Relevant bibliographies by topics / Phosphatidylinositol 3-Kinases

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Phosphatidylinositol 3-Kinases'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 June 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Phosphatidylinositol 3-Kinases.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Phosphatidylinositol 3-Kinases"

1

Abraham, Robert T. "Phosphatidylinositol 3-kinase related kinases." Current Opinion in Immunology 8, no. 3 (June 1996): 412–18. http://dx.doi.org/10.1016/s0952-7915(96)80132-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Suzuki, Takahiro, Osamu Hazeki, and Michio Ui. "Phosphatidylinositol 3-Kinases." membrane 21, no. 3 (1996): 158–64. http://dx.doi.org/10.5360/membrane.21.158.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Muftuoglu, Yagmur, Yi Xue, Xiang Gao, Dianqing Wu, and Ya Ha. "Mechanism of substrate specificity of phosphatidylinositol phosphate kinases." Proceedings of the National Academy of Sciences 113, no. 31 (July 20, 2016): 8711–16. http://dx.doi.org/10.1073/pnas.1522112113.

Full text
Abstract:
The phosphatidylinositol phosphate kinase (PIPK) family of enzymes is primarily responsible for converting singly phosphorylated phosphatidylinositol derivatives to phosphatidylinositol bisphosphates. As such, these kinases are central to many signaling and membrane trafficking processes in the eukaryotic cell. The three types of phosphatidylinositol phosphate kinases are homologous in sequence but differ in catalytic activities and biological functions. Type I and type II kinases generate phosphatidylinositol 4,5-bisphosphate from phosphatidylinositol 4-phosphate and phosphatidylinositol 5-phosphate, respectively, whereas the type III kinase produces phosphatidylinositol 3,5-bisphosphate from phosphatidylinositol 3-phosphate. Based on crystallographic analysis of the zebrafish type I kinase PIP5Kα, we identified a structural motif unique to the kinase family that serves to recognize the monophosphate on the substrate. Our data indicate that the complex pattern of substrate recognition and phosphorylation results from the interplay between the monophosphate binding site and the specificity loop: the specificity loop functions to recognize different orientations of the inositol ring, whereas residues flanking the phosphate binding Arg244 determine whether phosphatidylinositol 3-phosphate is exclusively bound and phosphorylated at the 5-position. This work provides a thorough picture of how PIPKs achieve their exquisite substrate specificity.
APA, Harvard, Vancouver, ISO, and other styles
4

Rane, M. J., S. L. Carrithers, J. M. Arthur, J. B. Klein, and K. R. McLeish. "Formyl peptide receptors are coupled to multiple mitogen-activated protein kinase cascades by distinct signal transduction pathways: role in activation of reduced nicotinamide adenine dinucleotide oxidase." Journal of Immunology 159, no. 10 (November 15, 1997): 5070–78. http://dx.doi.org/10.4049/jimmunol.159.10.5070.

Full text
Abstract:
Abstract Formyl peptide receptor activation of three mitogen-activated protein kinase (MAPK) cascades, extracellular signal-regulated kinases (ERKs), N-terminal kinases (JNKs), and p38 MAPK was examined in differentiated HL-60 granulocytes. FMLP stimulated a concentration- and time-dependent increase in ERK, JNK, and p38 MAPK activities, all of which were dependent on a pertussis toxin-sensitive G protein. Pharmacologic inhibitors were used to examine the roles of tyrosine kinases, phosphatidylinositol 3-kinase, protein kinase C, and phospholipase C. FMLP-stimulated ERK activity was dependent on tyrosine kinases, phosphatidylinositol 3-kinase, protein kinase C, and phospholipase C; p38 MAPK activation was dependent on phosphatidylinositol 3-kinase and phospholipase C; while JNK activation was independent of all of these signaling components. The mitogen-activated protein kinase/ERK kinase inhibitor PD098059 reduced ERK activation by 90%, while an inhibitor of p38 MAPK, SB203580, inhibited p38 MAPK activation by 80%. Both PD098059 and SB203580 inhibited FMLP-stimulated superoxide release, as did inhibitors directed against protein kinase C, tyrosine kinases, and phosphatidylinositol 3-kinase. We conclude that formyl peptide receptors are coupled to three MAPK cascades by Gi proteins. ERKs, p38 MAPK, and JNKs are each activated by distinct proximal signal transduction pathways. Activation of p38 MAPK is necessary for FMLP stimulation of respiratory burst activity; however, a second signal that may involve ERK is also required for this activity.
APA, Harvard, Vancouver, ISO, and other styles
5

Roymans, Dirk, and Herman Slegers. "Phosphatidylinositol 3-kinases in tumor progression." European Journal of Biochemistry 268, no. 3 (February 2001): 487–98. http://dx.doi.org/10.1046/j.1432-1327.2001.01936.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Imseng, Stefan, Christopher HS Aylett, and Timm Maier. "Architecture and activation of phosphatidylinositol 3-kinase related kinases." Current Opinion in Structural Biology 49 (April 2018): 177–89. http://dx.doi.org/10.1016/j.sbi.2018.03.010.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Shibasaki, F., Y. Fukui, and T. Takenawa. "Different properties of monomer and heterodimer forms of phosphatidylinositol 3-kinases." Biochemical Journal 289, no. 1 (January 1, 1993): 227–31. http://dx.doi.org/10.1042/bj2890227.

