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Pesquisa : D12.776.543.750.705.852.420.320.750 [Categoria DeCS]
Referências encontradas : 271 [refinar]
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  1 / 271 MEDLINE  
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PMID:29307521
Autor:Han W; Ni Q; Liu K; Yao Y; Zhao D; Liu X; Chen Y
Endereço:Department of Laboratory Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; Key Laboratory of Clinical In Vitro Diagnostic Techniques of Zhejiang Province, 79 Qingchun Road, Hangzhou 310003, China.
Título:Decreased CD122 on CD56 NK associated with its impairment in asymptomatic chronic HBV carriers with high levels of HBV DNA, HBsAg and HBeAg.
Fonte:Life Sci; 195:53-60, 2018 Feb 15.
ISSN:1879-0631
País de publicação:Netherlands
Idioma:eng
Resumo:AIMS: NK cells play important roles in inhibiting HBV replication and preventing HBV infection. However, NK-cell dysfunction has not been fully studied in asymptomatic chronic HBV carriers (ASC). This study aims to assess decreased expression of CD122 associated with impaired NK cells and the restoration of NK cells with IL-2 and IL-15 stimulation. MAIN METHODS: The experiments were performed by flow cytometer, cytotoxicity assay, ELISA and western blotting. KEY FINDINGS: The reduced CD122 on CD56 NK cells and CD56 NK cells is associated with high levels of HBV DNA, HBsAg or HBeAg in ASCs, in which CD56 NK-cell impairment is observed. Moreover, decreased IFN-γ and degranulation and low cytotoxicity by CD56 NK cells after CD122 blockade were revealed. IL-2 and/or IL-15 can restore impaired CD56 NK cells, together with increased p-STAT5, which can be reversed by CD122 blockade. Additionally, IL-2 or IL-15 can enhance IFN-α2-activated CD56 NK-cell immune responses via up-regulating interferon alpha and beta receptor subunit 2 (IFNAR2). SIGNIFICANCE: Down-regulated CD122 on CD56 NK cell in ASCs with massive viral antigens and high viremia is associated with its impairment, which can be restored by IL-2 and/or IL-15, or combined with IFN-α2.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (CD56 Antigen); 0 (DNA, Viral); 0 (Hepatitis B Surface Antigens); 0 (Hepatitis B e Antigens); 0 (IFNAR2 protein, human); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Interleukin-2 Receptor beta Subunit); 0 (STAT5 Transcription Factor); 156986-95-7 (Receptor, Interferon alpha-beta); 82115-62-6 (Interferon-gamma)


  2 / 271 MEDLINE  
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PMID:28855314
Autor:Muschaweckh A; Petermann F; Korn T
Endereço:Klinikum Rechts der Isar, Neurologische Klinik, Technische Universität München, 81675 Munich, Germany; and.
Título:IL-1ß and IL-23 Promote Extrathymic Commitment of CD27 CD122 γδ T Cells to γδT17 Cells.
Fonte:J Immunol; 199(8):2668-2679, 2017 Oct 15.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:γδT17 cells are a subset of γδ T cells committed to IL-17 production and are characterized by the expression of IL-23R and CCR6 and lack of CD27 expression. γδT17 cells are believed to arise within a narrow time window during prenatal thymic development. In agreement with this concept, we show in this study that adult recipient mice of (IL-23R reporter) bone marrow selectively lack IL-23R γδT17 cells. Despite their absence in secondary lymphoid tissues during homeostasis, γδT17 cells emerge in bone marrow chimeric mice upon induction of skin inflammation by topical treatment with imiquimod cream (Aldara). We demonstrate that IL-1ß and IL-23 together are able to promote the development of bona fide γδT17 cells from peripheral CD122 IL-23R γδ T cells, whereas CD122 γδ T cells fail to convert into γδT17 cells and remain stable IFN-γ producers (γδT1 cells). IL-23 is instrumental in expanding extrathymically generated γδT17 cells. In particular, TCR-Vγ4 chain-expressing CD122 IL-23R γδ T cells are induced to express IL-23R and IL-17 outside the thymus during skin inflammation. In contrast, TCR-Vγ1 γδ T cells largely resist this process because prior TCR engagement in the thymus has initiated their commitment to the γδT1 lineage. In summary, our data reveal that the peripheral pool of γδ T cells retains a considerable degree of plasticity because it harbors "naive" precursors, which can be induced to produce IL-17 and replenish peripheral niches that are usually occupied by thymus-derived γδT17 cells.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Aminoquinolines); 0 (Interleukin-17); 0 (Interleukin-1beta); 0 (Interleukin-2 Receptor beta Subunit); 0 (Interleukin-23); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-23 receptor, mouse); P1QW714R7M (imiquimod)


