Nuclear proteins interacting with the promoter region of the human granulocyte/macrophage colony-stimulating factor gene.

Shannon, M. Frances; Gamble, JR; Vadas, Mathew A.

doi:10.1073/pnas.85.3.674

Cited by 114 publications

(71 citation statements)

References 33 publications

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“…The Tax protein has been shown to activate transcription of the genes for IL-2 (52-54), the a chain of IL-2 receptor (IL-2Ra) (55-58), graulocyte-macrophage colony-stimulating factor (59)(60)(61)(62), nerve growth factor (NGF) (63), vimentine (64), and c-fos protooncogene (39). In CD4+ T lymphocytes, it has been postulated that the tax gene plays an important role in leukemogenesis through the IL-2/IL-2Ra autocrine pathway (65,66).…”

Section: Methodsmentioning

confidence: 99%

Overgrowth of human synovial cells driven by the human T cell leukemia virus type I tax gene.

Nakajima¹,

Aono²,

Hasunuma³

et al. 1993

J. Clin. Invest.

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One of the salient pathological features of rheumatoid arthritis is synovial cell proliferation with bone erosion. Despite extensive investigation, the factors essential for synovial cell proliferation remain to be identified. Recent studies suggest that human T cell leukemia virus type I (HTLV-I) may play an important role in synovial overgrowth observed in patients with one type of chronic inflammatory synovitis. In order to confirm and extend these observations, we have established synovial cell clones (SCCs) from three HTLV-I carriers who demonstrated synovial overgrowth but were otherwise asymptomatic. HTLV-I proviral DNA randomly integrated into the cellular genome was present in 20-30% of SCCs. The SCCs carrying HTLV-I proviral DNA and expressing the tax gene exhibited high levels of proliferative potential. HTLV-I was found to function as a transcriptional trans-activator in these SCCs. Moreover, transfection of the tax expression plasmid into SCCs resulted in the same phenotype of increased proliferation and cytokine expression as exhibited by HTLV-I provirus-carrying and tax-expressing SCCs. These data suggest that tax plays a critical role not only in leukemogenesis but also in synovial overgrowth in humans. (J. Clin. Invest. 1993. 92:186-193.)

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Section: Methodsmentioning

confidence: 99%

Overgrowth of human synovial cells driven by the human T cell leukemia virus type I tax gene.

Nakajima¹,

Aono²,

Hasunuma³

et al. 1993

J. Clin. Invest.

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“…2) regardless of orientation. Shannon et al (33) identified nuclear proteins that could form a complex with a DNA fragment carrying CLE1 and CLE2, although the significance of these binding data remains to be determined.…”

Section: Notesmentioning

confidence: 99%

T-cell activation signals and human T-cell leukemia virus type I-encoded p40x protein activate the mouse granulocyte-macrophage colony-stimulating factor gene through a common DNA element.

Miyatake¹,

Seiki²,

Yoshida³

et al. 1988

Mol. Cell. Biol.

141

106

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Activation of T cells by an antigen, a mitogen, or a combination of a phorbol ester ) and a calcium ionophore (A23187) leads to induction of a set of lymphokine genes. Treatment of human T-cell leukemia line Jurkat by a mitogen or p4OX, a transactivator protein encoded by human T-cell leukemia virus type I, activates many transfected lymphokine genes in a transient transfection assay. To study the mechanism of lymphokine gene induction, we examined the effects of mitogen stimulation and p4OX on the gene for the mouse granulocyte-macrophage colony-stimulating factor (GM-CSF) in Jurkat cells. Deletion and mutation analyses showed that the 5'-flanking region of the gene for the GM-CSF is composed of two types of regulatory elements. One sequence, located at positions -95 to -73, determines response to stimulation by either TPA-A23187 or p4OX. This region contains conserved lymphokine element 2, which appears in the gene for interleukin 3 (IL-3) and is followed by a GC-rich stretch. This GC-rich stretch alone specifies inducible response to p4oX but not to TPA-A23187. Another sequence, located at positions -113 to -96 upstream of a TATA-like sequence, mediates inducible response to p49X but not to TPA-A23187. This sequence includes conserved lymphokine element 1, which appears in several lymphokine-cytokine genes, such as those for IL-3, G-CSF, and IL-2. We previously showed that the simian virus 40 early region promoter was also induced by a mitogen or p4OX in Jurkat cells. Deletion analysis showed that the minimum regions required for stimulation by both signals are identical. These results, which indicate that p40X stimulates transcription of the gene for the GM-CSF or the simian virus 40 early region promoter through the same DNA element or an overlapping DNA element required for induction by a mitogen, lend further support to the notion that p4,X can exert its function by activating a component(s) of the T-cell signal transduction pathway which is activated by an antigen or a mitogen.Expression of many eucaryotic genes is regulated by hormones, growth factors, or other stimuli that interact with specific receptors to induce various intracellular processes.Activation of protein kinase C and increase of Ca"+ mobilization are used as signal transduction processes in many different types of cells (2, 26). When T cells are exposed to antigens, the T-cell antigen receptor-CD3 complex transduces the extracellular stimulus across the plasma membrane, generating intracellular signals. These signals activate phosphoinositide turnover, leading to production of diacylglycerol, which activates protein kinase C, and inositol trisphosphate, which results in increased Ca 2 mobilization or influx or both (42). Signal transduction events further downstream trigger a series of biochemical reactions in the nucleus which result in production of a battery of lymphokines. These can then mediate numerous effector functions to help coordinate the immune and inflammatory responses (20). Nuclear oncogenes, such as c-fos and c-myc, and th...