Full text
Abstract:
Phosphatidylinositol (PI) 3-kinase plays an important role in the signalling of cell growth. We previously purified two types of PI 3-kinase from bovine thymus, a monomer from (PI 3-kinase I) and a heterodimer form (PI 3-kinase II) [Shibasaki, Homma and Takenawa (1991) J. Biol. Chem. 266, 8108-8114]. Here we examine the properties of these purified PI 3-kinases. Both PI 3-kinases were inhibited strongly by quercetin and isoquercetin. The inhibition of PI 3-kinase I and PI 3-kinase II by quercetin appears to be non-competitive, with apparent Ki values of 4 microM and 2.5 microM respectively. PI 3-kinase II, but not PI 3-kinase I, co-immunoprecipitates with pp60v-src and polyoma middle T (mT)/pp60c-src, even under conditions where the PI 3-kinases are not phosphorylated, suggesting that non-phosphorylated PI 3-kinase recognizes autophosphorylated pp60v-src. PI 3-kinase II is phosphorylated by pp60v-src and binds to it. Anti-p85 (85 kDa subunit of PI 3-kinase II) antibody precipitates not only PI 3-kinase II but also co-immunoprecipitates pp60v-src in src-transformed cells, suggesting that PI 3-kinase II binds to pp60v-src in vivo. These data suggest that the two PI 3-kinases may be regulated independently.
APA, Harvard, Vancouver, ISO, and other styles
8

Yamboliev, Ilia A., Kevin M. Wiesmann, Cherie A. Singer, Jason C. Hedges, and William T. Gerthoffer. "Phosphatidylinositol 3-kinases regulate ERK and p38 MAP kinases in canine colonic smooth muscle." American Journal of Physiology-Cell Physiology 279, no. 2 (August 1, 2000): C352—C360. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c352.

Full text
Abstract:
In canine colon, M2/M3 muscarinic receptors are coupled to extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein (MAP) kinases. We tested the hypothesis that this coupling is mediated by enzymes of the phosphatidylinositol (PI) 3-kinase family. RT-PCR and Western blotting demonstrated expression of two isoforms, PI 3-kinase-α and PI 3-kinase-γ. Muscarinic stimulation of intact muscle strips (10 μM ACh) activated PI 3-kinase-γ, ERK and p38 MAP kinases, and MAP kinase-activated protein kinase-2, whereas PI 3-kinase-α activation was not detected. Wortmannin (25 μM) abolished the activation of PI 3-kinase-γ, ERK, and p38 MAP kinases. MAP kinase inhibition was a PI 3-kinase-γ-specific effect, since wortmannin did not inhibit recombinant activated murine ERK2 MAP kinase, protein kinase C, Raf-1, or MAP kinase kinase. In cultured muscle cells, newborn calf serum (3%) activated PI 3-kinase-α and PI 3-kinase-γ isoforms, ERK and p38 MAP kinases, and stimulated chemotactic cell migration. Using wortmannin and LY-294002 to inhibit PI 3-kinase activity and PD-098059 and SB-203580 to inhibit ERK and p38 MAP kinases, we established that these enzymes are functionally important for regulation of chemotactic migration of colonic myocytes.
APA, Harvard, Vancouver, ISO, and other styles
9

Choi, Suyong, Xander Houdek, and Richard A. Anderson. "Phosphoinositide 3-kinase pathways and autophagy require phosphatidylinositol phosphate kinases." Advances in Biological Regulation 68 (May 2018): 31–38. http://dx.doi.org/10.1016/j.jbior.2018.02.003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Christoforidis, Savvas, Marta Miaczynska, Keith Ashman, Matthias Wilm, Liyun Zhao, Shu-Chin Yip, Michael D. Waterfield, Jonathan M. Backer, and Marino Zerial. "Phosphatidylinositol-3-OH kinases are Rab5 effectors." Nature Cell Biology 1, no. 4 (July 15, 1999): 249–52. http://dx.doi.org/10.1038/12075.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Phosphatidylinositol 3-Kinases"

1

Valet, Colin. "Rôles de la PI3 kinase de classe II alpha et de la PI3K de classe III, vps34, dans la production et les fonctions plaquettaires." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30032.

