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Relevant bibliographies by topics / Id2 inhibiteur de E2A

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Academic literature on the topic 'Id2 inhibiteur de E2A'

Author: Grafiati

Published: 4 May 2024

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Journal articles on the topic "Id2 inhibiteur de E2A"

1

Nigten, Jeannet, Gorica Nikoloski, Theo De Witte, Bert A. Van der Reijden, and Joop H. Jansen. "Id1 and Id2 Are Retinoic Acid Responsive Genes and Induce a G0/G1 Arrest in Acute Promyelocytic Leukemia Cells." Blood 104, no. 11 (2004): 2029. http://dx.doi.org/10.1182/blood.v104.11.2029.2029.

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Abstract Acute promyelocytic leukemia (APL) is uniquely sensitive to treatment with all-trans retinoic acid (ATRA), which overcomes the differentiation arrest and induces terminal granulocytic differentiation of the leukemic blasts. In 98% of the cases of APL, the leukemic cells express a promyelocytic leukemia (PML)- retinoic acid receptor a (RARa) fusion protein as a result of a t(15;17) chromosome translocation. Previously, we have identified Id1 and Id2 as direct retinoic acid target genes being upregulated after ATRA stimulation in the APL cell line NB4 as well as in primary leukemic cell

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2

Gonda, Hiroyuki, Manabu Sugai, Yukiko Nambu, et al. "The Balance Between Pax5 and Id2 Activities Is the Key to AID Gene Expression." Journal of Experimental Medicine 198, no. 9 (2003): 1427–37. http://dx.doi.org/10.1084/jem.20030802.

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Pax5 activity is enhanced in activated B cells and is essential for class switch recombination (CSR). We show that inhibitor of differentiation (Id)2 suppresses CSR by repressing the gene expression of activation-induced cytidine deaminase (AID), which has been shown to be indispensable for CSR. Furthermore, a putative regulatory region of AID contains E2A- and Pax5-binding sites, and the latter site is indispensable for AID gene expression. Moreover, the DNA-binding activity of Pax5 is decreased in Id2-overexpressing B cells and enhanced in Id2−/− B cells. The kinetics of Pax5, but not E2A, o

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3

Kim, Wonil, Kimberly D. Klarmann, and Jonathan R. Keller. "Impaired Erythropoiesis Of Gfi-1 Null Hematopoietic Progenitor Cells Is Rescued By Reducing Id2 Levels." Blood 122, no. 21 (2013): 737. http://dx.doi.org/10.1182/blood.v122.21.737.737.

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Abstract The survival, self-renewal and differentiation of hematopoietic stem and progenitor cells (HSPC) are tightly regulated by extrinsic signals, and intrinsically by transcription factors and their regulatory networks. The molecular and cellular mechanisms, which regulate the complex process of hematopoiesis, depend upon the correct expression of transcription factors and their regulators. One such family of regulators is the inhibitor of DNA binding/differentiation (Id), which is helix-loop-helix proteins that function by acting as dominant negative regulators of transcription factors su

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4

Portis, Toni, and Richard Longnecker. "Epstein-Barr Virus LMP2A Interferes with Global Transcription Factor Regulation When Expressed during B-Lymphocyte Development." Journal of Virology 77, no. 1 (2003): 105–14. http://dx.doi.org/10.1128/jvi.77.1.105-114.2003.

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ABSTRACT Epstein-Barr virus (EBV) is associated with the development of malignant lymphomas and lymphoproliferative disorders in immunocompromised individuals. The LMP2A protein of EBV is thought to play a central role in this process by allowing the virus to persist in latently infected B lymphocytes. We have demonstrated that LMP2A, when expressed in B cells of transgenic mice, allows normal B-cell developmental checkpoints to be bypassed. To identify cellular genes targeted by LMP2A that are involved in this process, we have utilized DNA microarrays to compare gene transcription in B cells

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5

Yamamoto, Hideyuki, Fumihiko Hayakawa, Takahiko Yasuda, et al. "ZNF384-Fusion Proteins Have High Affinity to EP300, Which Increases Their Transcriptional Activities." Blood 132, Supplement 1 (2018): 1554. http://dx.doi.org/10.1182/blood-2018-99-114414.

