Calcium‐activated, phospholipid‐dependent protein kinase activity and protein phosphorylation in HL60 cells induced to differentiate by retinoic acid

Durham, John P.; Emler, Carol A.; Butcher, Fred R.; Fontana, Joseph A.

doi:10.1016/0014-5793(85)80761-4

Cited by 35 publications

(15 citation statements)

References 13 publications

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“…This membrane-bound kinase, originally identifled in brain (82) is widely distributed in cells, appears to be the target for the tumor promoting phorbol esters, and is important in the control of signal transduction and tumor differentiation (83). In myeloid precursors, there is a stimulation of PKC enzyme activity and phosphorylation of its various substrates correlating with RA-induced differentiation (81) occurring prior to the commitment of the cells to the myeloid pathway (84). In contrast, embryonal carcinoma cells exhibit an increase in PKC activity that accompanies but does not precede differentiation (85), suggesting that in the latter system, these effects may be a consequence rather than a cause of differentiation.…”

Section: Ra and Protein Kinase Activitymentioning

confidence: 99%

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Abemayor¹,

Sidell²

1989

Environ Health Perspect

143

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Neuroblastoma is a childhood solid tumor composed of primitive cells derived from precursors of the autonomic nervous system. This neoplasm has the highest rate of spontaneous regression of all cancer types and has been noted to undergo spontaneous and chemically induced differentiation into elements resembling mature nervous tissue. As such, neuroblastoma has been a prime model system for the study of neuronal differentiation and the process of cancer cell maturation. In this paper we review those agents that have been described to induce the differentiation of neuroblastoma, with an emphasis on the effects and possible mechanisms of action of a group of related compounds, the retinoids. With this model system and the availability of subclones that are both responsive and resistant to chemically induced differentiation, fundamental questions regarding the mechanisms and processes underlying cell maturation have become more amenable to in vitro study.

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Section: Ra and Protein Kinase Activitymentioning

confidence: 99%

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Abemayor¹,

Sidell²

1989

Environ Health Perspect

143

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“…Thus, PKC and PKA regulate a variety of developmental and mature neuronal and nonneuronal processes. Additional studies demonstrated differentiation-specific alterations in PKC and PKA activities (Abraham et al, 1991;Durham et al, 1985;Fontana et al, 1984;Kraft and Anderson, 1993;Plet et al, 1985Plet et al, , 1986Plet et al, , 1987Wooten et al, 1992). These data suggest that alterations in PKC and PKA activities are associated with the development of the mature cellular phenotype.…”

Section: Introductionmentioning

confidence: 83%

Protein kinase C and cAMP-dependent protein kinase regulate the neuronal differentiation of immortalized raphe neurons

Rind

Whittemore

1999

J. Neurosci. Res.

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These studies examined the extent to which protein kinase C (PKC) and cAMP-dependent protein kinase (PKA) regulate the neuronal differentiation of the raphe-derived neuronal cell line, RN33B. A differentiation-specific 2.25-fold increase in soluble PKA activity was observed. Neither membrane-associated-PKA, -PKC, or soluble PKC activities changed concomitant with differentiation. The PKC activity was derived from PKC alpha, gamma, epsilon, and theta isoenzymes. Activation of PKC inhibited the immunocytochemical expression of low and medium molecular weight neurofilament proteins, an effect due at least in part to decreased steady-state levels of protein. PKC activation also decreased glutamate immunoreactivity and increased cell number, protein synthesis, and bromodeoxyuridine uptake by 2.4-fold, 25%, and 32%, respectively. Coupled with the decrease in mature neuronal antigen expression, these data suggest that PKC activation inhibits neuronal differentiation by inducing proliferation. Inhibition of PKC markedly upregulated glutamate immunoreactivity. PKA activation potentiated the glutamatergic phenotype of RN33B cells, but inhibition of PKA was without effect on the expression of all neuronal antigens examined. Thus, both PKC and PKA regulate the differentiation of RN33B cells, although neither is absolutely necessary for expression of the differentiated neuronal phenotype. These results suggest the existence of parallel pathways regulating raphe neuronal differentiation.

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“…Granulocytic differentiation is a complex multistep process, involving irreversible changes in gene expression, which implies that many differentiation-inducing signal pathways terminate the nucleus. Modifications of protein kinase C activity in the process of retinoic acid-induced differentiation of HL-60 have been described by several authors (Zylber-Katz & Glazer, 1985;Durham et al, 1985;Makowske et al, 1988;Hashimoto et al, 1990;Devalia et al, 1992;Seibenhener & Wooten, 1992;Yat-Ming Yung & Ka-Way Hi, 1993;Yang et al, 1994). However, some discrepancies exist among these studies on the modifications of the PKC catalytic activity induced by ATRA as well as on its relative contribution to differentiation of the various PKC isoforms.…”

Section: Retinoids Induce Terminal Differentiation Of Blast Cells In mentioning

confidence: 97%

Nuclear translocation of protein kinase C‐α and ‐ζ isoforms in HL‐60 cells induced to differentiate along the granulocytic lineage by all‐trans retinoic acid

et al. 1996

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We investigated whether members of the protein kinase C (PKC) family of enzymes were involved in the nuclear events underlying granulocytic differentiation induced by 10(-6) M all-trans retinoic acid (ATRA) in HL-60 cells. PKC activity was analysed by using a serine substituted specific peptide which enabled the evaluation of the whole catalytic activity of both Ca2+ -dependent and Ca2+ -independent PKC isoforms. In parallel, the subcellular distribution of various PKC isoforms was evaluated by Western blot, immunoprecipitation and in situ immunocytochemistry analyses. The level of PKC catalytic activity in the nuclei of HL-60 cells significantly (P < 0.01) and progressively increased from 1 h of ATRA treatment onwards. Consistently, PKC-alpha and -zeta showed a striking and selective accumulation inside the nucleus upon treatment with ATRA. On the other hand, PKC-beta I and -beta II, the only two other isoforms present at nuclear level, did not show any significant modification upon ATRA treatment. The remaining PKC isoforms were not detectable inside the nucleus and showed only modest and non-significant variations, also in whole cell homogenates, upon ATRA treatment, except PKC-delta which showed a progressive down-regulation. Our data suggest that a selective nuclear translocation of PKC-alpha and -zeta might be involved in the process of granulocytic differentiation induced by ATRA in HL-60 cells.

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Calcium‐activated, phospholipid‐dependent protein kinase activity and protein phosphorylation in HL60 cells induced to differentiate by retinoic acid

Cited by 35 publications

References 13 publications

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Protein kinase C and cAMP-dependent protein kinase regulate the neuronal differentiation of immortalized raphe neurons

Nuclear translocation of protein kinase C‐α and ‐ζ isoforms in HL‐60 cells induced to differentiate along the granulocytic lineage by all‐trans retinoic acid

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