Full text
Abstract:
Les mégacaryocytes sont des cellules de la moelle osseuse qui par un processus complexe et encore mal caractérisé, mégacaryopoïèse/thrombopoïèse, donnent naissance, in fine, aux plaquettes sanguines. La différenciation mégacaryocytaire nécessite un intense remodelage nucléaire et cytoplasmique, guidé à la fois par des facteurs intrinsèques mais aussi par des facteurs extrinsèques tel que le microenvironnement médullaire. Les plaquettes sanguines sont des acteurs essentiels du maintien de l'intégrité vasculaire. Elles sont les premiers éléments cellulaires à intervenir dans l'arrêt du saignement lors d'une blessure vasculaire par la formation d'un thrombus via des mécanismes d'adhésion, de sécrétion et d'agrégation, trois étapes majeures de l'hémostase physiologique. Dans un premier temps, mes travaux de thèse visent à déterminer le rôle inconnu de l'isoforme alpha des PI3Ks de classe II (PI3KC2a), de la PI3K de classe III (Vps34) et de leur produit, le phosphatidylinositol 3 monophosphate (PI3P), dans la production et les fonctions plaquettaires. Grâce à un modèle murin présentant une inactivation partielle de la PI3KC2a, j'ai mis en évidence son rôle clé dans la génération d'un pool basal de PI3P dans les plaquettes. L'inactivation de la PI3KC2a affecte la composition du cortex sous-membranaire plaquettaire induisant une morphologie plaquettaire anormale, une accumulation de plaquettes à deux corps appelées " barbell-shaped proplatelets ", un défaut de formation du thrombus ex vivo et un retard d'occlusion de la carotide après lésion in vivo. Ainsi, la PI3KC2a joue un rôle majeur dans le maintien de l'intégrité du squelette membranaire contrôlant la structure et la dynamique membranaire, processus critique à la production de plaquettes fonctionnelles. D'autre part, la délétion de Vps34 spécifiquement dans la lignée mégacaryocyte/plaquette se traduit par une microthrombopénie modérée associée à une migration anormale des mégacaryocytes liées à un défaut de trafic vésiculaire et une diminution du taux de PI3P. De façon intéressante, Vps34 joue aussi un rôle dans l'activation plaquettaire en régulant la production de PI3P sous stimulation, la croissance du thrombus ex vivo et les capacités thrombotiques in vivo. Le rôle de Vps34 dans la plaquette indépendamment de son rôle dans le mégacaryocyte a été confirmé via l'utilisation de nouveaux inhibiteurs spécifiques de Vps34, SAR405 et INH1, ex vivo. Vps34 est donc critique dans la régulation de la production plaquettaire par les mégacaryocytes ainsi que dans l'activation plaquettaire. Dans un deuxième temps, je me suis intéressé à l'impact du microenvironnement médullaire sur la mégacaryopoïèse, et plus spécifiquement sur la communication entre adipocytes médullaires et progéniteurs hématopoïétiques lors de leur différenciation en mégacaryocytes. Grace à un système de coculture in vitro, j'ai montré que les adipocytes améliorent la différenciation mégacaryocytaire via un transfert direct de lipides, dans un but non-énergétique. Dans un contexte d'obésité, nous observons, in vivo, associée à une adiposité médullaire augmentée une maturation mégacaryocytaire exacerbée, une production et une demi-vie plaquettaire défectueuses ayant pour conséquence une macrothrombopénie. Ainsi, le microenvironnement médullaire et plus particulièrement l'adipocyte impacte directement sur la mégacaryopoïèse et la production plaquettaire. En conclusion, ces travaux de thèse contribuent à caractériser les mécanismes de production et de fonction plaquettaire régulés par des facteurs intrinsèques tels que le PI3KC2a et Vps34, ainsi que par des facteurs extrinsèques tels que l'adipocyte médullaire
Megakaryopoiesis is a highly specialised and complex process occurring in the bone marrow, by which megakaryocytes give rise to de novo circulating blood platelets. Megakaryocyte differentiation implies cytoplasmic and nuclear rearrangements regulated by intrinsic as well as extrinsic factors such as bone marrow microenvironment. Platelets play a critical role in preventing blood loss after vascular injury by orchestrating clot formation through mechanisms of adhesion, secretion and aggregation. These mechanisms are the three major steps of physiological haemostasis leading to the maintenance of vascular integrity. Firstly, my thesis work focused on characterizing the role of class II PI3K alpha isoform (PI3KC2a), class III PI3K (Vps34) and their common product the phosphatidylinositol 3 monophosphate (PI3P) in platelet production and function. Using a unique mouse model partially inactivated for PI3KC2a, I highlighted its key role in the production of a basal PI3P housekeeping pool in platelets. PI3KC2a partial inactivation affects platelet membrane skeleton composition leading to an abnormal platelet morphology, an enrichment of platelet with two cell bodies recently called "barbell-shaped proplatelets", an ex vivo defective thrombus formation and an in vivo delayed carotid occlusion following injury. Thus, PI3KC2a plays a major role in membrane structure and dynamics by maintaining membrane skeleton integrity, which is crucial for functional platelet production. On the other hand, Vps34 specific deletion in megakaryocyte/platelet lineage induced mild microthombopenia correlated to an abnormal megakaryocyte migration linked to an affected PI3P production as well as vesicular trafficking in megakaryocytes. In platelets, Vps34 plays a role in their activation by regulating PI3P production under stimulation, ex vivo thrombus growth and in vivo thrombotic capacity. Vps34 role in platelet independently from its role in megakaryocyte was confirmed using two recently developed inhibitors, SAR405 and INH1, which reproduced ex vivo thrombus growth defects. Therefore, Vps34 is critical for platelet production by megakaryocyte as well as platelet activation. Secondly, I studied the impact of bone marrow microenvironment on megakaryopoiesis and more specifically the crosstalk between medullar adipocytes and hematopoietic progenitors differentiating towards the megakaryocyte lineage. Using an in vitro coculture assay, I demonstrated that adipocytes enhanced megakaryocyte differentiation through a direct lipid transfer, in a non-energetic aim. In the context of obesity, increased marrow adipocity is associated to enhanced megakaryocyte differentiation and defective platelet production and lifespan leading to macrothrombopenia. Thus, bone marrow microenvironment through adipocytes impact directly on megakaryopoiesis and platelet production. Altogether my thesis work contributes to better understand platelet production and function, mechanisms regulated by intrinsic factors such as PI3KC2a and Vps34 as well as extrinsic factors like medullar adipocytes
APA, Harvard, Vancouver, ISO, and other styles
2

