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mab-monoclonal-antibody

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XMetA binds to the INSR at an allosteric site. <em>A</em>: CHO-hINS...
Published: 13 April 2012
FIG. 1. XMetA binds to the INSR at an allosteric site. A: CHO-hINSR cells were incubated with increasing concentrations of either XMetA (■) or isotype control antibody (○) and antibody binding measured by flow cytometry (n = 4). B: Increasing concentrations of CHO-hINSR cells were incubated with 80 pmol/L insulin and either 70 nmol/L XMetA (■) or isotype control antibody (○). Insulin binding to the INSR was determined by KinExA (n = 3). mAb, monoclonal antibody. FIG. 1. XMetA binds to the INSR at an allosteric site. A: CHO-hINSR cells were incubated with increasing concentrations of either XMetA (■) or isotype control antibody (○) and antibody binding measured by flow cytometry (n = 4). B: Increasing concentrations of CHO-hINSR cells were incubated with 80 pmol/L insulin and either 70 nmol/L XMetA (■) or isotype control antibody (○). Insulin binding to the INSR was determined by KinExA (n = 3). mAb, monoclonal antibody. More
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IL-2 pathway–targeted interventions in immunomodulatory therapy. Therapeuti...
Published: 12 December 2011
FIG. 5. IL-2 pathway–targeted interventions in immunomodulatory therapy. Therapeutic agents on the right (shaded green) enhance IL-2 signaling, whereas those on the left (shaded red) are designed to inhibit IL-2 signaling downstream of its receptor. Treatments suggested in this review that have no clinical history in type 1 diabetes therapy are outlined in dashed boxes. mAb, monoclonal antibody. FIG. 5. IL-2 pathway–targeted interventions in immunomodulatory therapy. Therapeutic agents on the right (shaded green) enhance IL-2 signaling, whereas those on the left (shaded red) are designed to inhibit IL-2 signaling downstream of its receptor. Treatments suggested in this review that have no clinical history in type 1 diabetes therapy are outlined in dashed boxes. mAb, monoclonal antibody. More
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XMetA promotes glucose uptake, but not cell growth. <em>A</em>: 3T3...
Published: 13 April 2012
FIG. 4. XMetA promotes glucose uptake, but not cell growth. A: 3T3 cells expressing hINSR were incubated with increasing concentrations of either XMetA (■), isotype control antibody (○), or insulin (▲), and 2-deoxy-d-glucose uptake was measured (n = 5). B: MCF-7 cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and cell proliferation was determined by CellTiter Glo assay (n = 6). C: MCF-7 cells were incubated with either 33 nmol/L XMetA (■) or isotype control antibody (○) with increasing concentrations of insulin. Cell proliferation was then measured (n = 3). mAb, monoclonal antibody. FIG. 4. XMetA promotes glucose uptake, but not cell growth. A: 3T3 cells expressing hINSR were incubated with increasing concentrations of either XMetA (■), isotype control antibody (○), or insulin (▲), and 2-deoxy-d-glucose uptake was measured (n = 5). B: MCF-7 cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and cell proliferation was determined by CellTiter Glo assay (n = 6). C: MCF-7 cells were incubated with either 33 nmol/L XMetA (■) or isotype control antibody (○) with increasing concentrations of insulin. Cell proliferation was then measured (n = 3). mAb, monoclonal antibody. More
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Generation of NOD mice with constitutive expression of the NKG2D ligand RAE...
Published: 13 June 2020
Figure 2 Generation of NOD mice with constitutive expression of the NKG2D ligand RAE1ε in the pancreas. A and B: Schematic of part of the vector used to generate the PCCALL-RAE1ε mice ( 7 ) (A) and breeding schema for generating NOD mice with constitutive RAE1ε expression in the islets (B). Note that rather than RAE1ε, PCCALL and RIP-cre mice have constitutive expression of β-gal or cre recombinase in islets, respectively. C: Flow cytometric analysis of nonimmune cells in the pancreas of RIP-cre or RIP-RAE1ε mice stained with an antibody specific for RAE1 (open histogram) or a control antibody (solid histogram). These data are representative of three independent experiments. D and E: The percentage of CD8+ T cells with detectable NKG2D expression in the pancreas (D) (n = 8) or spleen (E) (n = 6) of RIP-RAE1ε and RIP-cre mice as determined by flow cytometry. *P < 0.01 by Mann-Whitney U test. mAb, monoclonal antibody. Figure 2. Generation of NOD mice with constitutive expression of the NKG2D ligand RAE1ε in the pancreas. A and B: Schematic of part of the vector used to generate the PCCALL-RAE1ε mice (7) (A) and breeding schema for generating NOD mice with constitutive RAE1ε expression in the islets (B). Note that rather than RAE1ε, PCCALL and RIP-cre mice have constitutive expression of β-gal or cre recombinase in islets, respectively. C: Flow cytometric analysis of nonimmune cells in the pancreas of RIP-cre or RIP-RAE1ε mice stained with an antibody specific for RAE1 (open histogram) or a control antibody (solid histogram). These data are representative of three independent experiments. D and E: The percentage of CD8+ T cells with detectable NKG2D expression in the pancreas (D) (n = 8) or spleen (E) (n = 6) of RIP-RAE1ε and RIP-cre mice as determined by flow cytometry. *P < 0.01 by Mann-Whitney U test. mAb, monoclonal antibody. More
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XMetA is a partial agonist of the INSR that selectively activates the PI3K/...
