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Human Polyclonal IDO1 Primary Antibody pour ICC, FACS - ABIN1169196
Boasso, Herbeuval, Hardy, Anderson, Dolan, Fuchs, Shearer: HIV inhibits CD4+ T-cell proliferation by inducing indoleamine 2,3-dioxygenase in plasmacytoid dendritic cells. dans Blood 2007
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Mouse (Murine) Polyclonal IDO1 Primary Antibody pour ICC, IHC - ABIN1169195
Yadav, Burudi, Alirezaei, Flynn, Watry, Lanigan, Fox: IFN-gamma-induced IDO and WRS expression in microglia is differentially regulated by IL-4. dans Glia 2007
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Human Monoclonal IDO1 Primary Antibody pour FACS - ABIN4896116
Kaltenmeier, Gawanbacht, Beyer, Lindner, Trzaska, van der Merwe, Härter, Grüner, Fabricius, Lotfi, Schwarz, Schütz, Hönig, Schulz, Kern, Bommer, Schrezenmeier, Kirchhoff, Jahrsdörfer: CD4+ T cell-derived IL-21 and deprivation of CD40 signaling favor the in vivo development of granzyme B-expressing regulatory B cells in HIV patients. dans Journal of immunology (Baltimore, Md. : 1950) 2015
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Human Monoclonal IDO1 Primary Antibody pour FACS - ABIN4896118
Lood, Tydén, Gullstrand, Klint, Wenglén, Nielsen, Heegaard, Jönsen, Kahn, Bengtsson: Type I interferon-mediated skewing of the serotonin synthesis is associated with severe disease in systemic lupus erythematosus. dans PLoS ONE 2015
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Human Polyclonal IDO1 Primary Antibody pour IF (cc), IF (p) - ABIN1714836
Fu, Zhang, Song, Sheng, Li, Li, Song, Wang, Chu, Wei: Effect of bone marrow-derived CD11b(+)F4/80 (+) immature dendritic cells on the balance between pro-inflammatory and anti-inflammatory cytokines in DBA/1 mice with collagen-induced arthritis. dans Inflammation research : official journal of the European Histamine Research Society ... [et al.] 2014
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Human Monoclonal IDO1 Primary Antibody pour FACS - ABIN4896114
Chimal-Ramírez, Espinoza-Sánchez, Chávez-Sánchez, Arriaga-Pizano, Fuentes-Pananá: Monocyte Differentiation towards Protumor Activity Does Not Correlate with M1 or M2 Phenotypes. dans Journal of immunology research 2016
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Rat (Rattus) Polyclonal IDO1 Primary Antibody pour FACS, IHC (p) - ABIN2192173
Hill, Pereira, Chauveau, Zagani, Remy, Tesson, Mazal, Ubillos, Brion, Asghar, Ashgar, Mashreghi, Kotsch, Moffett, Doebis, Seifert, Boczkowski, Osinaga, Anegon: Heme oxygenase-1 inhibits rat and human breast cancer cell proliferation: mutual cross inhibition with indoleamine 2,3-dioxygenase. dans FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2005
Mouse (Murine) Monoclonal IDO1 Primary Antibody pour FACS, IP - ABIN1043733
Mellor, Munn: IDO expression by dendritic cells: tolerance and tryptophan catabolism. dans Nature reviews. Immunology 2004
Human Polyclonal IDO1 Primary Antibody pour IHC (p), WB - ABIN389194
Maghzal, Thomas, Hunt, Stocker: Cytochrome b5, not superoxide anion radical, is a major reductant of indoleamine 2,3-dioxygenase in human cells. dans The Journal of biological chemistry 2008
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Differential expression of CD25 (Montrer IL2RA Anticorps) and IDO mRNA with high and low virulence bovine viral diarrhea virus might reflect temporal differences in transcription during the immune response elicited by these viral strains.
IDO may be involved in downregulating immune responses to M. avium subsp. paratuberculosis and other virulent mycobacteria, which may be an example of the pathogen harnessing host immunoregulatory pathways to aid survival.
INDO participates in IFN-gama-induced death of bovine luteal cells, through a mechanism that involves degradation of tryptophan, thereby reducing tryptophan concentrations to a point insufficient to meet luteal cells needs
SIV-infected macaques exhibiting progression to AIDS displayed greater expression of TGF-beta (Montrer TGFB1 Anticorps) and indoleamine 2,3 dioxygenase in CD8 (Montrer CD8A Anticorps)+ T cells from mesentric lymph nodes.
High coexpression of cytoplasmic IDO1/COX2 (Montrer COX2 Anticorps) was found to be an independent predictor of poor outcome in colorectal cancer patients.
Report the crystal structures of IDO1 in complex with its substrate, Trp (Montrer TBPL1 Anticorps), an inhibitor, epacadostat, and/or an effector, indole ethanol (IDE (Montrer IDE Anticorps)). The data reveal structural features of the active site (Sa) critical for substrate activation; in addition, they disclose a new inhibitor-binding mode and a distinct small molecule binding site (Si).
IDO decreased glycolysis and glutaminolysis by activating GCN2K, resulting in activation of AMPactivated protein kinase.
