor (EGFR), mediating cell proliferation through the mitogen-activated protein kinase cascade in pancreatic cancer

IL-1beta induces serine protease inhibitor 3 (SPI-3) gene expression in rat pancreatic beta-cells. Detection by differential display of messenger RNA.

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Immune-mediated beta-cell damage induces diverse intracellular signals, leading to transcription of different genes which may either contribute to beta-cell repair and/or defence or lead to cell death. The cytokine interleukin-1beta (IL-1) is a potential mediator of beta-cell dysfunction and damage

Serine protease inhibitor 8 is a novel immunohistochemical marker for neuroendocrine tumors of the pancreas.

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OBJECTIVE The intracellular serine protease inhibitor 8 (SERPINB8) is expressed by squamous epithelium, monocytes, and a subset of neuroendocrine cells. Using immunohistochemistry, we now have further investigated the expression of SERPINB8 in normal neuroendocrine cells and its potential use as a

The processing of receptor-bound [125I-Tyr11]somatostatin by RINm5F insulinoma cells.

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The peptide somatostatin (SRIF) is secreted by delta cells of the endocrine pancreas and inhibits the secretion of insulin from pancreatic beta cells. We have previously shown that [125I-Tyr11]SRIF binds to specific, high affinity receptors on RINm5F insulinoma cells and that these receptors mediate

Protease inhibitors used in the treatment of HIV+ induce beta-cell apoptosis via the mitochondrial pathway and compromise insulin secretion.

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Inclusion of HIV protease inhibitors (PIs) in the treatment of people living with HIV+ has markedly decreased mortality but also increased the incidence of metabolic abnormalities, causes of which are not well understood. Here, we report that insulinopenia is exacerbated when Zucker fa/fa rats are

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