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Abstract ZNF384 fusion (Z-fusion) genes are recently identified recurrent fusion genes of B-acute lymphoblastic leukemia (ALL) and cause differentiation block of B-cells; however, its molecular mechanisms have yet to be clarified. Common structural character of Z-fusion proteins is that fusion partners are fused to the N-terminal end of full-length ZNF384 (Figure 1A), suggesting that protein-fusions confer specific transcriptional targets on ZNF384. We searched Z-fusion-specific transcriptional targets that could cause differentiation block of B-cells by analyzing the data of gene expression p

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6

Condorelli, G., L. Vitelli, M. Valtieri, et al. "Coordinate expression and developmental role of Id2 protein and TAL1/E2A heterodimer in erythroid progenitor differentiation." Blood 86, no. 1 (1995): 164–75. http://dx.doi.org/10.1182/blood.v86.1.164.bloodjournal861164.

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The Id proteins and basic helix-loop-helix (bHLH) proteins play major roles in specifying cell fate decisions in diverse biologic settings. A potential role for Id and TAL1/E2A bHLH genes in hematopoiesis has been suggested by studies on immortalized cell lines. However, it is uncertain whether these observations reflect normal hematopoiesis. We have investigated the expression pattern of Id2 and TAL1/E2A genes in liquid suspension culture of purified hematopoietic progenitor cell (HPCs) undergoing erythroid or granulopoietic differentiation in the first culture week and maturation to terminal

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7

Boos, Markus D., Yoshifumi Yokota, Gerard Eberl, and Barbara L. Kee. "Mature natural killer cell and lymphoid tissue–inducing cell development requires Id2-mediated suppression of E protein activity." Journal of Experimental Medicine 204, no. 5 (2007): 1119–30. http://dx.doi.org/10.1084/jem.20061959.

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The Id2 transcriptional repressor is essential for development of natural killer (NK) cells, lymphoid tissue–inducing (LTi) cells, and secondary lymphoid tissues. Id2 was proposed to regulate NK and LTi lineage specification from multipotent progenitors through suppression of E proteins. We report that NK cell progenitors are not reduced in the bone marrow (BM) of Id2−/− mice, demonstrating that Id2 is not essential for NK lineage specification. Rather, Id2 is required for development of mature (m) NK cells. We define the mechanism by which Id2 functions by showing that a reduction in E protei

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8

Ji, Ming, Huajie Li, Hyung Chan Suh, Kimberly D. Klarmann, Yoshifumi Yokota, and Jonathan R. Keller. "Id2 intrinsically regulates lymphoid and erythroid development via interaction with different target proteins." Blood 112, no. 4 (2008): 1068–77. http://dx.doi.org/10.1182/blood-2008-01-133504.

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Abstract Inhibitors of DNA binding (Id) family members are key regulators of cellular differentiation and proliferation. These activities are related to the ability of Id proteins to antagonize E proteins and other transcription factors. As negative regulators of E proteins, Id proteins have been implicated in lymphocyte development. Overexpression of Id1, Id2, or Id3 has similar effects on lymphocyte development. However, which Id protein plays a physiologic role during lymphocyte development is not clear. By analyzing Id2 knock-out mice and retroviral transduced hematopoietic progenitors, we

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9

Yan, W., A. Z. Young, V. C. Soares, R. Kelley, R. Benezra, and Y. Zhuang. "High incidence of T-cell tumors in E2A-null mice and E2A/Id1 double-knockout mice." Molecular and Cellular Biology 17, no. 12 (1997): 7317–27. http://dx.doi.org/10.1128/mcb.17.12.7317.

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The basic-helix-loop-helix (bHLH) proteins encoded by the E2A gene are broadly expressed transcription regulators which function through binding to the E-box enhancer sequences. The DNA binding activities of E2A proteins are directly inhibited upon dimerization with the Id1 gene product. It has been shown that disruption of the E2A gene leads to a complete block in B-lymphocyte development and a high frequency of neonatal death. We report here that nearly half of the surviving E2A-null mice develop acute T-cell lymphoma between 3 to 10 months of age. We further show that disruption of the Id1

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10

Masson, Frederick, Margherita Ghisi, Joanna R. Groom, et al. "Id2 represses E2A-mediated activation of IL-10 expression in T cells." Blood 123, no. 22 (2014): 3420–28. http://dx.doi.org/10.1182/blood-2014-03-561456.

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Key Points Loss of Id2 in T cells results in overexpression of IL-10 during influenza infection and GVHD and protects against GVHD immunopathology. Id2 represses the direct E2A-mediated activation of the Il10 locus in effector T cells.

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