Data suggest that IDO1 is constitutively expressed in insulin (Montrer INS Anticorps)-secreting cells from donors without diabetes; IDO1 appears to be down-regulated in insulin (Montrer INS Anticorps)-containing beta-cells from double autoantibody-positive donors and donors with recent-onset type 1 diabetes; this study was conducted on donor tissues obtained from cadavers.
Twenty-nine percent (n = 2/7) of the PD-L1 (Montrer CD274 Anticorps) positive poorly differentiated thyroid carcinomas also co-expressed IDO1
In non-ST segment elevation myocardial infarction, the tolerogenic mechanism of the immune response related to IDO production by activated monocytes derived dendritic cells is altered, supporting their role in T-cell dysregulation.
These data suggest that the expression of immunosuppressive molecules, including PD-1 (Montrer PDCD1 Anticorps) ligands and IDO1, by macrophage/microglia may be involved in immune evasion of lymphoma cells.
Our data demonstrate that high intratumoral IDO1 mRNA levels correlate with a poor glioblastoma (GBM) patient prognosis. It also confirms the positive correlation between increased GBM IDO1 levels and human-infiltrating T cells
Among the 89 patients, CD274 (Montrer CD274 Anticorps), LAG3 (Montrer LAG3 Anticorps), and IDO1 expressions in TIICs were observed in 68.6% (61 cases), 13.5% (12), and 28.1% (25) of patients, respectively. CD274 (Montrer CD274 Anticorps), CTLA4 (Montrer CTLA4 Anticorps), and IDO1 were expressed in tumor cells of 24.7% (22 cases), 4.5% (4), and 72.0% (64) of patients, respectively.
Multivariate analysis indicated indoleamine 2,3-dioxygenase (IDO) expression as independent prognostic factors in overall survival (OS).
The treatment of Salmonella enterica serovar choleraesuis or resveratrol in murine melanoma cells demonstrated the ability of reducing IDO1 production through upregulating Cx43 (Montrer GJA1 Anticorps).
Study showed that the knockout of IDO prevented vascular smooth muscle cells apoptosis in AngII -treated Ldlr (Montrer LDLR Anticorps)-/- mice fed with HFD, suggesting a detrimental role of IDO in abdominal aortic aneurysm formation.
The KYNurenine pathway of IDO1-mediated Tryptophan metabolism plays a critical role in depressive symptoms associated with IFN-alpha therapy.
IDO is a critical regulator of acute pulmonary inflammation .
Data suggest that Indoleamine 2,3-dioxygenase 1 (IDO1) appears to be a potential hallmark of liver lesions, and its deficiency protects mice from CCl4 (Montrer CCL4 Anticorps)-induced fibrosis mediated by Th17 cells down-regulation and tryptophan 2,3-dioxygenase (TDO (Montrer TDO2 Anticorps)) compensatory increase.
Findings suggest non-redundant neurophysiological roles for indoleamine 2,3-dioxygenase 1, indoleamine 2,3-dioxygenase 2 (Montrer IDO2 Anticorps) and tryptophan 2,3-dioxygenase (Montrer TDO2 Anticorps) in modulating brain activities and metabolism.
These results show IDO is upregulated with RSV infection and this upregulation likely participates with IFN-gamma (Montrer IFNG Anticorps) in inhibition of virus replication and suppression of some host cell responses to infection.
Lipopolysaccharide (LPS (Montrer TLR4 Anticorps)) stimulation increased the expression and activity of the immunoregulatory enzyme IDO1 in hepatic stellate cells (HSCs), and LPS (Montrer TLR4 Anticorps)/HSCs stimulated aryl hydrocarbon receptor (AhR (Montrer AHR Anticorps)) signaling in cocultured regulatory T cells.
this study shows that the presence of IFN-alpha at antigen sensitization activates an IDO1/TGF-beta (Montrer TGFB1 Anticorps)-dependent anti-inflammatory program that upon antigenic rechallenge prevents inflammation via plasmacytoid dendritic cells
Across strains, networks depicted a predominance of genes under-expressed in microglia relative to macrophages that may be a precursor for the different response of both cell types to challenges. The detected transcriptome differences enhance the understanding of the role of IDO1 in the microglia transcriptome under unchallenged conditions.
This gene encodes indoleamine 2,3-dioxygenase (IDO) - a heme enzyme that catalyzes the first and rate-limiting step in tryptophan catabolism to N-formyl-kynurenine. This enzyme acts on multiple tryptophan substrates including D-tryptophan, L-tryptophan, 5-hydroxy-tryptophan, tryptamine, and serotonin. This enzyme is thought to play a role in a variety of pathophysiological processes such as antimicrobial and antitumor defense, neuropathology, immunoregulation, and antioxidant activity. Through its expression in dendritic cells, monocytes, and macrophages this enzyme modulates T-cell behavior by its peri-cellular catabolization of the essential amino acid tryptophan.
indoleamine-pyrrole 2,3 dioxygenase
, indoleamine 2,3-dioxygenase 2
, putative indoleamine 2,3-dioxygenase
, indoleamine 2,3-dioxygenase 1
, indolamine 2,3 dioxygenase
, indole 2,3-dioxygenase
, indoleamine-pyrrole 2,3-dioxygenase
, indoleamine 23-dioxygenase