Published: 13 April 2012
FIG. 2. XMetA is a partial agonist of the INSR that selectively activates the PI3K/Akt pathway. A: CHO-hINSR cells were incubated with increasing concentrations of either XMetA (■), isotype control antibody (○), or insulin (▲), and INSR autophosphorylation was measured by ELISA (n = 3). B: CHO-hINSR cells were incubated with either 33 nmol/L XMetA (■) or isotype control antibody (○) with increasing concentrations of insulin. INSR autophosphorylation was then measured (n = 3). C: CHO-hINSR cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and Akt phosphorylation was measured by ELISA (n = 3). D: CHO-hINSR cells were incubated with either 33 nmol/L XMetA (■) or isotype control antibody (○) with increasing concentrations of insulin. Akt phosphorylation was then measured (n = 3). E: CHO-hINSR cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and extracellular signal–related kinase (Erk)1/2 phosphorylation was measured by ELISA (n = 3). mAb, monoclonal antibody. FIG. 2. XMetA is a partial agonist of the INSR that selectively activates the PI3K/Akt pathway. A: CHO-hINSR cells were incubated with increasing concentrations of either XMetA (■), isotype control antibody (○), or insulin (▲), and INSR autophosphorylation was measured by ELISA (n = 3). B: CHO-hINSR cells were incubated with either 33 nmol/L XMetA (■) or isotype control antibody (○) with increasing concentrations of insulin. INSR autophosphorylation was then measured (n = 3). C: CHO-hINSR cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and Akt phosphorylation was measured by ELISA (n = 3). D: CHO-hINSR cells were incubated with either 33 nmol/L XMetA (■) or isotype control antibody (○) with increasing concentrations of insulin. Akt phosphorylation was then measured (n = 3). E: CHO-hINSR cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and extracellular signal–related kinase (Erk)1/2 phosphorylation was measured by ELISA (n = 3). mAb, monoclonal antibody. More
Journal Articles
Journal: Diabetes
Diabetes 1996;45(9):1181–1186
Published: 01 September 1996
... associated antigen (LFA)-l, anti-integrin α4, anti-intercellular adhesion molecule (ICAM)-1, and anti-L-selectin antibodies (monoclonal antibodies [mAbs]) gave rise to a partial or complete prevention of diabetes via different mechanisms of protection. On day 20 posttransfer, diabetes was only observed...
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Macrophage-derived OSM prevents stem cell mobilization. <em>A</em>:...
Published: 24 March 2015
Figure 5 Macrophage-derived OSM prevents stem cell mobilization. A: CXCL12 gene expression by MSCs induced by increasing concentrations of OSM. *P < 0.05 vs. 0. B: OSM protein concentration in M0, M1, and M2 macrophage CM. *P < 0.05 vs. M0. C: OSM gene expression in cultured M0, M1, and M2 macrophages. *P < 0.05 vs. M0. D: OSM gene expression in the BM as a whole at baseline and after treatment with clodronate liposomes in nondiabetic and diabetic mice. *P < 0.05 vs. baseline. E: CXCL12 gene expression by MSCs treated with M0, M1, and M2 CM in the presence or in the absence of an anti-OSM neutralizing antibody (αOSM). mAb, monoclonal antibody. *P < 0.05 vs. M0. LKS cell mobilization in response to G-CSF alone (F) or G-CSF plus a neutralizing anti-OSM antibody (G) in nondiabetic and diabetic mice. *P < 0.05 vs. baseline. Endothelial progenitor cell mobilization in response to G-CSF alone (H) or G-CSF plus a neutralizing anti-OSM antibody (I) in nondiabetic and diabetic mice. *P < 0.05 vs. baseline. J: OSM protein concentration in BM plasma of patients without (n = 6) and with (n = 6) diabetes. *P < 0.05. K: BM-to-PB ratio of CD34+ cells, a surrogate of steady-state SC mobilization, in patients without and with diabetes. *P < 0.05. L: Linear correlation between OSM concentrations and the BM-to-PB CD34+ cell ratio. Figure 5. Macrophage-derived OSM prevents stem cell mobilization. A: CXCL12 gene expression by MSCs induced by increasing concentrations of OSM. *P < 0.05 vs. 0. B: OSM protein concentration in M0, M1, and M2 macrophage CM. *P < 0.05 vs. M0. C: OSM gene expression in cultured M0, M1, and M2 macrophages. *P < 0.05 vs. M0. D: OSM gene expression in the BM as a whole at baseline and after treatment with clodronate liposomes