Long-term tracking of murine hematopoietic cells transduced with a bicistronic retrovirus containing CD24 and EGFP genes

Kume, Akihiro; Xu, Ruifang; Ueda, Yasuji; Urabe, Masashi; Ozawa, Keiya

doi:10.1038/sj.gt.3301225

Cited by 21 publications

(26 citation statements)

References 43 publications

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“…The primers possessing BamHI site at each 5Ј end, were 5Ј-GTTAAGGAT-CCATGTCTGTGGATGAGAGACCT-3Ј and 5Ј-GTTAAGGATCCCTAG-GCATAATCTTTCCTGGG-3Ј (initiation and stop codons are underlined). A 2.5-kilobase pair NotI and HindIII fragment was isolated from the pcDNAFLAGBach2, filled in, and inserted into the HpaI site of MSCV/IRES-EGFP (28). To construct Bach2⌬BTBFLAG, the EcoRIBamHI fragment was isolated from Bach2 cDNA, filled in, and cloned into the blunt-ended KpnI site of pcDNA3.1FLAG, resulting in pF-⌬BT-BB2.…”

Section: Methodsmentioning

confidence: 99%

“…To evaluate the effect of Bach2 expression on cellular function at the level of a single cell, we employed a bicistronic retroviral system possessing the encephalomyocarditis virus-derived IRES and the EGFP with a murine stem cell virus backbone (28). Virus-infected cells can be monitored individually without selecting clonal stable cell lines.…”

Section: Effects Of Bach2 On the Related Enhancers Tre Mare Andmentioning

confidence: 99%

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Activation of Maf/AP-1 Repressor Bach2 by Oxidative Stress Promotes Apoptosis and Its Interaction with Promyelocytic Leukemia Nuclear Bodies

Muto¹,

Tashiro²,

Tsuchiya³

et al. 2002

Journal of Biological Chemistry

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The oxidative stress response operates by inducing the expression of genes that counteract the stress. We show here that the oxidative stress-responsive transcription factor Bach2 is a generic inhibitor of gene expression directed by the 12-O-tetradecanoylphorbol-13-acetate response element, the Maf recognition element, and the antioxidant-responsive element. The Bach2-enhanced green fluorescent protein bicistronic retrovirus was used to monitor the fate of Bach2-expressing cells at the single cell level. Bach2 exerted an inhibitory effect on NIH3T3 cell proliferation and caused massive apoptosis upon mild oxidative stress in both NIH3T3 and Raji B-lymphoid cells. Interestingly, Bach1, a highly homologous protein, could not induce cell death, demonstrating the specificity for the apoptosis induction. Although both oxidative stress and leptomycin B, an inhibitor of nuclear export, induce nuclear accumulation of Bach2, the leptomycin B-induced nuclear accumulation of Bach2 was not sufficient to elicit apoptosis. Upon oxidative stress, Bach2 formed nuclear foci that associated with promyelocytic leukemia nuclear bodies. Our results suggest that Bach2 constitutes a cell lineage-specific system that couples oxidative stress and cell death and that inhibition of 12-O-tetradecanoylphorbol-13-acetate response element, the Maf recognition element, and the antioxidant-responsive element upon oxidative stress may be critical determinants for apoptosis.

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Section: Methodsmentioning

confidence: 99%

Section: Effects Of Bach2 On the Related Enhancers Tre Mare Andmentioning

confidence: 99%

Activation of Maf/AP-1 Repressor Bach2 by Oxidative Stress Promotes Apoptosis and Its Interaction with Promyelocytic Leukemia Nuclear Bodies

Muto¹,

Tashiro²,

Tsuchiya³

et al. 2002

Journal of Biological Chemistry

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“…25 We also established a TF-1-fms clone expressing enhanced green fluorescent protein (EGFP). This was achieved with a retrovirus vector (MSCV2.2/IRES-EGFP), 26 as described previously. 27 In brief, the amphotropic packaging PT67 cells (Clontech, Palo Alto, CA) were transfected with MSCV2.2/IRES-EGFP vector using LipofectAMINE2000 reagent (Invitrogen, Carlsbad, CA) according to the manufacturer's recommendations.…”

Section: Cells and Culture Conditionsmentioning

confidence: 99%

HIV-1 Nef interferes with M-CSF receptor signaling through Hck activation and inhibits M-CSF bioactivities