Riojas, Ramon Alberto. "Characterization of PDK1 regulation and function in the insulin-stimulated PI3-kinase pathway : a dissertation /." San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1372010131&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Cox, Sian Sarah Eileen. "Characterisation of putative phosphatidylinositol-3 kinases in the parasitic protozoan giardia instestinalis." Thesis, Royal Holloway, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498208.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Fos, Camille. "Etude de la signalisation P 13-kinase induite par le récepteur de costimulation ICOS au cours de l'activation lymphocytaire T." Aix-Marseille 2, 2008. http://theses.univ-amu.fr.lama.univ-amu.fr/2008AIX22012.pdf.

Full text
Abstract:
Il est maintenant communément admis qu’une activation lymphocytaire T efficace requiert deux signaux indépendants. Le premier, qui détermine la spécificité de la réponse immunitaire, est délivré au travers de l’interaction du récepteur à l’antigène sur la cellule T (TcR) avec le complexe CMH-peptide antigénique à la surface des cellules présentatrices d’antigène. Un signal additionnel (ou signal 2) aussi appelé costimulateur, est critique pour la régulation de l’activation lymphocytaire T. La signalisation induite par le couple ICOS/ICOS-L fournit à la cellule un second signal positif qui contribue à l’activation des lymphocytes T. La signalisation induite par l’engagement du récepteur ICOS est actuellement peu référencée dans la littérature et ne semble engager que la voie PI3-kinase. Les résultats obtenus in vitro, nous ont montré que l’engagement du récepteur ICOS par son ligand induit le recrutement de p50α au sein de sa partie intracellulaire via son motif consensus motif YxxM. L’engagement du récepteur ICOS augmente également le recrutement intracellulaire de p85α, déjà présent au sein du récepteur à l’état basal. De manière assez surprenante, nous avons constaté que la stimulation du récepteur ICOS semble renforcer la signalisation PI3K induite sous CD28 selon un mécanisme encore inconnu et a mit en évidence un "crosstalk" entre les deux molécules. Nous avons pu montré pour la première fois que le récepteur de costimulation ICOS se localise à la synapse immunologique, zone de la membrane où le récepteur semble influencer le recrutement de p50α. Enfin, dans notre système de stimulation de lymphocytes T primaires, ICOS est capable d’activer la voie de signalisation PI3K beaucoup plus fortement que CD28 comme en témoigne les niveaux élevés de phosphorylation de la sérine/thréonine kinase Akt après engagement de ce récepteur
Inducible costimulator (ICOS) ligation in concert with TcR stimulation results in strong phosphoinositide 3-kinase (PI3K) activation in T lymphocytes. The ICOS cytoplasmic tail contains an YMFM motif that binds the p85α subunit of class IA PI3K, similar to the YMNM motif of CD28, suggesting a redundant function of the two receptors in PI3K signaling. However, ICOS costimulation shows greater PI3K activity than CD28 in T cells. We show in this report that ICOS expression in activated T cells triggers the participation of p50, one of the regulatory subunits of class IA PI3Ks. Using different T-APC cell conjugate systems, we report that p50α accumulates at the immunological synapse in activated but not in resting T cells. Our results demonstrate that ICOS membrane expression is involved in this process and that p50α plasma membrane accumulation requires a functional YMFM SH2-binding motif in ICOS. We also show that ICOS triggering with its ligand, ICOSL, induces the recruitment of p50α at the synapse of T cell/APC conjugates. In association with the p110 catalytic subunit, p50 is known to carry a stronger lipid kinase activity compared to p85α. Accordingly, we observed that ICOS engagement results in a stronger activation of PI3K. Together, these findings provide evidence that p50α is likely a determining factor in ICOS mediated PI3K activity in T cells. These results also suggest that a differential recruitment and activity of class IA PI3K subunits represents a novel mechanism in the control of PI3K signaling by costimulatory molecules
APA, Harvard, Vancouver, ISO, and other styles
5

