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  1. AU=Cismasiu Valeriu B
  2. AU="Töpfer, Änne"
  3. AU="Lemcke, Johannes"
  4. AU=Cousins Emily
  5. AU="Clarke Aileen"
  6. AU="Aparecido Corrêa, Nivaldo"
  7. AU="Meng-Ju Wang"
  8. AU=Verrills Paul
  9. AU="Chaudhari, Amol"
  10. AU="Planagumà, Jesús"
  11. AU="de Rezende, Grazielli Rocha"
  12. AU="Mohadeseh NEZAM"
  13. AU="Daniel Pecos-Martín"
  14. AU="Gentle, Popular"
  15. AU=Wang Jirui
  16. AU="Bielik, Martin"
  17. AU="Simon A.F. Darroch"
  18. AU="Suzuki, Kenichi G N"
  19. AU="Hu, Yizhong"
  20. AU=Sasaki Kotaro
  21. AU=Abd-Elsayed Alaa
  22. AU="Jung, Hee-Jun"
  23. AU="Struckmann, Stephan"
  24. AU=Coward Richard
  25. AU="Ghazizadeh, Shabnam"
  26. AU="Rebecca A Butcher"
  27. AU="Kimberlyn Roosa"
  28. AU=Chian Ri-Cheng
  29. AU="Alzalzalah, Sayed"
  30. AU=Kaufman Jonathan J
  31. AU="Kim, Jin K"
  32. AU="Zevakov, S A"
  33. AU="Sui Phang"
  34. AU="Kolomeichuk, Lilia V"
  35. AU="Sabuj Kanti Mistry"
  36. AU="Basurto-Lozada, Daniela"
  37. AU="Takashima, Shin-Ichiro"
  38. AU="Teresinha Leal"
  39. AU="Angélique B van 't Wout"
  40. AU="Roberts, Nicholas J"
  41. AU="Chauhan, Gaurav B"
  42. AU=Hanjaya-Putra Donny
  43. AU=Powell James
  44. AU="Russell, Todd"
  45. AU=Forth Scott
  46. AU="Kreutzer, Susanne" AU="Kreutzer, Susanne"
  47. AU="St John, Maie"
  48. AU=Gerhardy A
  49. AU="Qi, Huixin"
  50. AU="Dobosiewicz, May"
  51. AU="Srivastava, Rakesh"
  52. AU="Grevtsov K.I."

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  1. Artikel ; Online: Telocytes transfer extracellular vesicles loaded with microRNAs to stem cells.

    Cismaşiu, Valeriu B / Popescu, Laurentiu M

    Journal of cellular and molecular medicine

    2015  Band 19, Heft 2, Seite(n) 351–358

    Abstract: Telocytes (TCs) are cells ubiquitously distributed in the body and characterized by very long and thin prolongations named telopodes (Tps). Cardiac TCs are the best characterized TCs for the moment. Tps release extracellular vesicles (EVs) in vivo and in ...

    Abstract Telocytes (TCs) are cells ubiquitously distributed in the body and characterized by very long and thin prolongations named telopodes (Tps). Cardiac TCs are the best characterized TCs for the moment. Tps release extracellular vesicles (EVs) in vivo and in vitro suggesting that TCs regulate the activity of other cells by vesicular paracrine signals. TCs have been found within the stem cell niche of several organs. Electron microscopy or electron tomography has shown that Tps are located in close vicinity of stem cells (SC). Since stem cell regulation by niche components involves paracrine signalling, we have investigated if TCs could be part of this mechanism. Using fluorescent labelling of cells and EVs with calcein and Cy5-miR-21 oligos, we provide evidence that TCs can modulate SC through EVs loaded with microRNAs. TCs deliver microRNA to cardiac stem cells (CSCs), as well as to other types of SCs (e.g. hematopoietic SC) indicating that this mechanism is not restricted to cardiac tissue. We also found that CSCs deliver microRNA loaded EVs to TCs, suggesting that there is a continuous, post-transcriptional regulatory signal back and forth between TCs and SC. In conclusion, our data reveal the existence of a reciprocal (bidirectional) epigenetic signalling between TCs and SC.
    Mesh-Begriff(e) Animals ; Cells, Cultured ; Heart/physiology ; Mice ; Mice, Inbred C57BL ; MicroRNAs/metabolism ; Rats ; Rats, Wistar ; Stem Cell Niche/physiology ; Stem Cells/metabolism ; Transport Vesicles/metabolism
    Chemische Substanzen MicroRNAs
    Sprache Englisch
    Erscheinungsdatum 2015-02
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.12529
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Bcl11b sustains multipotency and restricts effector programs of intestinal-resident memory CD8