  3 / 271 MEDLINE  
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PMID:28678791
Autor:Charych D; Khalili S; Dixit V; Kirk P; Chang T; Langowski J; Rubas W; Doberstein SK; Eldon M; Hoch U; Zalevsky J
Endereço:Nektar Therapeutics, San Francisco, California, United States of America.
Título:Modeling the receptor pharmacology, pharmacokinetics, and pharmacodynamics of NKTR-214, a kinetically-controlled interleukin-2 (IL2) receptor agonist for cancer immunotherapy.
Fonte:PLoS One; 12(7):e0179431, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:Cytokines are potent immune modulating agents but are not ideal medicines in their natural form due to their short half-life and pleiotropic systemic effects. NKTR-214 is a clinical-stage biologic that comprises interleukin-2 (IL2) protein bound by multiple releasable polyethylene glycol (PEG) chains. In this highly PEG-bound form, the IL2 is inactive; therefore, NKTR-214 is a biologic prodrug. When administered in vivo, the PEG chains slowly release, creating a cascade of increasingly active IL2 protein conjugates bound by fewer PEG chains. The 1-PEG-IL2 and 2-PEG-IL2 species derived from NKTR-214 are the most active conjugated-IL2 species. Free-IL2 protein is undetectable in vivo as it is eliminated faster than formed. The PEG chains on NKTR-214 are located at the region of IL2 that contacts the alpha (α) subunit of the heterotrimeric IL2 receptor complex, IL2Rαßγ, reducing its ability to bind and activate the heterotrimer. The IL2Rαßγ complex is constitutively expressed on regulatory T cells (Tregs). Therefore, without the use of mutations, PEGylation reduces the affinity for IL2Rαßγ to a greater extent than for IL2Rßγ, the receptor complex predominant on CD8 T cells. NKTR-214 treatment in vivo favors activation of CD8 T cells over Tregs in the tumor microenvironment to provide anti-tumor efficacy in multiple syngeneic models. Mechanistic modeling based on in vitro and in vivo kinetic data provides insight into the mechanism of NKTR-214 pharmacology. The model reveals that conjugated-IL2 protein derived from NKTR-214 occupy IL-2Rßγ to a greater extent compared to free-IL2 protein. The model accurately describes the sustained in vivo signaling observed after a single dose of NKTR-214 and explains how the properties of NKTR-214 impart a unique kinetically-controlled immunological mechanism of action.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-2 Receptor beta Subunit); 0 (NKTR-214); 0 (Prodrugs); 0 (Receptors, Interleukin-2); 0 (STAT5 Transcription Factor); 30IQX730WE (Polyethylene Glycols)


  4 / 271 MEDLINE  
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PMID:28657314
Autor:Quéméner A; Maillasson M; Arzel L; Sicard B; Vomiandry R; Mortier E; Dubreuil D; Jacques Y; Lebreton J; Mathé-Allainmat M
Endereço:CRCINA, INSERM, CNRS, University of Nantes , Nantes 44007, France.
Título:Discovery of a Small-Molecule Inhibitor of Interleukin 15: Pharmacophore-Based Virtual Screening and Hit Optimization.
Fonte:J Med Chem; 60(14):6249-6272, 2017 Jul 27.
ISSN:1520-4804
País de publicação:United States
Idioma:eng
Resumo:Interleukin (IL)-15 is a pleiotropic cytokine, which is structurally close to IL-2 and shares with it the IL-2 ß and γ receptor (R) subunits. By promoting the activation and proliferation of NK, NK-T, and CD8+ T cells, IL-15 plays important roles in innate and adaptative immunity. Moreover, the association of high levels of IL-15 expression with inflammatory and autoimmune diseases has led to the development of various antagonistic approaches targeting IL-15. This study is an original approach aimed at discovering small-molecule inhibitors impeding IL-15/IL-15R interaction. A pharmacophore and docking-based virtual screening of compound libraries led to the selection of 240 high-scoring compounds, 36 of which were found to bind IL-15, to inhibit the binding of IL-15 to the IL-2Rß chain or the proliferation of IL-15-dependent cells or both. One of them was selected as a hit and optimized by a structure-activity relationship approach, leading to the first small-molecule IL-15 inhibitor with sub-micromolar activity.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Interleukin-15); 0 (Interleukin-2 Receptor beta Subunit); 0 (Phthalazines); 0 (Small Molecule Libraries); 0 (Triazoles)