Pomerance, Martine. "Etapes précoces de la transmission du signal des facteurs de croissance : phosphatidylinositol-3 kinase et protéines serine/threonine kinases." Paris 11, 1994. http://www.theses.fr/1994PA11T008.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bardet, Valérie. "Anomalies de la signalisation dans les leucémies aiguës myéloïdes." Paris 7, 2006. http://www.theses.fr/2006PA077070.

Full text
Abstract:
Les leucémies aiguës myéloïdes (LAM) sont des maladies clonales qui atteignent des progéniteurs de la lignée myéloïde. Elles résultent de la coexistence d'au moins deux anomalies : un blocage de la différenciation et une prolifération cellulaire anormale. Des activations anormales de voies de signalisation, en particulier des voies PI3K/Akt/mTOR, Ras/MAPK et JAK/STAT ont été mises en évidence dans ces hémopathies. Nous nous sommes intéressés dans ce travail à l'étude des anomalies de la voie PI3K/Akt. Nous avons retrouvé une activation constitutive de cette voie de signalisation dans 50% des échantillons de cellules blastiques prélevés au diagnostic chez les patients atteints de LAM de novo. Nous avons également mis en évidence le rôle prédominant de l'isoforme delta de la sous unité catalytique p110 de la PI3K dans cette activation anormale. L'abolition de cette activité catalytique par un inhibiteur spécifique, I'IC87114, nous a permis de démontrer que la voie PI3K/Akt contrôle chez nos patients la prolifération cellulaire mais pas la survie. Ce composé, qui n'est pas toxique et n'a pas d'effet sur la prolifération des progéniteurs normaux, ou un de ses analogues, pourrait avoir un intérêt thérapeutique en association aux chimiothérapies conventionnelles. Des mutations activatrices de la sous unité p110 alpha étant décrites dans certaines tumeurs solides, nous avons recherché si l'activation constitutive anormale de la voie PI3K était causée par des mutations activatrices de p110 delta. Il ne semble pas que cette hypothèse soit à privilégier car les 42 patients testés ne présentent pas de mutation de p110 delta dans leurs blastes. Ces activations anormales ne sont pas non plus corrélées aux anomalies génétiques décrites dans les LAM comme la présence d'un récepteur Flt3 ou c-kit muté ou les mutations des protéines de la famille ras. Il est possible que l'activation anormale de la PI3K observée chez nos patients soit en relation avec des mécanismes d'auto ou de paracrinie de facteurs de croissance. Nous testons actuellement l'implication du système IGF-1/IGF-1R dans cette signalisation anormale. Nos travaux nous ont également permis de montrer grâce à des techniques de cytométrie en flux multi couleurs que lorsqu'une activation anormale de la voie PI3K est détectée dans la population blastique, cette activation est déjà détectable dans la fraction de cellules blastiques les plus immatures de phénotype CD34+ CD38-/low CD123+ qui contient les cellules souches leucémiques. Ces résultats laissent suggérer que l'utilisation en thérapeutique d'inhibiteurs de voies de signalisation en association à la chimiothérapie conventionnelle a un rationnel dans les LAM qui sont des maladies dont le pronostic est actuellement médiocre en raison de la fréquence élevée des rechutes
Acute myeloid leukemia (AML) is an aggressive malignancy resulting from a blockade of differentiation and abnormal proliferation of myeloid progenitor. Abnormal activation of several signal transduction pathways such as PI3K/Akt/mTOR, Ras/MAPK and JAK/STAT has been reported in AML. In this work, we focused on the role of PI3K/Akt signaling abnormalities in the biology of AML. We identified an abnormal and constitutive activation of thé PI3K pathway in half of the blast cell'samples from patients with de novo AML at diagnosis. We pointed out the major role of the delta isoform of the p110 catalytic unit of PI3K. Using a specific inhibitor, IC87114, we were able to demonstrate that the PI3K pathway controls in our patients cell proliferation but not survival. This compound which has no toxicity or inhibitory effect on proliferation of normal progenitors, could therefore be of therapeutic interest associated with conventional chemotherapy. As activating mutations of another catalytic isoform, pHOalpha, were described in various solid tumors, we asked whether the abnormal activation of p110delta can be related with such mutations in p110delta. No mutation could be evidenced in the 42 patients tested, so it is unlikely that one activating mutation could be responsible for this abnormal activation. Moreover, we did not find any association with the genetic abnormalities frequently found in AML like mutated Flt3 or kit receptor or ras mutations. The PI3K activation present in our patients can possibly be due to auto or paracrine growth factor stimulation. We are currently evaluating the role of the IGF-1/1GF-1R System in this abnormal signaling. Using multicolor flow cytometry, we were able to identify in the positive samples, an immature blast cell population with the CD34+ CD38-/low CD123+ among the whole leukemic bulk that already harbored PI3K activation. These results suggest that targeted therapies could be of interest in AML whose prognosis remains poor
APA, Harvard, Vancouver, ISO, and other styles
7

