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Journal articles on the topic 'ICA512/IA-2'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Torkko, Juha M., M. Evangelina Primo, Ronald Dirkx, Anne Friedrich, Antje Viehrig, Elisa Vergari, Barbara Borgonovo, et al. "Stability of proICA512/IA-2 and Its Targeting to Insulin Secretory Granules Require β4-Sheet-Mediated Dimerization of Its Ectodomain in the Endoplasmic Reticulum." Molecular and Cellular Biology 35, no. 6 (January 5, 2015): 914–27. http://dx.doi.org/10.1128/mcb.00994-14.

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The type 1 diabetes autoantigen ICA512/IA-2/RPTPN is a receptor protein tyrosine phosphatase of the insulin secretory granules (SGs) which regulates the size of granule stores, possibly via cleavage/signaling of its cytosolic tail. The role of its extracellular region remains unknown. Structural studies indicated that β2- or β4-strands in the mature ectodomain (ME ICA512) form dimers in vitro . Here we show that ME ICA512 prompts proICA512 dimerization in the endoplasmic reticulum. Perturbation of ME ICA512 β2-strand N-glycosylation upon S508A replacement allows for proICA512 dimerization, O -glycosylation, targeting to granules, and conversion, which are instead precluded upon G553D replacement in the ME ICA512 β4-strand. S508A/G553D and N506A/G553D double mutants dimerize but remain in the endoplasmic reticulum. Removal of the N-terminal fragment (ICA512-NTF) preceding ME ICA512 allows an ICA512-ΔNTF G553D mutant to exit the endoplasmic reticulum, and ICA512-ΔNTF is constitutively delivered to the cell surface. The signal for SG sorting is located within the NTF RESP18 homology domain (RESP18-HD), whereas soluble NTF is retained in the endoplasmic reticulum. Hence, we propose that the ME ICA512 β2-strand fosters proICA512 dimerization until NTF prevents N506 glycosylation. Removal of this constraint allows for proICA512 β4-strand-induced dimerization, exit from the endoplasmic reticulum, O -glycosylation, and RESP18-HD-mediated targeting to granules.

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2

Trajkovski, Mirko, Hassan Mziaut, Anke Altkrüger, Joke Ouwendijk, Klaus-Peter Knoch, Stefan Müller, and Michele Solimena. "Nuclear translocation of an ICA512 cytosolic fragment couples granule exocytosis and insulin expression in β-cells." Journal of Cell Biology 167, no. 6 (December 13, 2004): 1063–74. http://dx.doi.org/10.1083/jcb.200408172.

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Islet cell autoantigen 512 (ICA512)/IA-2 is a receptor tyrosine phosphatase-like protein associated with the insulin secretory granules (SGs) of pancreatic β-cells. Here, we show that exocytosis of SGs and insertion of ICA512 in the plasma membrane promotes the Ca2+-dependent cleavage of ICA512 cytoplasmic domain by μ-calpain. This cleavage occurs at the plasma membrane and generates an ICA512 cytosolic fragment that is targeted to the nucleus, where it binds the E3-SUMO ligase protein inhibitor of activated signal transducer and activator of transcription-y (PIASy) and up-regulates insulin expression. Accordingly, this novel pathway directly links regulated exocytosis of SGs and control of gene expression in β-cells, whose impaired insulin production and secretion causes diabetes.

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3

Myers, M. A., M. R. Laks, S. J. Feeney, T. E. Mandel, M. Koulmanda, A. Bone, J. Barley, M. J. Rowley, and I. R. Mackay. "Antibodies to ICA512/IA-2 in Rodent Models of IDDM." Journal of Autoimmunity 11, no. 3 (June 1998): 265–72. http://dx.doi.org/10.1006/jaut.1998.0192.