in nondiabetic and diabetic mice. *P < 0.05 vs. baseline. E: CXCL12 gene expression by MSCs treated with M0, M1, and M2 CM in the presence or in the absence of an anti-OSM neutralizing antibody (αOSM). mAb, monoclonal antibody. *P < 0.05 vs. M0. LKS cell mobilization in response to G-CSF alone (F) or G-CSF plus a neutralizing anti-OSM antibody (G) in nondiabetic and diabetic mice. *P < 0.05 vs. baseline. Endothelial progenitor cell mobilization in response to G-CSF alone (H) or G-CSF plus a neutralizing anti-OSM antibody (I) in nondiabetic and diabetic mice. *P < 0.05 vs. baseline. J: OSM protein concentration in BM plasma of patients without (n = 6) and with (n = 6) diabetes. *P < 0.05. K: BM-to-PB ratio of CD34+ cells, a surrogate of steady-state SC mobilization, in patients without and with diabetes. *P < 0.05. L: Linear correlation between OSM concentrations and the BM-to-PB CD34+ cell ratio. More
Images
XMetA improves hyperglycemia and other metabolic markers of disease in diab...
Published: 13 April 2012
FIG. 5. XMetA improves hyperglycemia and other metabolic markers of disease in diabetic mice. A: CHO-mINSR cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and Akt phosphorylation was measured by ELISA (n = 3). B: Fasting blood glucose measurements were obtained weekly for 6 weeks from control mice treated with 10 mg/kg isotype control antibody (○) and diabetic mice treated with either 10 mg/kg XMetA (■) or isotype control antibody (●). C: After 3 weeks of treatment, fasting blood glucose was measured in control mice treated with 10 mg/kg isotype control antibody (white bar), diabetic mice treated with 10 mg/kg isotype control antibody (gray bar), and diabetic mice treated with the indicated doses of XMetA (black bars). D: Nonfasted blood glucose measurements were obtained weekly for 6 weeks from control mice treated with 10 mg/kg isotype control antibody (○) and diabetic mice treated with either 10 mg/kg XMetA (■) or isotype control antibody (●). After 6 weeks of treatment, blood hemoglobin A1c (E) and nonfasted plasma β-hydroxybutyrate (F) were measured in control mice treated with 10 mg/kg isotype control antibody (white bar) and diabetic mice treated with either 10 mg/kg isotype control antibody (gray bar) or XMetA (black bar). Values shown are mean ± SEM. *P < 0.05 for diabetic mice treated with XMetA compared with isotype control; n = 8 mice/group. mAb, monoclonal antibody. FIG. 5. XMetA improves hyperglycemia and other metabolic markers of disease in diabetic mice. A: CHO-mINSR cells were incubated with increasing concentrations of XMetA (■), isotype control antibody (○), or insulin (▲), and Akt phosphorylation was measured by ELISA (n = 3). B: Fasting blood glucose measurements were obtained weekly for 6 weeks from control mice treated with 10 mg/kg isotype control antibody (○) and diabetic mice treated with either 10 mg/kg XMetA (■) or isotype control antibody (●). C: After 3 weeks of treatment, fasting blood glucose was measured in control mice treated with 10 mg/kg isotype control antibody (white bar), diabetic mice treated with 10 mg/kg isotype control antibody (gray bar), and diabetic mice treated with the indicated doses of XMetA (black bars). D: Nonfasted blood glucose measurements were obtained weekly for 6 weeks from control mice treated with 10 mg/kg isotype control antibody (○) and diabetic mice treated with either 10 mg/kg XMetA (■) or isotype control antibody (●). After 6 weeks of treatment, blood hemoglobin A1c (E) and nonfasted plasma β-hydroxybutyrate (F) were measured in control mice treated with 10 mg/kg isotype control antibody (white bar) and diabetic mice treated with either 10 mg/kg isotype control antibody (gray bar) or XMetA (black bar). Values shown are mean ± SEM. *P < 0.05 for diabetic mice treated with XMetA compared with isotype control; n = 8 mice/group. mAb, monoclonal antibody. More
Journal Articles
Journal: Diabetes
Diabetes 2006;55(10):2843–2848
Published: 01 October 2006
... output (HGO) and hyperglycemia. Antagonizing the effects of glucagon is therefore considered an attractive target for treatment of type 2 diabetes. In the current study, effects of eliminating glucagon signaling with a glucagon monoclonal antibody (mAb) were investigated in the diabetic ob/ob...