Mujalli, Abdulrahman. "Phosphoinositides in blood platelet : mapping of molecular species and evidence for a new localization and role of PI3P." Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30110.

Full text
Abstract:
Les phosphoinositides (PIs) sont des phospholipides membranaires qui jouent un rôle crucial dans le contrôle de l'organisation spatio-temporelle de nombreuses voies de signalisation intracellulaire, du réarrangement du cytosquelette d'actine et du trafic de vésicules. Dans la plaquette, le métabolisme des PIs est particulièrement actif et génère, par le jeu de kinases, phosphatases et phospholipases spécifiques, des seconds messagers indispensables à l'activation plaquettaire, notamment le phosphatidylinositol 3,4,5-trisphosphate (PIP3). La première partie de la thèse concerne l'étude des différentes espèces moléculaires (composition en acides gras) des 4 grandes classes de PIs (PI, PIP, PIP2 et PIP3) dans les plaquettes humaines et de souris au repos ou lors de leur activation. Cette analyse, jamais réalisée précédemment, a été possible grâce à une technique de spectrométrie de masse (LC-MS), basée sur la méthylation avec le TMS-diazomethane des groupements phosphates des PIs. Cette étude montre une augmentation rapide et transitoire de 2 espèces moléculaires majoritaires de PIP3 lors d'une stimulation plaquettaire avec une réactivité différente des plaquettes humaines et de souris en réponse aux agonistes plaquettaires (thrombine et CRP). En utilisant des modèles murins présentant une inactivation des PI3-kinases (PI3K) dans la lignée mégacaryocytaire et des inhibiteurs spécifiques de PI3K, j'ai montré que l'isoforme PI3Kß (p110ß) de classe I est très majoritairement responsable de la production des diverses espèces moléculaires de PI(3,4,5)P3 en réponse à la thrombine ou au CRP alors que la PI3Ka (p110a) est faiblement impliquée. Les résultats montrent également une grande variété d'espèces moléculaires de PI et seulement 2 espèces moléculaires prédominantes pour les PIP, PIP2 et PIP3, aussi bien chez l'homme que chez la souris malgré des régimes alimentaires très différents. Nous montrons des différences importantes dans le métabolisme des espèces moléculaires de PI, PIP et PIP2 dans les plaquettes humaines et de souris lors de la stimulation. Dans cette étude, nous avons identifié pour la première fois des espèces moléculaires minoritaire de PIP2 mais qui augmentent de façon importante lors de la stimulation plaquettaire. Ce travail permet de dresser la première cartographie des différentes espèces moléculaires de PIs présents dans les plaquettes humaines et de souris et les modifications induites par leur activation. La deuxième partie de la thèse montre pour la première fois une localisation atypique du phosphatidylinositol 3- monophosphate (PI3P), dans le feuillet externe de la membrane plasmique plaquettaire. Je démontre que ce lipide minoritaire (environ 10% de PIP), connu pour être intracellulaire et impliqué dans le trafic vésiculaire, est également présent à la surface des plaquettes au repos. Aucun autre PI n'a pu être détecté dans le feuillet externe de la membrane plasmique plaquettaire. Ce résultat a été obtenu en utilisant différentes sondes fluorescentes se liant spécifiquement au PI3P et leurs contrôles mutées. Nous montrons que le traitement des plaquettes avec des enzymes métabolisant spécifiquement le PI3P (MTM1 et ABH) réduit significativement ce pool de PI3P. Les plaquettes de souris déficientes en PI3K de classe II et III présentent une diminution du PI3P de surface. De manière intéressante, ce pool externe de PI3P permet l'endocytose des protéines circulantes liant le PI3P, in vitro, ex vivo et in vivo. Les sondes PI3P spécifiques internalisées dans la plaquette sont stockées dans les granules a puis sécrétées lors de l'activation plaquettaire. Cette étude montre que le PI3P se comporte comme un récepteur permettant l'endocytose de protéines plasmatiques spécifiques