  5 / 271 MEDLINE  
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PMID:28652399
Autor:Schuster M; Plaza-Sirvent C; Matthies AM; Heise U; Jeron A; Bruder D; Visekruna A; Huehn J; Schmitz I
Endereço:Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
Título:c-REL and IκB Govern Common and Independent Steps of Regulatory T Cell Development from Novel CD122-Expressing Pre-Precursors.
Fonte:J Immunol; 199(3):920-930, 2017 Aug 01.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:Foxp3-expressing regulatory T cells (Tregs) are essential regulators of immune homeostasis and, thus, are prime targets for therapeutic interventions of diseases such as cancer and autoimmunity. c-REL and IκB are important regulators of Foxp3 induction in Treg precursors upon γ-chain cytokine stimulation. In c-REL/IκB double-deficient mice, Treg numbers were dramatically reduced, indicating that together, c-REL and IκB are pivotal for Treg development. However, despite the highly reduced Treg compartment, double-deficient mice did not develop autoimmunity even when aged to more than 1 y, suggesting that c-REL and IκB are required for T cell effector function as well. Analyzing Treg development in more detail, we identified a CD122 subset within the CD25 Foxp3 precursor population, which gave rise to classical CD25 Foxp3 Treg precursors. Importantly, c-REL, but not IκB , controlled the generation of classical CD25 Foxp3 precursors via direct binding to the locus. Thus, we propose that CD4 GITR CD122 CD25 Foxp3 cells represent a Treg pre-precursor population, whose transition into Treg precursors is mediated via c-REL.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Il2ra protein, mouse); 0 (Il2rb protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-2 Receptor beta Subunit); 0 (Proto-Oncogene Proteins c-rel); 139874-52-5 (NF-KappaB Inhibitor alpha)


  6 / 271 MEDLINE  
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PMID:28507024
Autor:Meghnem D; Morisseau S; Frutoso M; Trillet K; Maillasson M; Barbieux I; Khaddage S; Leray I; Hildinger M; Quéméner A; Jacques Y; Mortier E
Endereço:Centre de Recherche en Cancérologie et Immunologie Nantes-Angers, CNRS, Inserm, Université de Nantes, Nantes 44007, France.
Título:Cutting Edge: Differential Fine-Tuning of IL-2- and IL-15-Dependent Functions by Targeting Their Common IL-2/15Rß/γc Receptor.
Fonte:J Immunol; 198(12):4563-4568, 2017 Jun 15.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:Interleukin 2 and IL-15 are two closely related cytokines, displaying important functions in the immune system. They share the heterodimeric CD122/CD132 receptor to deliver their signals within target cells. Their specificity of action is conferred by their α receptor chains, IL-2Rα and IL-15Rα. By combining an increased affinity for CD122 and an impaired recruitment of CD132, we have generated an original molecule named IL-2Rß/γ (CD122/CD132) inhibitor (BiG), targeting the CD122/CD132 receptor. BiG efficiently inhibited IL-15- and IL-2-dependent functions of primary cells, including CD8 T and NK cells, in vitro and in vivo. We also report a differential dynamic of action of these cytokines by highlighting a major role played by the IL-2Rα receptor. Interestingly, due to the presence of IL-2Rα, BiG had no impact on IL-2-dependent regulatory T cell proliferation. Thus, by acting as a fine switch in the immune system, BiG emphasizes the differential roles of these two cytokines.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (IL2RA protein, human); 0 (IL2RB protein, human); 0 (IL2RG protein, human); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-15); 0 (Interleukin-15 Receptor alpha Subunit); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-2 Receptor beta Subunit)