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4

Kawasaki, Eiji, Liping Yu, Roberto Gianani, Charles F. Verge, Sunanda Babu, Ezio Bonifacio, and George S. Eisenbarth. "Evaluation of Islet Cell Antigen (ICA) 512/IA-2 Autoantibody Radioassays Using Overlapping ICA512/IA-2 Constructs1." Journal of Clinical Endocrinology & Metabolism 82, no. 2 (February 1997): 375–80. http://dx.doi.org/10.1210/jcem.82.2.3723.

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5

Kawasaki, E. "Evaluation of Islet Cell Antigen (ICA) 512/IA-2 Autoantibody Radioassays Using Overlapping ICA512/IA-2 Constructs." Journal of Clinical Endocrinology & Metabolism 82, no. 2 (February 1, 1997): 375–80. http://dx.doi.org/10.1210/jc.82.2.375.

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6

Sosa, Laura, Juha M. Torkko, María E. Primo, Ramiro E. Llovera, Pamela L. Toledo, Antonella S. Rios, F. Luis Gonzalez Flecha, et al. "Biochemical, biophysical, and functional properties of ICA512/IA-2 RESP18 homology domain." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1864, no. 5 (May 2016): 511–22. http://dx.doi.org/10.1016/j.bbapap.2016.01.013.

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7

Miao, Dongmei, Liping Yu, Claudio Tiberti, David D. Cuthbertson, Marian Rewers, Umberto di Mario, George S. Eisenbarth, and Francesco Dotta. "ICA512(IA-2) Epitope Specific Assays Distinguish Transient from Diabetes Associated Autoantibodies." Journal of Autoimmunity 18, no. 2 (March 2002): 191–96. http://dx.doi.org/10.1006/jaut.2001.0577.

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8

Eisenbarth, George S., and Joy Jeffrey. "The natural history of type 1A diabetes." Arquivos Brasileiros de Endocrinologia & Metabologia 52, no. 2 (March 2008): 146–55. http://dx.doi.org/10.1590/s0004-27302008000200002.

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We can now predict the development of Type 1A (Immune Mediated) diabetes primarily through the determination of four biochemically characterized islet autoantibodies [insulin, GAD65, IA-2 (ICA512) and (Znt8)]. Prediction is possible because beta-cell destruction is chronically progressive and very slow in most, but not all individuals. We can also prevent type 1A diabetes in animal models and a major goal is the prevention of type 1A diabetes in man with multiple clinical trials underway.

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9

Cunningham, JL, ET Janson, B. Eriksson, K. Oberg, and AE Gobl. "Transmembrane protein tyrosine phosphatase IA-2 (ICA512) is expressed in human midgut carcinoids but is not detectable in normal enterochromaffin cells." Journal of Endocrinology 164, no. 3 (March 1, 2000): 315–22. http://dx.doi.org/10.1677/joe.0.1640315.

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A potential upregulation of receptor type protein tyrosine phosphatase IA-2 (ICA512) expression was detected by differential display and investigated in midgut carcinoid tumours. Normal intestine tissue and tumour tissue from 13 midgut carcinoid patients were studied by in situ hybridisation using an IA-2 ribonucleotide probe and confocal microscopy using specific IA-2 antibodies. Previously, it had been shown that IA-2 is located in the secretory granules of virtually all neuroendocrine cells. However, we found that IA-2 was not detectable in resting normal enterochromaffin (EC) cells of the small intestine, while high expression of IA-2 mRNA and protein was confirmed in both primary and metastatic carcinoid tissue. This difference in expression was not observed with chromogranin A or serotonin, two secretory granule hormones known to be expressed in EC cells, indicating that IA-2 was seemingly not necessary for the basal production and packaging of these hormones. When comparing patients receiving biotherapy before operation with untreated patients, we found expression of IA-2 to be lower in tumours from patients that had been treated with a combination of alpha-interferon and the somatostatin analogue, octreotide. There was no correlation between IA-2 expression and proliferation rates as measured by immunohistochemistry with antibodies against the Ki 67 antigen. Furthermore, we show that IA-2 is co-localised with serotonin in carcinoid tumours as well as in the pancreatic tumour cell line, BON1, which is interesting as serotonin secretion rate is presumably higher in tumour cells than in resting EC cells. Taken together, these findings may indicate a role for IA-2 in the later stages of the regulated secretory process.