Phosphoinositides (PIs) are membrane phospholipids that play a crucial role in controlling the spatiotemporal organization of many intracellular signaling pathways, actin cytoskeleton rearrangement, and vesicle trafficking. In platelet, the metabolism of PIs is highly active and generates, by the interplay of specific kinases, phosphatases and phospholipases, second messengers essential for platelet activation, in particular phosphatidylinositol 3,4,5-trisphosphate (PIP3). The first part of the thesis concerns the study of the different molecular species (fatty-acyl composition) of 4 PIs classes (PI, PIP, PIP2 and PIP3) in resting and stimulated human and mouse platelets. This analysis, never realized previously, was possible thanks to a mass spectrometry (LC-MS) technique, based on methylation of PIs phosphates groups with TMS- diazomethane. This study shows a rapid and transient increase in the 2 major molecular species of PIP3 during platelet stimulation with a different reactivity of human and mice platelets according to the used agonists (thrombin and CRP). Using mice models with selective deletion of PI3-kinases (PI3K) in the megakaryocyte lineage and specific PI3K inhibitor, I showed that the class I PI3Kß (p110ß) is the major isoform responsible for the production of the various molecular species of PIP3 in response to thrombin or CRP whereas class I PI3Ka (p110a) is weakly involved. The results also show a large variety of molecular species of PI while only 2 predominant molecular species for PIP, PIP2 and PIP3, both in humans and mice platelets despite very different diet. We show a significant difference in terms of PI, PIP and PIP2 molecular species metabolism in human and mice platelets during stimulation. In this study, we identified for the first time the presence of low-abundance molecular species of PIP2 but which increase significantly during platelet stimulation. This work constitutes the first comprehensive analysis of PIs molecular species and the changes in their actual mass during platelet stimulation. The second part of the thesis shows for the first time an atypical localization of phosphatidylinositol 3-monophosphate (PI3P), in the outer leaflet of the platelet plasma membrane. I demonstrate that this minor lipid (about 10% of PIP), known to be intracellular and involved in vesicular trafficking, is also present at the surface of resting platelet. No other PIs could be detected in the outer leaflet of the platelet plasma membrane. This result was obtained using fluorescent probes binding specifically to PI3P and their mutated controls. Treatment of platelets with PI3P specific metabolizing enzymes (MTM1 and ABH) significantly reduced this particular pool of PI3P. Class II and III PI3K deficient mouse platelets showed a decrease in surface PI3P. Interestingly, this external pool of PI3P was able to mediate endocytosis of circulating PI3P- binding proteins, in vitro, ex vivo and in vivo. Internalized specific PI3P probes were stored into platelets a-granules and could then be secreted during platelets activation. This study shows that PI3P acts as a receptor allowing endocytosis of specific plasma proteins
APA, Harvard, Vancouver, ISO, and other styles
8

Gobin, Bérengère. "Approches thérapeutiques des ostéosarcomes par ciblage des activités kinases." Nantes, 2013. http://archive.bu.univ-nantes.fr/pollux/show.action?id=38b2d404-a1cc-40e0-b8c7-038cf56a7994.