Suzu

Harada

Μatsumoto

et al. 2005

Blood

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IntroductionNef is an accessory protein of HIV-1, a causative virus for AIDS. A number of reports, including studies of HIV-1-infected patients and of animal models, have demonstrated that the Nef protein is a major determinant of the pathogenicity of HIV-1. [1][2][3][4] Transgenic mice expressing the complete coding sequences of HIV-1 under the regulatory sequences of human CD4 gene developed severe AIDS-like abnormalities: loss of CD4 ϩ T cells, thymus atrophy, failure to thrive, diarrhea, wasting, premature death, interstitial pneumonitis, and tubulo-interstitial nephritis. 4 Using this mouse model and the introduction of mutation into selected HIV-1 gene(s), Hanna et al 4 clearly demonstrated that Nef harbored a major disease determinant. Therefore, much attention has been given to Nef to explain its contribution to HIV-1 pathogenesis and to investigate it as a target for antiviral drug development.CD4 ϩ T cells and monocytes/macrophages are the principal target cells for HIV-1, and the functions of Nef in CD4 ϩ T cells are generally accepted as accounting for many aspects of viral pathogenesis (reviewed in Fackler and Baur 5 and Peterlin and Trono 6 ). For example, Nef has been shown to cause the downregulation of cell surface molecules such as cell surface receptor CD4 7 and major histocompatibility complex (MHC) class I in CD4 ϩ T cells. 8 The down-regulation of MHC class I is considered to diminish the recognition of HIV-1-infected cells by cytotoxic T cells. In contrast, the contribution of monocytes/macrophages to viral pathogenesis is less well understood. Several lines of evidence support the idea that monocytes/macrophages and CD4 ϩ T cells are important for the development and progression of AIDS. Recent studies have demonstrated that Nef induces the production of CC chemokines (macrophage inflammatory proteins-1␣ and -1␤) and soluble forms of CD23 and intracellular adhesion molecule-1 by macrophages. 9,10 These Nef-induced factors from macrophages might stimulate the chemotaxis and activation of resting CD4 ϩ T cells, thereby promoting the permissiveness of CD4 ϩ T cells to HIV-1 infection. 9,10 This Nef function is likely to be mediated by the activation of NF-B transcription factor. 10 Another important feature of Nef is the binding at high affinity to myeloid lineage-specific Src family kinase Hck to activate its kinase activity. 11,12 The proline-rich (PxxP) motif in Nef binds to the Src homology 3 (SH3) domain of Hck. 11 Interestingly, Hck was found to bind preferentially and with higher affinity to Nef than other Src kinases. 11 The pathologic relevance of the molecular interaction in vivo was revealed by studies of HIV-1 transgenic mice. The mutation in the SH3-binding motif of Nef abolished the development of AIDS-like disease in the HIV-1 transgenic mice. 13 Moreover, the breeding of transgenic mice expressing the complete coding sequences of HIV-1 on a hck Ϫ/Ϫ background resulted in the delay of disease development. 13 These studies suggest that the modulation of macrophage functions by ...

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“…41 Various GATA-2 mutants and fusion proteins were constructed by PCR. Transcriptional activities of the VP16 activation domain 42 GATA-2 zinc finger fusion protein (VP-F) and engrailed repressor domain 43 GATA-2 zinc finger fusion protein (Eng-F) were confirmed based on their Luciferase reporter activity.…”

Section: Retroviral Overexpression Of the Gata-2 Genementioning

confidence: 99%

Expression and domain-specific function of GATA-2 during differentiation of the hematopoietic precursor cells in midgestation mouse embryos

Minegishi

Suzuki

Yokomizo

et al. 2003

Blood

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The aorta-gonads-mesonephros (AGM) region of the mouse embryo has been assigned as the origin of definitive hematopoiesis. The transcription factor GATA-2 has specific but unclarified roles in early hematopoiesis. To elucidate the expression profile of GATA-2, we prepared transgenic mouse lines containing the green fluorescent protein (GFP ) gene driven by GATA-2 gene regulatory elements. We also prepared a mouse line in which GFP reporter sequences were inserted into the endogenous GATA-2 gene. Both mouse

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Long-term tracking of murine hematopoietic cells transduced with a bicistronic retrovirus containing CD24 and EGFP genes

Cited by 21 publications

References 43 publications

Activation of Maf/AP-1 Repressor Bach2 by Oxidative Stress Promotes Apoptosis and Its Interaction with Promyelocytic Leukemia Nuclear Bodies

Activation of Maf/AP-1 Repressor Bach2 by Oxidative Stress Promotes Apoptosis and Its Interaction with Promyelocytic Leukemia Nuclear Bodies

HIV-1 Nef interferes with M-CSF receptor signaling through Hck activation and inhibits M-CSF bioactivities

Expression and domain-specific function of GATA-2 during differentiation of the hematopoietic precursor cells in midgestation mouse embryos

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