  7 / 271 MEDLINE  
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PMID:28241741
Autor:Chiu YC; Wang LJ; Lu TP; Hsiao TH; Chuang EY; Chen Y
Endereço:Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
Título:Differential correlation analysis of glioblastoma reveals immune ceRNA interactions predictive of patient survival.
Fonte:BMC Bioinformatics; 18(1):132, 2017 Feb 28.
ISSN:1471-2105
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Recent studies illuminated a novel role of microRNA (miRNA) in the competing endogenous RNA (ceRNA) interaction: two genes (ceRNAs) can achieve coexpression by competing for a pool of common targeting miRNAs. Individual biological investigations implied ceRNA interaction performs crucial oncogenic/tumor suppressive functions in glioblastoma multiforme (GBM). Yet, a systematic analysis has not been conducted to explore the functional landscape and prognostic significance of ceRNA interaction. RESULTS: Incorporating the knowledge that ceRNA interaction is highly condition-specific and modulated by the expressional abundance of miRNAs, we devised a ceRNA inference by differential correlation analysis to identify the miRNA-modulated ceRNA pairs. Analyzing sample-paired miRNA and gene expression profiles of GBM, our data showed that this alternative layer of gene interaction is essential in global information flow. Functional annotation analysis revealed its involvement in activated processes in brain, such as synaptic transmission, as well as critical tumor-associated functions. Notably, a systematic survival analysis suggested the strength of ceRNA-ceRNA interactions, rather than expressional abundance of individual ceRNAs, among three immune response genes (CCL22, IL2RB, and IRF4) is predictive of patient survival. The prognostic value was validated in two independent cohorts. CONCLUSIONS: This work addresses the lack of a comprehensive exploration into the functional and prognostic relevance of ceRNA interaction in GBM. The proposed efficient and reliable method revealed its significance in GBM-related functions and prognosis. The highlighted roles of ceRNA interaction provide a basis for further biological and clinical investigations.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (CCL22 protein, human); 0 (Chemokine CCL22); 0 (IL2RB protein, human); 0 (Interferon Regulatory Factors); 0 (Interleukin-2 Receptor beta Subunit); 0 (MicroRNAs); 0 (RNA, Neoplasm); 0 (interferon regulatory factor-4)


  8 / 271 MEDLINE  
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PMID:28111009
Autor:Luque Y; Cathelin D; Vandermeersch S; Xu X; Sohier J; Placier S; Xu-Dubois YC; Louis K; Hertig A; Bories JC; Vasseur F; Campagne F; Di Santo JP; Vosshenrich C; Rondeau E; Mesnard L
Endereço:Unité Mixte de Recherche (UMR) 1155, Institut National de la Santé et de la Recherche Médicale (Inserm), Paris, France; Sorbonne Universités, Université Pierre et Marie Curie Paris 06, Paris, France; Urgences Néphrologiques et Transplantation Rénale, Hôpital Tenon, Assistance Publique - Hôpitaux de
Título:Glomerular common gamma chain confers B- and T-cell-independent protection against glomerulonephritis.
Fonte:Kidney Int; 91(5):1146-1158, 2017 May.
ISSN:1523-1755
País de publicação:United States
Idioma:eng
Resumo:Crescentic glomerulonephritis is a life-threatening renal disease that has been extensively studied by the experimental anti-glomerular basement membrane glomerulonephritis (anti-GBM-GN) model. Although T cells have a significant role in this model, athymic/nude mice and rats still develop severe renal disease. Here we further explored the contribution of intrinsic renal cells in the development of T-cell-independent GN lesions. Anti-GBM-GN was induced in three strains of immune-deficient mice (Rag2 , Rag2 Il2rg , and Rag2 Il2rb ) that are devoid of either T/B cells or T/B/NK cells. The Rag2 Il2rg or Rag2 Il2rb mice harbor an additional deletion of either the common gamma chain (γC) or the interleukin-2 receptor ß subunit (IL-2Rß), respectively, impairing IL-15 signaling in particular. As expected, all these strains developed severe anti-GBM-GN. Additionally, bone marrow replenishment experiments allowed us to deduce a protective role for the glomerular-expressed γC during anti-GBM-GN. Given that IL-15 has been found highly expressed in nephritic kidneys despite the absence of lymphocytes, we then studied this cytokine in vitro on primary cultured podocytes from immune-deficient mice (Rag2 Il2rg and Rag2 Il2rb ) compared to controls. IL-15 induced downstream activation of JAK1/3 and SYK in primary cultured podocytes. IL-15-dependent JAK/SYK induction was impaired in the absence of γC or IL-2Rß. We found γC largely induced on podocytes during human glomerulonephritis. Thus, renal lesions are indeed modulated by intrinsic glomerular cells through the γC/IL-2Rß receptor response, to date classically described only in immune cells.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Autoantibodies); 0 (DNA-Binding Proteins); 0 (Il2rb protein, mouse); 0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-15); 0 (Interleukin-2 Receptor beta Subunit); 0 (Rag2 protein, mouse); 0 (antiglomerular basement membrane antibody); EC 2.7.10.2 (Jak1 protein, mouse); EC 2.7.10.2 (Jak3 protein, mouse); EC 2.7.10.2 (Janus Kinase 1); EC 2.7.10.2 (Janus Kinase 3); EC 2.7.10.2 (Syk Kinase); EC 2.7.10.2 (Syk protein, mouse)


