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| - artículu científicu espublizáu en 2002 (ast)
- vědecký článek publikovaný v roce 2002 (cs)
- مقالة علمية (نشرت في يونيو 2002) (ar)
- наукова стаття, опублікована в червні 2002 (uk)
- 2002 թուականի Յունիսին հրատարակուած գիտական յօդուած (hyw)
- 2002 թվականի հունիսին հրատարակված գիտական հոդված (hy)
- vedecký článok (publikovaný 2002/06/01) (sk)
- wetenschappelijk artikel (gepubliceerd op 2002/06/01) (nl)
- im Juni 2002 veröffentlichter wissenschaftlicher Artikel (de)
- scientific journal article (en)
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| author name string
| - Min Zhu
- Abner Louis Notkins
- Jingping Xie
- Atsutaka Kubosaki
- Keiichi Saeki
- Michael S. Lan
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| - Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (en)
- Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (nl)
- Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (ast)
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| skos:prefLabel
| - Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (en)
- Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (nl)
- Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (ast)
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| name
| - Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (en)
- Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (nl)
- Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (ast)
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| title
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| title
| - Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion (en)
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| DOI
| - 10.2337/DIABETES.51.6.1842
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| is cites work
of | - MicroRNA 144 impairs insulin signaling by inhibiting the expression of insulin receptor substrate 1 in type 2 diabetes mellitus
- Structural genomics of protein phosphatases
- Mitochondrial dysfunction and oxidative stress mediate the physiological impairment induced by the disruption of autophagy
- The IA-2 interactome
- Sorting nexin 19 regulates the number of dense core vesicles in pancreatic β-cells
- Disturbances in the secretion of neurotransmitters in IA-2/IA-2beta null mice: changes in behavior, learning and lifespan
- The dense core transmembrane vesicle protein IA-2 is a regulator of vesicle number and insulin secretion
- IA-2 modulates dopamine secretion in PC12 cells
- Deletion of the secretory vesicle proteins IA-2 and IA-2beta disrupts circadian rhythms of cardiovascular and physical activity.
- Overexpression of the autoantigen IA-2 puts beta cells into a pre-apoptotic state: autoantigen-induced, but non-autoimmune-mediated, tissue destruction.
- Loss of the transcriptional repressor PAG-3/Gfi-1 results in enhanced neurosecretion that is dependent on the dense-core vesicle membrane protein IDA-1/IA-2.
- Insulinoma-Associated Protein IA-2, a Vesicle Transmembrane Protein, Genetically Interacts with UNC-31/CAPS and Affects Neurosecretion in Caenorhabditis elegans.
- Deconstructing pancreas developmental biology
- ICA512 signaling enhances pancreatic beta-cell proliferation by regulating cyclins D through STATs
- Deletion of Ia-2 and/or Ia-2β in mice decreases insulin secretion by reducing the number of dense core vesicles
- Mechanisms of dense core vesicle recapture following "kiss and run" ("cavicapture") exocytosis in insulin-secreting cells
- A novel strategy for the development of selective active-site inhibitors of the protein tyrosine phosphatase-like proteins islet-cell antigen 512 (IA-2) and phogrin (IA-2beta).
- An extended tyrosine-targeting motif for endocytosis and recycling of the dense-core vesicle membrane protein phogrin
- Nuclear translocation of an ICA512 cytosolic fragment couples granule exocytosis and insulin expression in {beta}-cells
- Synergy of glucose and growth hormone signalling in islet cells through ICA512 and STAT5
- Co-regulation of intragenic microRNA miR-153 and its host gene Ia-2 β: identification of miR-153 target genes with functions related to IA-2β in pancreas and brain
- Relationship between increased relative birthweight and infections during pregnancy in children with a high-risk diabetes HLA genotype.
- Diabetes-associated HLA genotypes affect birthweight in the general population
- Immunologic and genetic factors in type 1 diabetes
- A transcription factor map as revealed by a genome-wide gene expression analysis of whole-blood mRNA transcriptome in multiple sclerosis
- Protein tyrosine phosphatases: functional inferences from mouse models and human diseases.
- Neonatal β cell development in mice and humans is regulated by calcineurin/NFAT
- IA-2beta, but not IA-2, is induced by ghrelin and inhibits glucose-stimulated insulin secretion
- Regulation of insulin granule turnover in pancreatic beta-cells by cleaved ICA512.
- Islet autoantigens: structure, function, localization, and regulation
- IA-2 is not required for the development of diabetes in NOD mice
- Receptor type protein tyrosine phosphatases (RPTPs) - roles in signal transduction and human disease
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