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“…The pattern of G-methylation interference observed with complex IV showed protein-DNA contacts at a nucleotide sequence (-659 to -649) that corresponds to a consensus found in the upstream region of several lymphokines and cytokines (33) and for this reason is called cytokine 1 (CK-1). Formation of this complex was prevented by an oligonucleotide containing the CK-1 but not the KB motif (32a).…”

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confidence: 99%

Regulation of tumor necrosis factor alpha transcription in macrophages: involvement of four kappa B-like motifs and of constitutive and inducible forms of NF-kappa B.

Collart¹,

Baeuerle²,

Vassalli³

1990

Mol. Cell. Biol.

835

509

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This study characterizes the interaction of murine macrophage nuclear proteins with the tumor necrosis factor alpha (TNF-a) promoter. Gel retardation and methylation interference assays showed that stimulation of TNF-aL gene transcription in peritoneal exudate macrophages was accompanied by induction of DNAbinding proteins that recognized with different affinities four elements related to the KB consensus motif and a Y-box motif. We suggest that the basal level of TNF-a expression in macrophages is due to the binding of a constitutive form of NF-KB, present at low levels in nuclei from resting thioglycolate exudate peritoneal macrophages, to some if not all of the KB motifs; we postulate that this constitutive form contains only the 50-kilodalton (kDa) DNA-binding protein subunits of NF-KB, not the 65-kDa protein subunits (P. Baeuerle and D. Baltimore, Genes Dev. 3:1689-1698). Agents such as glucocorticoids, which decrease TNF-c transcription, diminished the basal level of nuclear NF-KB. Stimulation of TNF-a transcription in macrophages by lipopolysaccharide, gamma interferon, or cycloheximide led to an increased content of nuclear NF-KB. This induced factor represents a different form of NF-KB, since it generated protein-DNA complexes of slower mobility; we propose that this induced form of NF-KB contains both the 50-and 65-kDa protein subunits, the latter ones being necessary to bind NF-KB to its cytoplasmic inhibitor in uninduced cells (Baeuerle and Baltimore, Genes Dev., 1989). In resting cells, this inducible form of NF-KB was indeed detectable in the cytosol after deoxycholate treatment. UV cross-linking experiments and gel retardation assays indicated that the inducible form of NF-KB is in a higher-order complex with other proteins.

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Nuclear proteins interacting with the promoter region of the human granulocyte/macrophage colony-stimulating factor gene.

Cited by 114 publications

References 33 publications

Overgrowth of human synovial cells driven by the human T cell leukemia virus type I tax gene.

Overgrowth of human synovial cells driven by the human T cell leukemia virus type I tax gene.

T-cell activation signals and human T-cell leukemia virus type I-encoded p40x protein activate the mouse granulocyte-macrophage colony-stimulating factor gene through a common DNA element.

Regulation of tumor necrosis factor alpha transcription in macrophages: involvement of four kappa B-like motifs and of constitutive and inducible forms of NF-kappa B.

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