Efficient in vitro and in vivo gene regulation of a retrovirally delivered pro-apoptotic factor under the control of the Drosophila HSP70 promoter

Romano, Gaetano; Reiss, Krzysztof; Tu, Xiao; Peruzzi, Francesca; Belletti, Barbara; Wang, J Y; Zanocco-Marani, Tommaso; Baserga, Renato

doi:10.1038/sj.gt.3301441

Cited by 14 publications

(10 citation statements)

References 24 publications

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“…The difference in IRS-1 expression is also not crucial. When single cell clones are generated from mixed populations, the levels of expression of IRS-1 vary greatly from one clone to another (45), yet all clones grow equally well. In fact, even low levels of IRS-1 expression can make 32D IGF-IR cells tumorigenic in mice (30).…”

Section: Cell Linesmentioning

confidence: 99%

Signaling Differences from the A and B Isoforms of the Insulin Receptor (IR) in 32D Cells in the Presence or Absence of IR Substrate-1

Sciacca

Prisco

et al. 2003

Endocrinology

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The A isoform of the insulin receptor (IR) is frequently overexpressed in cancer cells and is activated by IGF-II as well as by insulin, whereas the B isoform is predominant in differentiated tissues and responds poorly to IGF-II. The IR substrate-1 (IRS-1), a docking protein for the IR, is known to send a mitogenic signal and to be a powerful inhibitor of cell differentiation. We have investigated the biological effects of the two IR isoforms in parental 32D hemopoietic cells, which do not express IRS-1, and in 32D-derived cells in which IRS-1 is ectopically expressed. The effects of the two isoforms on cell survival, differentiation markers and nuclear translocation of IRS-1 were compared. The results confirm that the A isoform responds to IGF-II and preferentially sends mitogenic, antiapoptotic signals, whereas the B form, poorly responsive to IGF-II, tends to send differentiation signals.

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Section: Cell Linesmentioning

confidence: 99%

Signaling Differences from the A and B Isoforms of the Insulin Receptor (IR) in 32D Cells in the Presence or Absence of IR Substrate-1

Sciacca

Prisco

et al. 2003

Endocrinology

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“…The feasibility of the approach has been demonstrated both in vitro [25][26][27] and in vivo [28] for the expression of suicide genes in implanted mammary cancer cell lines after targeting by HVJ-anionic liposomes [29], and the expression of a reporter gene in implanted C6 cells [30]. This promoter is strongly induced in heat-shocked cells, and is already used in other studies, with liposomes [29] or viral constructions [25,31,32].…”

Section: Introductionmentioning

confidence: 98%

Spatial and temporal control of transgene expression in vivo using a heat‐sensitive promoter and MRI‐guided focused ultrasound

Guilhon

Voisin

Zwart

et al. 2002

The Journal of Gene Medicine

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“…The self-inactivating form of MSCV retroviral vector was generated as described elsewhere (26). The various mutants of IRS-1 were generated by site-directed mutagenesis, as previously described (24,27). The mutants thus generated are described in Results.…”

Section: Materials and Methods Plasmidsmentioning

confidence: 99%

Regulation of Id2 Gene Expression by the Type 1 IGF Receptor and the Insulin Receptor Substrate-1

et al. 2001

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The Id family of helix-loop-helix proteins is known to be involved in the proliferation and differentiation of several types of cells. The type 1 IGF receptor (IGF-IR) induces either proliferation or differentiation in 32D cells, a murine hemopoietic cell line, depending on the availability of the appropriate substrates for the receptor. We have previously reported that the IGF-IR regulates the expression of the Id2 gene in 32D cells. We now show that the IGF-IR controls the increase in Id2 gene expression through at least three pathways. These three pathways originate from the tyrosine residue at 950, a domain in the C-terminus, and the activation of the insulin receptor substrate-1 (IRS-1) by the receptor. IRS-1 is the preponderant signal, and its effect on Id2 gene expression requires a functional phosphotyrosine binding domain. With wild-type IRS-1, Id2 gene expression is increased, even in those cells that express IGF-I receptors defective in Id2 signaling. Rapamycin, an inhibitor of p70(S6K), a downstream effector of IRS-1 signaling, partially inhibits (but does not completely abrogate) the increase in Id2 gene expression. A mutant IRS-1 with a deletion of the Pleckstrin domain is as effective as wild-type IRS-1 in up-regulating Id2 gene expression. In addition, it seems to increase the stability of p70(S6K). Our results indicate that the IGF-IR regulates Id2 gene expression through different pathways. At least in 32D cells, increased Id2 gene expression seems to correlate more with inhibition of differentiation than with proliferation.

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Efficient in vitro and in vivo gene regulation of a retrovirally delivered pro-apoptotic factor under the control of the Drosophila HSP70 promoter

Cited by 14 publications

References 24 publications

Signaling Differences from the A and B Isoforms of the Insulin Receptor (IR) in 32D Cells in the Presence or Absence of IR Substrate-1

Signaling Differences from the A and B Isoforms of the Insulin Receptor (IR) in 32D Cells in the Presence or Absence of IR Substrate-1

Spatial and temporal control of transgene expression in vivo using a heat‐sensitive promoter and MRI‐guided focused ultrasound

Regulation of Id2 Gene Expression by the Type 1 IGF Receptor and the Insulin Receptor Substrate-1

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