    Helm, Eric Y / Zelenka, Tomas / Cismasiu, Valeriu B / Islam, Shamima / Silvane, Leonardo / Zitti, Beatrice / Holmes, Tim D / Drashansky, Theodore T / Kwiatkowski, Alexander J / Tao, Christine / Dean, Joseph / Obermayer, Alyssa N / Chen, Xianghong / Keselowsky, Benjamin G / Zhang, Weizhou / Huo, Zhiguang / Zhou, Liang / Sheridan, Brian S / Conejo-Garcia, Jose R /
    Shaw, Timothy I / Bryceson, Yenan T / Avram, Dorina

    Science immunology

    2023  Band 8, Heft 82, Seite(n) eabn0484

    Abstract: The networks of transcription factors (TFs) that control intestinal-resident memory ... ...

    Abstract The networks of transcription factors (TFs) that control intestinal-resident memory CD8
    Mesh-Begriff(e) Mice ; Animals ; CD8-Positive T-Lymphocytes/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Cell Differentiation ; Intestines ; Tumor Suppressor Proteins/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism
    Chemische Substanzen Transcription Factors ; Tumor Suppressor Proteins ; Bcl11b protein, mouse ; Repressor Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-04-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abn0484
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: BCL11B is a general transcriptional repressor of the HIV-1 long terminal repeat in T lymphocytes through recruitment of the NuRD complex.

    Cismasiu, Valeriu B / Paskaleva, Elena / Suman Daya, Sneha / Canki, Mario / Duus, Karen / Avram, Dorina

    Virology

    2008  Band 380, Heft 2, Seite(n) 173–181

    Abstract: In this study we provide evidence that the transcription factor BCL11B represses expression from the HIV-1 long terminal repeat (LTR) in T lymphocytes through direct association with the HIV-1 LTR. We also demonstrate that the NuRD corepressor complex ... ...

    Abstract In this study we provide evidence that the transcription factor BCL11B represses expression from the HIV-1 long terminal repeat (LTR) in T lymphocytes through direct association with the HIV-1 LTR. We also demonstrate that the NuRD corepressor complex mediates BCL11B transcriptional repression of the HIV-1 LTR. In addition, BCL11B and the NuRD complex repressed TAT-mediated transactivation of the HIV-1 LTR in T lymphocytes, pointing to a potential role in initiation of silencing. In support of all the above results, we demonstrate that BCL11B affects HIV-1 replication and virus production, most likely by blocking LTR transcriptional activity. BCL11B showed specific repression for the HIV-1 LTR sequences isolated from seven different HIV-1 subtypes, demonstrating that it is a general transcriptional repressor for all LTRs.
    Mesh-Begriff(e) Artificial Gene Fusion ; Cell Line ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation, Viral ; Genes, Reporter ; HIV Long Terminal Repeat ; HIV-1/physiology ; Histone Deacetylases/metabolism ; Humans ; Luciferases/biosynthesis ; Luciferases/genetics ; Mi-2 Nucleosome Remodeling and Deacetylase Complex ; Protein Binding ; Repressor Proteins/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/virology ; Tumor Suppressor Proteins/metabolism ; Virus Replication ; tat Gene Products, Human Immunodeficiency Virus/antagonists & inhibitors
    Chemische Substanzen BCL11B protein, human ; DNA-Binding Proteins ; Repressor Proteins ; Tumor Suppressor Proteins ; tat Gene Products, Human Immunodeficiency Virus ; Luciferases (EC 1.13.12.-) ; Histone Deacetylases (EC 3.5.1.98) ; Mi-2 Nucleosome Remodeling and Deacetylase Complex (EC 3.5.1.98)
    Sprache Englisch
    Erscheinungsdatum 2008-09-02
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 200425-2
    ISSN 1096-0341 ; 0042-6822
    ISSN (online) 1096-0341
    ISSN 0042-6822
    DOI 10.1016/j.virol.2008.07.035
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: BCL11B enhances TCR/CD28-triggered NF-kappaB activation through up-regulation of Cot kinase gene expression in T-lymphocytes.