  9 / 271 MEDLINE  
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PMID:27463037
Autor:Osinalde N; Sanchez-Quiles V; Akimov V; Aloria K; Arizmendi JM; Blagoev B; Kratchmarova I
Endereço:Department of Biochemistry and Molecular Biology, University of Southern Denmark , 5230 Odense M, Denmark.
Título:Characterization of Receptor-Associated Protein Complex Assembly in Interleukin (IL)-2- and IL-15-Activated T-Cell Lines.
Fonte:J Proteome Res; 16(1):106-121, 2017 Jan 06.
ISSN:1535-3907
País de publicação:United States
Idioma:eng
Resumo:It remains a paradox that IL-2 and IL-15 can differentially modulate the immune response using the same signaling receptors. We have previously dissected the phosphotyrosine-driven signaling cascades triggered by both cytokines in Kit225 T-cells, unveiling subtle differences that may contribute to their functional dichotomy. In this study, we aimed to decipher the receptor complex assembly in IL-2- and IL-15-activated T-lymphocytes that is highly orchestrated by site-specific phosphorylation events. Comparing the cytokine-induced interactome of the interleukin receptor beta and gamma subunits shared by the two cytokines, we defined the components of the early IL-2 and IL-15 receptor-associated complex discovering novel constituents. Additionally, phosphopeptide-directed analysis allowed us to detect several cytokine-dependent and -independent phosphorylation events within the activated receptor complex including novel phosphorylated sites located in the cytoplasmic region of IL-2 receptor ß subunit (IL-2Rß). We proved that the distinct phosphorylations induced by the cytokines serve for recruiting different types of effectors to the initial receptor/ligand complex. Overall, our study sheds new light into the initial molecular events triggered by IL-2 and IL-15 and constitutes a further step toward a better understanding of the early signaling aspects of the two closely related cytokines in T-lymphocytes.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (IL15 protein, human); 0 (IL2RB protein, human); 0 (IL2RG protein, human); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Interleukin-2 Receptor beta Subunit); 0 (Recombinant Proteins); 21820-51-9 (Phosphotyrosine); EC 2.7.10.2 (JAK1 protein, human); EC 2.7.10.2 (JAK3 protein, human); EC 2.7.10.2 (Janus Kinase 1); EC 2.7.10.2 (Janus Kinase 3)


  10 / 271 MEDLINE  
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PMID:27799311
Autor:Kuwabara T; Kasai H; Kondo M
Endereço:Department of Molecular Immunology, Toho University School of Medicine, Tokyo 143-8540, Japan; and kuwabara@med.toho-u.ac.jp.
Título:Acetylation Modulates IL-2 Receptor Signaling in T Cells.
Fonte:J Immunol; 197(11):4334-4343, 2016 Dec 01.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:Ligand binding to the cognate cytokine receptors activates intracellular signaling by recruiting protein tyrosine kinases and other protein modification enzymes. However, the roles of protein modifications other than phosphorylation remain unclear. In this study, we examine a novel regulatory mechanism of Stat5, based on its acetylation. As for phosphorylation, IL-2 induces the acetylation of signaling molecules, including Stat5, in the murine T cell line CTLL-2. Stat5 is acetylated in the cytoplasm by CREB-binding protein (CBP). Acetylated Lys and Lys on Stat5 are critical indicators for limited proteolysis, which leads to the generation of a truncated form of Stat5. In turn, the truncated form of Stat5 prevents transcription of the full-length form of Stat5. We also demonstrate that CBP physically associates with the IL-2 receptor ß-chain. CBP, found in the nucleus in resting CTLL-2 cells, relocates to the cytoplasm after IL-2 stimulation in an MEK/ERK pathway-dependent manner. Thus, IL-2-mediated acetylation plays an important role in the modulation of cytokine signaling and T cell fate.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Il2rb protein, mouse); 0 (Interleukin-2); 0 (Interleukin-2 Receptor beta Subunit); 0 (STAT5 Transcription Factor); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, mouse)



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