Journal Articles
Journal: Diabetes
Diabetes 1995;44(8):871–877
Published: 01 August 1995
... of C57BL/KsJ mice, and CD4+, CD8+, or both subsets of cells were transiently depleted with monoclonal antibodies (mAbs). After T-cell repopulation, animals that had received intrathymic islets followed by anti-CD8 mAb (P < 0.05) or both anti-CD4 and anti-CD8 mAbs...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(5):967–974
Published: 01 May 1999
...T G Markees; D V Serreze; N E Phillips; C H Sorli; E J Gordon; L D Shultz; R J Noelle; B A Woda; D L Greiner; J P Mordes; A A Rossini A protocol consisting of a single donor-specific transfusion (DST) plus a brief course of anti-CD154 monoclonal antibody (anti-CD40 ligand mAb) induces permanent...
Journal Articles
Journal: Diabetes
Diabetes 2007;56(8):2103–2109
Published: 01 August 2007
...Hiroki Ishikawa; Hirofumi Ochi; Mei-Ling Chen; Dan Frenkel; Ruth Maron; Howard L. Weiner Anti-CD3 monoclonal antibody (mAb) has been shown to induce tolerance and to be an effective treatment for diabetes both in animal models and in human trials. We have shown that anti-CD3 mAb given orally...
Journal Articles
Journal: Diabetes
Diabetes 1995;44(3):354–359
Published: 01 March 1995
... by preparing Southern blots of T-cell receptor (TCR) β-chain genes amplified by polymerase chain reaction (PCR) from islets from C57BL/KsJ mice given multiple doses of STZ. The relative abundance of TCR gene products in islets was compared with spleen cells stimulated with anti-CD3 monoclonal antibody (mAb...
Journal Articles
Journal: Diabetes
Diabetes 2008;57(5):1293–1301
Published: 01 May 2008
... with a panel of 11 human monoclonal antibodies (mAbs), supplemented by use of recombinant Fab to cross-inhibit reactivity with GAD65 by radioimmunoprecipitation of the same mAbs. RESULTS— The COOH-terminal region on GAD65 was the major autoantigenic site. B-cell epitopes were distributed within two separate...
Journal Articles
Journal: Diabetes
Diabetes 1997;46(3):363–371
Published: 01 March 1997
...Jose A Pinies; Yineng Fu; J A Vazquez; Denise Faustman New cellular-based reagents are needed to diagnose type I diabetes as well as to monitor the outcomes of clinical trials at early time points. Four new monoclonal antibodies (mAbs) have been shown to demonstrate reduced binding to lymphocytes...
Journal Articles
Journal: Diabetes
Diabetes 2012;61(5):1263–1271
Published: 13 April 2012
... cells were incubated with 80 pmol/L insulin and either 70 nmol/L XMetA (■) or isotype control antibody (○). Insulin binding to the INSR was determined by KinExA (n = 3). mAb, monoclonal antibody. FIG. 1. XMetA binds to the INSR at an allosteric site. A: CHO-hINSR cells were incubated...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(2):270–276
Published: 01 February 2001
... diabetes in humans. CD40-CD154 (CD40 ligand) interaction blockade by the use of anti-CD154 monoclonal antibody (mAb) has shown efficacy in preventing allorejection in several models of organ and cell transplantation. Here we report the beneficial effect of the chronic administration of a hamster anti...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(12):3238–3245
Published: 01 December 2006
... and following immune therapy with anti-CD3 monoclonal antibodies (mAbs) or immune regulatory T-cells (Tregs). β-Cell replication increases in pre-diabetic mice, after adoptive transfer of diabetes with increasing islet inflammation but before an increase in blood glucose concentration or a significant decrease...
Journal Articles
Journal: Diabetes
Diabetes 1995;44(7):744–752
Published: 01 July 1995
.... However, immunohistochemical staining under electron microscopy revealed that islet β-cells adjacent to infiltrating lymphocytes were clearly stained by an anti-ICAM-1 monoclonal antibody (mAb). Flow cytometric analysis showed that the ICAM-1 expression on NOD islet cells and NOD-derived insulinoma cells...
Journal Articles
Journal: Diabetes
Diabetes 2002;51(2):265–270
Published: 01 February 2002
... immunosuppression regimen (rapamycin and anti–IL-2R monoclonal antibody [mAb]) or the base immunosuppression and LEA29Y. Animals receiving the LEA29Y/rapamycin/anti–IL-2R regimen (n = 5) had significantly prolonged islet allograft survival (204, 190, 216, 56, and >220 days). In contrast, those animals...