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10

Yokota, I., J. Matsuda, E. Naito, M. Ito, K. Shima, and Y. Kuroda. "Comparison of GAD and ICA512/IA-2 Antibodies at and After the Onset of IDDM." Diabetes Care 21, no. 1 (January 1, 1998): 49–52. http://dx.doi.org/10.2337/diacare.21.1.49.

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11

Park, Y. S., E. Kawasaki, K. Kelemen, L. Yu, M. R. Schiller, M. Rewers, M. Mizuta, G. S. Eisenbarth, and J. C. Hutton. "Humoral autoreactivity to an alternatively spliced variant of ICA512/IA-2 in Type I diabetes." Diabetologia 43, no. 10 (October 2, 2000): 1293–301. http://dx.doi.org/10.1007/s001250051525.

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12

Robert, S., K. Van Huynegem, C. Gysemans, C. Mathieu, P. Rottiers, and L. Steidler. "Trimming of two major type 1 diabetes driving antigens, GAD65 and IA-2, allows for successful expression in Lactococcus lactis." Beneficial Microbes 6, no. 4 (August 2015): 591–601. http://dx.doi.org/10.3920/bm2014.0083.

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Type 1 diabetes (T1D) is a chronic autoimmune disease characterised by excessive immune reactions against auto-antigens of pancreatic β-cells. Restoring auto-antigen tolerance remains the superior therapeutic strategy. Oral auto-antigen administration uses the tolerogenic nature of the gut-associated immune system to induce antigen-specific tolerance. However, due to gastric degradation, proper mucosal product delivery often imposes a challenge. Recombinant Lactococcus lactis have proven to be effective and safe carriers for gastrointestinal delivery of therapeutic products: L. lactis secreting diabetes-associated auto-antigens in combination with interleukin (IL)-10 have demonstrated therapeutic efficacy in a well-defined mouse model for T1D. Here, we describe the construction of recombinant L. lactis secreting the 65 kDa isoform of glutamic acid decarboxylase (GAD65) and tyrosine phosphatase-like protein ICA512 (IA-2), two major T1D-related auto-antigens. Attempts to secrete full size human GAD65 and IA-2 protein by L. lactis were unsuccessful. Trimming of GAD65 and IA-2 was investigated to optimise antigen secretion while maintaining sufficient bacterial growth. GAD65370-575 and IA-2635-979 showed to be efficiently secreted by recombinant L. lactis. Antigen secretion was verified by immunoblotting. Plasmid-derived GAD65 and IA-2 expression was combined in single strains with human IL-10 expression, a desired combination to allow tolerance induction. This study reports the generation of recombinant L. lactis secreting two major diabetes-related auto-antigens: human GAD65 and IA-2, by themselves or combined with the anti-inflammatory cytokine human IL-10. Prohibitive sequence obstacles hampering antigen secretion were resolved by trimming the full size proteins.

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13

Bergert, Hendrik, Klaus-Peter Knoch, Ronny Meisterfeld, Melanie Jäger, Joke Ouwendijk, Stephan Kersting, Hans Detlev Saeger, and Michele Solimena. "Effect of Oxygenated Perfluorocarbons on Isolated Rat Pancreatic Islets in Culture." Cell Transplantation 14, no. 7 (August 2005): 441–48. http://dx.doi.org/10.3727/000000005783982873.

