Isolation and assay of red-cell inositol polyphosphates

Bartlett, Grant R.

doi:10.1016/0003-2697(82)90060-4

Cited by 35 publications

(13 citation statements)

References 18 publications

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“…The analysis of the phosphate chromatograms obtained for samples showed differences among the profiles. In both the seasons ADP was at levels, similar to described by other authors in other species of birds (Issacks et al 1976a;Issacks et al 1976b;Issacks et al 1976c;Bartlett 1982c). However, the most interesting was the presence of GTP in the winter and its absence in the summer.…”

Section: Discussionsupporting

confidence: 87%

Intraerythrocytic organic phosphates and hemoglobins of skua - Catharacta maccormicki (Stercoraridae): at two different stages of the year in relation to Antartic migration

Landini

Neto

Schwantes

et al. 2013

Braz. arch. biol. technol.

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Section: Discussionsupporting

confidence: 87%

Intraerythrocytic organic phosphates and hemoglobins of skua - Catharacta maccormicki (Stercoraridae): at two different stages of the year in relation to Antartic migration

Landini

Neto

Schwantes

et al. 2013

Braz. arch. biol. technol.

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“…lnositol phosphates were measured by the method o f Berridge et al (1983) with the exception that a perchloric acid stop solution was used to extract water-soluble inositol phosphates from the cells (Bartlett, 1982). Cells were incubated in medium with serum as described above containing 5-10 pCi/ml of ['Hlinositol at 37°C for approximately 24 h. We have labeled cells for 48 h or in inositol-free RPMI with similar results.…”

Section: Inositol Phosphate Measurementsmentioning

confidence: 83%

Nerve Growth Factor Potentiates Bradykinin‐Induced Calcium Influx and Release in PC12 Cells

Bush

Borden

Greene

et al. 1991

Journal of Neurochemistry

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To investigate how the response to agonists changes during neuronal differentiation, we examined the effect of nerve growth factor (NGF) on bradykinin-induced calcium increases in PC12 cells. Short-term (1 h) treatment with NGF increased the potency of bradykinin to raise intracellular calcium by about 10-fold, whereas long-term (1 week) treatment, which was associated with the expression of the differentiated phenotype, increased the potency about 100-fold. Neither treatment affected the maximal response to bradykinin. NGF alone had no acute effect on calcium levels. Short-term potentiation appeared to be mainly a result of greater release of calcium from intracellular stores, whereas the effect of long-term treatment apparently was due to increases in both release from intracellular stores and calcium influx. [3H]Bradykinin binding to intact PC12 cells was unaltered by short-term NGF treatment, whereas differentiated cells displayed a 50% increase in receptor number and about a twofold increase in affinity as compared with cells not treated with NGF. The production of inositol phosphates in response to bradykinin correlated poorly with the calcium transients, in that large calcium responses were associated with small increases in inositol phosphates. Neither NGF treatment had a significant effect on the appearance of inositol phosphates in response to bradykinin. Experiments with permeabilized cells revealed that differentiated cells did not display a heightened response to exogenously added inositol 1,4,5-trisphosphate. Our results demonstrate that NGF modulates the bradykinin signaling pathway without acutely activating this pathway itself.

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“…Higher-order inositol phosphates have been described in several systems. InsP5 has been described in avian erythrocytes (27), where it serves to alter the oxygen-hemoglobin dissociation curve in much the same way that 2,3-diphosphoglycerate does in mammalian erythrocytes (28). InsP6 or phytic acid is a prominent component of plant seeds (29).…”

Section: Discussionmentioning

confidence: 99%

Perturbation of the human T-cell antigen receptor-T3 complex leads to the production of inositol tetrakisphosphate: evidence for conversion from inositol trisphosphate.

Stewart¹,

Prpić²,

Powers³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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Antibodies directed against the T-cell antigen receptor-T3 complex mimic antigen and lead to cellular changes consistent with activation. When cells of the human T-cell line Jurkat were stimulated with a monoclonal antibody directed against T3, inositol phosphates were produced. In addition to inositol trisphosphate, which is the product of phosphatidylinositol bisphosphate cleavage, a second inositol polyphosphate was formed. This compound was more polar than inositol trisphosphate but less polar than inositol pentakisphosphate. It cochromatographed with inositol tetrakisphosphate from ostrich erythrocytes. In permeabilized Jurkat cells, this compound was shown to be formed from inositol 1,4,5-trisphosphate, but only in the presence of ATP, and 32p was incorporated into it from [y-32P]ATP. There also was coincident formation of inositol 1,3,4-trisphosphate. We conclude that the more polar compound is inositol tetrakisphosphate, which is formed by phosphorylation of inositol 1,4,5-trisphosphate and may be the precursor of inositol 1,3,4-trisphosphate.Activation of several receptor-mediated cellular systems has been shown to be calcium dependent and mediated by breakdown products of polyphosphate derivatives of phosphatidylinositol (1-6). In these systems, stimulation of the relevant receptor leads to phosphodiesterase (phospholipase C)-catalyzed cleavage of phosphatidylinositol bisphosphate to inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and 1,2-diacylglycerol (4, 5). In turn, Ins(1,4,5)P3 and diacylglycerol act as second messengers to release intracellular stores of calcium and activate protein kinase C (6), respectively. Antibodies directed against the T-lymphocyte receptor for nominal antigen or its closely associated structure, T3 (Leu-4) have been shown to mimic antigen (7) and lead to changes characteristic of activation. These changes include production of lymphokines (8) and interleukin-2 receptors (9) and proliferation (10, 11). In a series of papers (12-14), Stobo and colleagues have shown that perturbation of the T-cell receptor-T3 complex on cells of the human T-cell leukemia line Jurkat leads to production of inositol phosphates (14) and rapid increases in intracellular calcium concentration (12,13). Furthermore, in studies using permeabilized Jurkat cells, they have demonstrated that addition of inositol trisphosphate causes release of calcium from iniracellular stores (14).We report here that perturbation of the T-cell antigen receptor-T3 complex with a monoclonal antibody leads to the production of not only Ins(1,4,5)P3, but also a second inositol polyphosphate. We present evidence that this compound isThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. inositol tetrakisphosphate (InsP4). Furthermore, we present evidence that it is generated by the ATP-dependent phosphorylation of Ins(1,4,5)P3. MATERIALS AND METHODSCells and Antibo...

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Isolation and assay of red-cell inositol polyphosphates

Cited by 35 publications

References 18 publications

Intraerythrocytic organic phosphates and hemoglobins of skua - Catharacta maccormicki (Stercoraridae): at two different stages of the year in relation to Antartic migration

Intraerythrocytic organic phosphates and hemoglobins of skua - Catharacta maccormicki (Stercoraridae): at two different stages of the year in relation to Antartic migration

Nerve Growth Factor Potentiates Bradykinin‐Induced Calcium Influx and Release in PC12 Cells

Perturbation of the human T-cell antigen receptor-T3 complex leads to the production of inositol tetrakisphosphate: evidence for conversion from inositol trisphosphate.

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