    Cismasiu, Valeriu B / Duque, Javier / Paskaleva, Elena / Califano, Danielle / Ghanta, Sailaja / Young, Howard A / Avram, Dorina

    The Biochemical journal

    2009  Band 417, Heft 2, Seite(n) 457–466

    Abstract: BCL11B is a transcriptional regulator with an important role in T-cell development and leukaemogenesis. We demonstrated recently that BCL11B controls expression from the IL (interleukin)-2 promoter through direct binding to the US1 (upstream site 1). In ... ...

    Abstract BCL11B is a transcriptional regulator with an important role in T-cell development and leukaemogenesis. We demonstrated recently that BCL11B controls expression from the IL (interleukin)-2 promoter through direct binding to the US1 (upstream site 1). In the present study, we provide evidence that BCL11B also participates in the activation of IL-2 gene expression by enhancing NF-kappaB (nuclear factor kappaB) activity in the context of TCR (T-cell receptor)/CD28-triggered T-cell activation. Enhanced NF-kappaB activation is not a consequence of BCL11B binding to the NF-kappaB response elements or association with the NF-kappaB-DNA complexes, but rather the result of higher translocation of NF-kappaB to the nucleus caused by enhanced degradation of IkappaB (inhibitor of NF-kappaB). The enhanced IkappaB degradation in cells with increased levels of BCL11B was specific for T-cells activated through the TCR, but not for cells activated through TNFalpha (tumour necrosis factor alpha) or UV light, and was caused by increased activity of IkappaB kinase, as indicated by its increase in phosphorylation. As BCL11B is a transcription factor, we investigated whether the expression of genes upstream of IkappaB kinase in the TCR/CD28 signalling pathway was affected by increased BCL11B expression, and found that Cot (cancer Osaka thyroid oncogene) kinase mRNA levels were elevated. Cot kinase is known to promote enhanced IkappaB kinase activity, which results in the phosphorylation and degradation of IkappaB and activation of NF-kappaB. The implied involvement of Cot kinase in BCL11B-mediated NF-kappaB activation in response to TCR activation is supported by the fact that a Cot kinase dominant-negative mutant or Cot kinase siRNA (small interfering RNA) knockdown blocked BCL11B-mediated NF-kappaB activation. In support of our observations, in the present study we report that BCL11B enhances the expression of several other NF-kappaB target genes, in addition to IL-2. In addition, we provide evidence that BCL11B associates with intron 2 of the Cot kinase gene to regulate its expression.
    Mesh-Begriff(e) CD28 Antigens/immunology ; CD28 Antigens/metabolism ; Cell Line, Tumor ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Genes, Reporter/genetics ; Humans ; I-kappa B Kinase/metabolism ; Interleukin-2/genetics ; Interleukin-2/metabolism ; Lymphocyte Activation/immunology ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/metabolism ; NF-kappa B/metabolism ; Phosphorylation ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; RNA, Messenger/genetics ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes/radiation effects ; Transcription, Genetic/genetics ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Up-Regulation/genetics
    Chemische Substanzen BCL11B protein, human ; CD28 Antigens ; DNA-Binding Proteins ; Interleukin-2 ; NF-kappa B ; Proto-Oncogene Proteins ; RNA, Messenger ; Repressor Proteins ; Tumor Suppressor Proteins ; I-kappa B Kinase (EC 2.7.11.10) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP3K8 protein, human (EC 2.7.11.25)
    Sprache Englisch
    Erscheinungsdatum 2009-01-15
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2969-5
    ISSN 1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
    ISSN (online) 1470-8728
    ISSN 0006-2936 ; 0306-3275 ; 0264-6021
    DOI 10.1042/BJ20080925
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: BCL11B functionally associates with the NuRD complex in T lymphocytes to repress targeted promoter.