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One impediment for a wider application of islet transplantation is the limited number of donor pancreata for islet isolation. A more efficient utilization of available organs could in part alleviate this problem. Perfluorocarbons (PFCs) have a high oxygen solubility coefficient and maintain high oxygen partial pressures for extended time. They serve also as oxygen “reservoirs” for harvested organs in pancreas organ transplantation. The aim of this study was to test whether the use of PFCs could also be beneficial for the secretory activity and overall viability of cultured purified islets before transplantation. Purified rat islets were cultured in static conditions with or without oxygen-saturated PFCs for 1 or 7 days. Cell death and apoptosis were assessed by trypan blue staining, DNA strand breaks, and caspase 3/7 activity. mRNA levels of insulin and ICA512/IA-2, a membrane marker of secretory granules (SGs), were quantitated by real-time PCR, whereas insulin content and secretion were measured by RIA. Polypyrimidine tract binding protein (PTB), which promotes SG biogenesis, was assessed by Western blotting. The number of SGs and the ultrastructural appearance of β-cells were analyzed by cryoimmunoelectronmicroscopy for insulin. Various parameters, including caspase activity, insulin and ICA512/IA-2 mRNA levels, PTB expression, number of secretory granules, and ultrastructural appearance did not significantly differ between control and PFC-cultured islets. On the other hand, PFC culture islets showed significantly increased DNA fragmentation and a reduced insulin stimulation index at both time points compared to control islets. While advantageous for the transport of human harvested organs, the use of PFH in the culture may be comparable to and/or not provide advantage over conventional protocols for culture of islets for transplantation.

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14

Kawasaki, E., G. S. Eisenbarth, C. Wasmeier, and J. C. Hutton. "Autoantibodies to Protein Tyrosine Phosphatase-Like Proteins In Type I Diabetes: Overlapping Specificities To Phogrin And ICA512/IA-2." Diabetes 45, no. 10 (October 1, 1996): 1344–49. http://dx.doi.org/10.2337/diab.45.10.1344.

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15

Kawasaki, E., G. S. Eisenbarth, C. Wasmeier, and J. C. Hutton. "Autoantibodies to protein tyrosine phosphatase-like proteins in type I diabetes. Overlapping specificities to phogrin and ICA512/IA-2." Diabetes 45, no. 10 (October 1, 1996): 1344–49. http://dx.doi.org/10.2337/diabetes.45.10.1344.

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16

Fernando, Roshini, Andrew Vonberg, Stephen J. Atkins, Susan Pietropaolo, Massimo Pietropaolo, and Terry J. Smith. "Human Fibrocytes Express Multiple Antigens Associated With Autoimmune Endocrine Diseases." Journal of Clinical Endocrinology & Metabolism 99, no. 5 (May 1, 2014): E796—E803. http://dx.doi.org/10.1210/jc.2013-3072.

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Context: Factors common to multiple autoimmune diseases have been sought vigorously. Graves' disease (GD) and type 1 diabetes mellitus (T1DM) involve end-organ remodeling. Fibrocytes participate in inflammatory diseases and were recently shown to express thyroid-specific proteins such as the thyrotropin receptor and thyroglobulin. Objective: The objective of the study was to determine whether a broader repertoire of autoantigen expression, such as proteins associated with T1DM, can be ascribed to fibrocytes. Design, Setting, and Participants: Fibrocytes and fibroblasts were collected and analyzed from healthy individuals and those with autoimmune diseases in an academic clinical practice. Main Outcome Measures: Real-time PCR, Western blot analysis, gene promoter analysis, cell transfections, and flow cytometric cell sorting were performed. Results: Islet cell antigen ICA512 (IA-2) and islet cell autoantigen of 69 kDa (ICA69), two islet-specific proteins implicated in T1DM, are expressed by fibrocytes from healthy donors and those with T1DM, GD, and multiple sclerosis. Both transcripts are detected by PCR, the proteins are resolved on Western blots, and both gene promoters are active in fibrocytes. Levels of ICA69 are substantially higher than those of IA-2 in fibrocytes. ICA69 localizes to CD34+ GD orbital fibroblasts putatively derived from fibrocytes, whereas higher levels of IA-2 are found in CD34− fibroblasts. Conclusions: In addition to autoantigens implicated in thyroid autoimmunity, fibrocytes and derivative fibroblasts express multiple autoantigens associated with T1DM. This expression results from active gene promoters and abundant steady-state mRNA encoding ICA69 and IA-2. These latest findings demonstrate that fibrocytes express antigens relevant to multiple forms of endocrine autoimmunity. They suggest the potential for these cells playing a direct role in immune reactivity directed at the thyroid and pancreatic islets.

