HL60 Cells Halted in G1 or S Phase Differentiate Normally

Brown, Geoffrey; Drayson, Mark T.; Durham, Jennifer N.; Toellner, Kai‐Michael; Hughes, Philip; Choudhry, M. A.; Taylor, D.L.; Bird, Roger; Michell, Robert H.

doi:10.1006/excr.2002.5654

Cited by 29 publications

(21 citation statements)

References 39 publications

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“…It is intriguing that 32D IGF-IR cells expressing PES1 and UBF1 remain very large even when differentiated. Brown et al (5) reported that HL60 cells halted in G 1 or S phase differentiate normally. Morphological analysis of size in differentiated cells (6 days after a shift to IGF-I) was confirmed by FACS analysis (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Role of Pescadillo and Upstream Binding Factor in the Proliferation and Differentiation of Murine Myeloid Cells

Prisco

Maiorana

Guerzoni

et al. 2004

Molecular and Cellular Biology

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Section: Discussionmentioning

confidence: 99%

Role of Pescadillo and Upstream Binding Factor in the Proliferation and Differentiation of Murine Myeloid Cells

Prisco

Maiorana

Guerzoni

et al. 2004

Molecular and Cellular Biology

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“…Since both early embryonic and iPS cells are rapidly proliferating, a significant question is whether differentiation per se affects APA in a system where proliferation and differentiation could be uncoupled. For example, the leukemic cell line HL60 is capable of differentiating into neutrophils or monocytes (in response to different stimuli) even when the cell cycle is blocked in early G1 or S phase, indicating that differentiation and proliferation can be regulated independently (Brown et al, 2002). It would be of interest to compare changes in usage of APA sites before and after differentiation, independently from alterations in the proliferation rate.…”

Section: Genome-wide Analyses Of Apamentioning

confidence: 99%

Mechanisms and Consequences of Alternative Polyadenylation

2011

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Summary Alternative polyadenylation (APA) is emerging as a widespread mechanism used to control gene expression. Like alternative splicing, usage of alternative poly(A) sites allows a single gene to encode multiple mRNA transcripts. In some cases, this changes the mRNA coding potential; in other cases, the code remains unchanged but the 3’UTR length is altered, influencing the fate of mRNAs in several ways, for example, by altering the availability of RNA binding protein sites and microRNA binding sites. The mechansims governing both global and gene-specific APA are only starting to be deciphered. Here we review what is known about these mechanisms and the functional consequences of alternative polyadenlyation.

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“…In hemopoietic cell lines, the induction of differentiation is often preceded by a period of vigorous cell proliferation (1,14,15). It has been hypothesized that in hemopoietic cells, like 32D myeloid cells, sustained cell proliferation requires not only stimulation of cell growth, but also the extinction of a differentiation program.…”

Section: Cells Are Murine Myeloid Cells That Depend Onmentioning

confidence: 99%

Deletion of the Pleckstrin and Phosphotyrosine Binding Domains of Insulin Receptor Substrate-2 Does Not Impair Its Ability to Regulate Cell Proliferation in Myeloid Cells

Sun

Baserga

2004

Endocrinology

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32D IGF-I receptor (IR) cells are IL-3-dependent myeloid cells that can be induced to differentiate into granulocytes by IGF-I. Like the parental 32D cells, 32D IGF-IR cells do not express the insulin receptor substrate (IRS)-1 or IRS-2. We investigated the effect of ectopic expression of IRS-2 in 32D IGF-IR cells. Expression in these cells of a wild-type IRS-2 inhibits IGF-I-induced differentiation, and the cells grow indefinitely in the absence of IL-3. We also investigated the effect of a mutant IRS-2 lacking both the pleckstrin (PH) and the phosphotyrosine-binding (PTB) domains, which are known to bind to the IR. The partial differentialPHPTB IRS-2 is fully as capable as the wild-type IRS-2 (and wild-type IRS-1) to stimulate the growth and inhibit the differentiation of 32D IGF-IR cells. In contrast, an IRS-1 protein lacking the same PH and PTB domains is completely inactive in blocking differentiation and stimulating IL-3-independent growth of 32D IGF-IR cells. The partial differentialPHPTB IRS-2 protein is dependent for its effect on an activated IGF-IR, is cytoplasmic, binds to the beta-subunit of the IGF-IR, and requires for its action the presence of phosphatidylinositol 3-kinase binding sequences. These experiments show that the PH and PTB domains of IRS-2 (but not IRS-1) are dispensable for the IGF-I/IRS-2-mediated growth of 32D myeloid cells. Our results also indicate that IRS-2 (either wild type or partial differentialPHPTB) is capable of inhibiting the differentiation of 32D cells.

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HL60 Cells Halted in G1 or S Phase Differentiate Normally

Cited by 29 publications

References 39 publications

Role of Pescadillo and Upstream Binding Factor in the Proliferation and Differentiation of Murine Myeloid Cells

Role of Pescadillo and Upstream Binding Factor in the Proliferation and Differentiation of Murine Myeloid Cells

Mechanisms and Consequences of Alternative Polyadenylation

Deletion of the Pleckstrin and Phosphotyrosine Binding Domains of Insulin Receptor Substrate-2 Does Not Impair Its Ability to Regulate Cell Proliferation in Myeloid Cells

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