    Cismasiu, Valeriu B / Adamo, Karen / Gecewicz, Jennifer / Duque, Javier / Lin, Qishan / Avram, Dorina

    Oncogene

    2005  Band 24, Heft 45, Seite(n) 6753–6764

    Abstract: ... with hematopoietic malignancies. Specifically, disruption of the BCL11B (B-cell chronic lymphocytic leukemia/lymphoma 11B) locus ...

    Abstract BCL11 genes play crucial roles in lymphopoiesis and have been associated with hematopoietic malignancies. Specifically, disruption of the BCL11B (B-cell chronic lymphocytic leukemia/lymphoma 11B) locus is linked to T-cell acute lymphoblastic leukemia, and the loss of heterozygosity in mice results in T-cell lymphoma. BCL11 proteins are related C2H2 zinc-finger transcription factors that act as transcriptional repressors. Here, we demonstrate the association of the endogenous BCL11B with the nucleosome remodeling and histone deacetylase (NuRD) complex, one of the major transcriptional corepressor complexes in mammalian cells. BCL11B complexes from T lymphocytes possess trichostatin A-sensitive histone deacetylase activity, confirming the functionality of the complexes. Analysis of the BCL11B-NuRD association demonstrated that BCL11B directly interacted with the metastasis-associated proteins MTA1 and MTA2 through the amino-terminal region. We provide evidence for the functional requirement of MTA1 in transcriptional repression mediated by BCL11B through the following: (1) overexpression of MTA1 enhanced the transcriptional repression mediated by BCL11B, (2) knockdown of MTA1 expression by small interfering RNA inhibited BCL11B transcriptional repression activity and (3) MTA1 was specifically recruited to a BCL11B targeted promoter. Taken together, these data support the hypothesis that the NuRD complex mediates transcriptional repression function of BCL11B.
    Mesh-Begriff(e) Amino Acid Sequence ; Animals ; CD4-Positive T-Lymphocytes/enzymology ; CD4-Positive T-Lymphocytes/metabolism ; Cell Line ; DNA-Binding Proteins/metabolism ; Histone Deacetylases/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Mi-2 Nucleosome Remodeling and Deacetylase Complex ; Molecular Sequence Data ; Promoter Regions, Genetic ; Repressor Proteins/metabolism ; Tumor Suppressor Proteins/metabolism
    Chemische Substanzen BCL11B protein, human ; DNA-Binding Proteins ; Hydroxamic Acids ; Repressor Proteins ; Tumor Suppressor Proteins ; trichostatin A (3X2S926L3Z) ; Histone Deacetylases (EC 3.5.1.98) ; Mi-2 Nucleosome Remodeling and Deacetylase Complex (EC 3.5.1.98)
    Sprache Englisch
    Erscheinungsdatum 2005-10-13
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/sj.onc.1208904
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Dicer is selectively important for the earliest stages of erythroid development.

