Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis.

James Murray

Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis.

James Murray

Research output: Contribution to journal › Article › peer-review

Original language	English
Pages (from-to)	610-618
Number of pages	9
Journal	Inflammation research : official journal of the European Histamine Research Society ... [et al.]
Volume	49(11)
Issue number	11
Publication status	Published - 2000

ASJC Scopus subject areas

Toxicology
Pharmacology (medical)
Immunology
Cell Biology

Cite this

Murray, J. (2000). Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis. Inflammation research : official journal of the European Histamine Research Society ... [et al.], 49(11)(11), 610-618.

Murray, James. / Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis. In: Inflammation research : official journal of the European Histamine Research Society ... [et al.]. 2000 ; Vol. 49(11), No. 11. pp. 610-618.

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title = "Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis.",

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volume = "49(11)",

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Murray, J 2000, 'Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis.', Inflammation research : official journal of the European Histamine Research Society ... [et al.], vol. 49(11), no. 11, pp. 610-618.

Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis. / Murray, James.
In: Inflammation research : official journal of the European Histamine Research Society ... [et al.], Vol. 49(11), No. 11, 2000, p. 610-618.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis.

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M3 - Article

C2 - 11131301

VL - 49(11)

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EP - 618

JO - Inflammation research : official journal of the European Histamine Research Society ... [et al.]

JF - Inflammation research : official journal of the European Histamine Research Society ... [et al.]

IS - 11

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Mechanism of phosphatidylinositol 3-kinase-dependent increases in BAC1.2F5 macrophage-like cell density in response to M-CSF: phosphatidylinositol 3-kinase inhibitors increase the rate of apoptosis rather than inhibit DNA synthesis.

ASJC Scopus subject areas

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