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17

Eisenbarth, George S. "Etiology of Organ-Specific Autoimmunity: Basic Research and Clinical Implications in IBD." Canadian Journal of Gastroenterology 10, no. 2 (1996): 121–25. http://dx.doi.org/10.1155/1996/909212.

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Autoimmunity develops in the setting of genetic susceptibility and can be monogenic (eg, autoimmune polyendocrine syndrome type I with Addison’s disease, mucocutaneous candidiasis and hypoparathyroidism, which is autosomal recessive with the causative gene on the tip of chromosome 21) or polygenic (usually with important alleles within the major histocompatibility complex [eg, type I diabetes]). In addition to genetic susceptibility, many autoimmune disorders can be classified into etiological categories (oncogenic, drug-induced, diet-induced, infectious or idiopathic). For most autoimmune disorders there are multiple target autoantigens and, for type I diabetes, a combinatorial approach (eg, expression of at least two autoantibodies of insulin, glutamic acid decarboxylase and/or ICA512/IA-2) is the best predictor of diabetes risk. Finally, antigen-specific therapies hold promise for the prevention and therapy of autoimmunity, eg, parenteral or oral therapy with insulin delays or prevents type I diabetes in animal models, and a small pilot trial of parenteral insulin in humans suggests that such therapy may similarly prevent diabetes in humans.

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18

Papakonstantinou, Theo, Mark A. Myers, Jennifer Jois, Xavier Roucou, Mark Prescott, Merill J. Rowley, and Ian R. Mackay. "Expression of Protein Tyrosine Phosphatase-like Molecule ICA512/IA-2 Induces Growth Arrest in Yeast Cells and Transfected Mammalian Cell Lines." Journal of Autoimmunity 17, no. 1 (August 2001): 51–61. http://dx.doi.org/10.1006/jaut.2001.0516.

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19

Acevedo-Calado, Maria, Eddie A. James, Michael P. Morran, Susan L. Pietropaolo, Qin Ouyang, David Arribas-Layton, Marco Songini, et al. "Identification of Unique Antigenic Determinants in the Amino Terminus of IA-2 (ICA512) in Childhood and Adult Autoimmune Diabetes: New Biomarker Development." Diabetes Care 40, no. 4 (February 7, 2017): 561–68. http://dx.doi.org/10.2337/dc16-1527.

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20

Pietropaolo, Massimo, Mark Peakman, Susan L. Pietropaolo, Maria M. Zanone, Thomas P. Foley Jr, Dorothy J. Becker, and Massimo Trucco. "Combined Analysis of GAD65 and ICA512(IA-2) Autoantibodies in Organ and Non-organ-specific Autoimmune Diseases Confers High Specificity for Insulin-dependent Diabetes Mellitus." Journal of Autoimmunity 11, no. 1 (February 1998): 1–10. http://dx.doi.org/10.1006/jaut.1997.0170.

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21

Zanone, M. M., E. Catalfamo, S. L. Pietropaolo, I. Rabbone, C. Sacchetti, F. Cerutti, M. Trucco, and P. Cavallo-Perin. "Glutamic acid decarboxylase and ICA512/IA-2 autoantibodies as disease markers and relationship to residual β-cell function and glycemic control in young type 1 diabetic patients." Metabolism 52, no. 1 (January 2003): 25–29. http://dx.doi.org/10.1053/meta.2003.50003.

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22

Payton, M. A., C. J. Hawkes, and M. R. Christie. "Relationship of the 37,000- and 40,000-M(r) tryptic fragments of islet antigens in insulin-dependent diabetes to the protein tyrosine phosphatase-like molecule IA-2 (ICA512)." Journal of Clinical Investigation 96, no. 3 (September 1, 1995): 1506–11. http://dx.doi.org/10.1172/jci118188.

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