    Buza-Vidas, Natalija / Cismasiu, Valeriu B / Moore, Susan / Mead, Adam J / Woll, Petter S / Lutteropp, Michael / Melchiori, Luca / Luc, Sidinh / Bouriez-Jones, Tiphaine / Atkinson, Deborah / O'Carroll, Donal / Jacobsen, Sten Eirik W / Nerlov, Claus

    Blood

    2012  Band 120, Heft 12, Seite(n) 2412–2416

    Abstract: MicroRNAs (miRs) are involved in many aspects of normal and malignant hematopoiesis, including hematopoietic stem cell (HSC) self-renewal, proliferation, and terminal differentiation. However, a role for miRs in the generation of the earliest stages of ... ...

    Abstract MicroRNAs (miRs) are involved in many aspects of normal and malignant hematopoiesis, including hematopoietic stem cell (HSC) self-renewal, proliferation, and terminal differentiation. However, a role for miRs in the generation of the earliest stages of lineage committed progenitors from HSCs has not been identified. Using Dicer inactivation, we show that the miR complex is not only essential for HSC maintenance but is specifically required for their erythroid programming and subsequent generation of committed erythroid progenitors. In bipotent pre-MegEs, loss of Dicer up-regulated transcription factors preferentially expressed in megakaryocyte progenitors (Gata2 and Zfpm1) and decreased expression of the erythroid-specific Klf1 transcription factor. These results show a specific requirement for Dicer in acquisition of erythroid lineage programming and potential in HSCs and their subsequent erythroid lineage differentiation, and in particular indicate a role for the miR complex in achieving proper balance of lineage-specific transcriptional regulators necessary for HSC multilineage potential to be maintained.
    Mesh-Begriff(e) Animals ; Biomarkers/metabolism ; Blotting, Western ; Cell Differentiation ; Cell Lineage ; DEAD-box RNA Helicases/antagonists & inhibitors ; DEAD-box RNA Helicases/physiology ; Erythroid Cells/cytology ; Erythroid Cells/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Integrases/metabolism ; Megakaryocyte Progenitor Cells/cytology ; Megakaryocyte Progenitor Cells/metabolism ; Mice ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonuclease III/antagonists & inhibitors ; Ribonuclease III/physiology ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemische Substanzen Biomarkers ; RNA, Messenger ; Transcription Factors ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-) ; Dicer1 protein, mouse (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Sprache Englisch
    Erscheinungsdatum 2012-08-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2011-10-383653
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: The MAM (meprin/A5-protein/PTPmu) domain is a homophilic binding site promoting the lateral dimerization of receptor-like protein-tyrosine phosphatase mu.

    Cismasiu, Valeriu B / Denes, Stefan A / Reiländer, Helmut / Michel, Hartmut / Szedlacsek, Stefan E

    The Journal of biological chemistry

    2004  Band 279, Heft 26, Seite(n) 26922–26931

    Abstract: The MAM (meprin/A5-protein/PTPmu) domain is present in numerous proteins with diverse functions. PTPmu belongs to the MAM-containing subclass of protein-tyrosine phosphatases (PTP) able to promote cell-to-cell adhesion. Here we provide experimental ... ...

    Abstract The MAM (meprin/A5-protein/PTPmu) domain is present in numerous proteins with diverse functions. PTPmu belongs to the MAM-containing subclass of protein-tyrosine phosphatases (PTP) able to promote cell-to-cell adhesion. Here we provide experimental evidence that the MAM domain is a homophilic binding site of PTPmu. We demonstrate that the MAM domain forms oligomers in solution and binds to the PTPmu ectodomain at the cell surface. The presence of two disulfide bridges in the MAM molecule was evidenced and their integrity was found to be essential for MAM homophilic interaction. Our data also indicate that PTPmu ectodomain forms oligomers and mediates the cellular adhesion, even in the absence of MAM domain homophilic binding. Reciprocally, MAM is able to interact homophilically in the absence of ectodomain trans binding. The MAM domain therefore contains independent cis and trans interaction sites and we predict that its main role is to promote lateral dimerization of PTPmu at the cell surface. This finding contributes to the understanding of the signal transduction mechanism in MAM-containing PTPs.
    Mesh-Begriff(e) Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Baculoviridae/genetics ; Binding Sites ; Cell Adhesion ; Cell Line ; Cysteine/genetics ; Cysteine/metabolism ; Dimerization ; Disulfides/chemistry ; Disulfides/metabolism ; Humans ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Protein Binding ; Protein Structure, Tertiary ; Protein Tyrosine Phosphatases/chemistry ; Protein Tyrosine Phosphatases/genetics ; Protein Tyrosine Phosphatases/metabolism ; Receptor-Like Protein Tyrosine Phosphatases, Class 2 ; Receptor-Like Protein Tyrosine Phosphatases, Class 8 ; Receptors, Cell Surface/chemistry ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Sequence Alignment ; Spodoptera/cytology ; Tiopronin/chemistry ; Tiopronin/metabolism
    Chemische Substanzen Disulfides ; Receptors, Cell Surface ; Recombinant Proteins ; Tiopronin (C5W04GO61S) ; PTPRN protein, human (EC 3.1.3.48) ; Protein Tyrosine Phosphatases (EC 3.1.3.48) ; Receptor-Like Protein Tyrosine Phosphatases, Class 2 (EC 3.1.3.48) ; Receptor-Like Protein Tyrosine Phosphatases, Class 8 (EC 3.1.3.48) ; Cysteine (K848JZ4886)
    Sprache Englisch
    Erscheinungsdatum 2004-04-14
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M313115200
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: BCL11B participates in the activation of IL2 gene expression in CD4+ T lymphocytes.

    Cismasiu, Valeriu B / Ghanta, Sailaja / Duque, Javier / Albu, Diana I / Chen, Hong-Mei / Kasturi, Rohini / Avram, Dorina

    Blood

    2006  Band 108, Heft 8, Seite(n) 2695–2702

    Abstract: BCL11A and BCL11B are transcriptional regulators important for lymphopoiesis and previously associated with hematopoietic malignancies. Ablation of the mouse Bcl11b locus results in failure to generate double-positive thymocytes, implicating a critical ... ...

    Abstract BCL11A and BCL11B are transcriptional regulators important for lymphopoiesis and previously associated with hematopoietic malignancies. Ablation of the mouse Bcl11b locus results in failure to generate double-positive thymocytes, implicating a critical role of Bcl11b in T-cell development. However, BCL11B is also expressed in CD4+ T lymphocytes, both in resting and activated states. Here we show both in transformed and primary CD4+ T cells that BCL11B participates in the control of the interleukin-2 (IL2) gene expression following activation through T-cell receptor (TCR). BCL11B augments expression from the IL2 promoter through direct binding to the US1 site. In addition, BCL11B associates with the p300 coactivator in CD4+ T cells activated through TCR, which may account for its transcriptional activation function. These results provide the first evidence that BCL11B, originally described as a transcriptional repressor, activates transcription of a target gene in the context of T-cell activation.
    Mesh-Begriff(e) Animals ; Base Sequence ; Binding Sites ; CD4-Positive T-Lymphocytes/immunology ; Cells, Cultured ; DNA/genetics ; DNA/metabolism ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Humans ; Interleukin-2/genetics ; Jurkat Cells ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Promoter Regions, Genetic ; RNA, Small Interfering/genetics ; Receptors, Antigen, T-Cell/metabolism ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Repressor Proteins/antagonists & inhibitors ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transduction, Genetic ; Tumor Suppressor Proteins/antagonists & inhibitors ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; p300-CBP Transcription Factors/metabolism
    Chemische Substanzen Bcl11b protein, mouse ; DNA-Binding Proteins ; Interleukin-2 ; RNA, Small Interfering ; Receptors, Antigen, T-Cell ; Recombinant Proteins ; Repressor Proteins ; Tumor Suppressor Proteins ; DNA (9007-49-2) ; p300-CBP Transcription Factors (EC 2.3.1.48)
    Sprache Englisch
    Erscheinungsdatum 2006-06-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2006-05-021790
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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