Full text
Abstract:
L'ostéosarcome est la plus fréquente des tumeurs osseuses primitives malignes et est caractérisé par la production de tissu ostéoide tumoral avec ou sans lésions ostéolytiques. Malgré des avancées en termes de chimiothérapie et de chirurgie, le taux de survie des patients reste inchangé depuis plusieurs années. L'absence de réponse aux drogues et l'établissement de résistance montre l'urgence d'explorer de nouvelles voies thérapeutiques. Durant la dernière décade, les avancées biologiques et technologiques ont permis l'émergence de nouvelles thérapies ciblées. Ces drogues inhibitrices sont regroupées en 2 familles majeures (anticorps monoclonaux et petites molécules inhibitrices des activités tyrosine kinase) et ciblent spécifiquement un acteur clé du développement tumoral, et montrent de plus en plus un intérêt majeur dans le ciblage du microenvironnement tumoral. Dans ce contexte, nous nous sommes intéressés aux petites molécules inhibitrices des activités tyrosine kinase: l'imatinib mésylate, inhibiteur des plusieurs récepteurs tyrosine kinase, le NVP-BEZ235, inhibiteur de PI3K et de mTOR, et le BYL719, inhibiteur de la sous-unité p110a de l'enzyme PI3K. Nos résultats ont révélé un effet anti-tumoral direct de ces inhibiteurs in vitro ainsi que in vivo dans plusieurs modèles précliniques d'ostéosarcome. De plus, des études histomorphométriques ont montré l'implication de ces inhibiteurs dans le ciblage de l'angiogenèse tumorale. Nous avons également pu mettre en évidence un impact de ces molécules sur la physiologie osseuse. L'ensemble des résultats de ce travail permet donc de mettre en avant l'intérêt thérapeutique des thérapies ciblées dans l'ostéosarcome
Osteosarcoma is the most common type of primary malignant bone tumor, characterized by osteoid production with or without osteolytic lesions. Despite recent improvements in chemotherapy and surgery, the survival rate remains unchanged for several years. Due to the lack of response to drugs and establishment of resistance there is an important need to explore new therapeutic approaches. During the last decade, biological and technological advances enabled the emergence of targeted therapies. These inhibitors are divided into 2 families (monoclonal antibodies and small molecule inhibitors of tyrosine kinase activities) and specifically target a key player in tumor development and show an increasing interest in targeting the tumor microenvironment. In this context, we are interested in small molecule inhibitors of tyrosine kinase activities: imatinib mesylate, an inhibitor of several tyrosine kinase receptors, NVP-BEZ235, an inhibitor of both PI3K and mTOR, and BYL719, a specific inhibitor of p110a subunit of PI3K enzyme. Our results showed direct in vitro and in vivo anti-tumoral effects of these inhibitors in several preclinical models of osteosarcoma. In addition, histomorphometric studies have shown the involvement of these inhibitors in targeting tumor angiogenesis. We were also able to demonstrate an impact of these drugs on bone biology. Taken together, these results highlight the therapeutic benefit of targeted therapy in osteosarcoma
APA, Harvard, Vancouver, ISO, and other styles
9

Chen, Xi. "The role of PI3K and ERK/MAPK signal transduction cascades in long-term memory formation /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6248.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Rojnuckarin, Ponlapat. "Mitogen-activated protein kinase pathways in megakaryocyte development /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/9200.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Phosphatidylinositol 3-Kinases"

1

Devereaux, Kelly Anne. The role of phosphatidylinositol 3-kinases in autophagy regulation. [New York, N.Y.?]: [publisher not identified], 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Falcioni, Lisa. The role of the phosphatidylinositol-3 kinase-Akt pathway in determining radiation sensivity in the breast cancer cell line MDA-MB 231. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Analysis of Complex Diseases: A Mathematical Perspective. Taylor & Francis Group, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ban, Kiwon. The role of phosphatidylinositol-3 kinase isomers in myocardial ischemic preconditioning. 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wang, Guanyu. Analysis of Complex Diseases: A Mathematical Perspective. Taylor & Francis Group, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wang, Guanyu. Analysis of Complex Diseases: A Mathematical Perspective. Taylor & Francis Group, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Wang, Guanyu. Analysis of Complex Diseases: A Mathematical Perspective. Taylor & Francis Group, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Menon, Deepa U. Autism and Intellectual Disabilities. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0053.

Full text
Abstract:
PTEN (phosphatase and tensin homologue) on chromosome 10q23.3 is a tumor suppressor gene that encodes for a dual specificity phosphatase that regulates the phosphatidylinositol 3- kinase pathway and has an important role in brain development by affecting neuronal survival, neurite outgrowth, synaptic plasticity, and learning memory. Germline mutations of the PTEN gene have been implicated in a group of related tumor syndromes with autosomal dominant inheritance and variable expression and include the Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Juvenile Polyposis syndrome. These syndromes are collectively called the PTEN hamartoma tumor syndromes (PHTS) because they have a predisposition to tumors and hamartomas. PTEN germ line mutations have also been recently linked to autism and macrocephaly and the prevalence of PTEN mutation in children with autism spectrum disorder, and macrocephaly is reported to range from 1.1% to 16.7%.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Phosphatidylinositol 3-Kinases"

1

Burke, John E., and Roger L. Williams. "Phosphatidylinositol 3-Kinases." In Encyclopedia of Metalloproteins, 1686–92. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_53.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "Phosphatidylinositol 3-Kinase." In Encyclopedia of Signaling Molecules, 1369. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101025.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Robert, Jacques. "Phosphatidylinositol 3-Kinase Pathway." In Textbook of Cell Signalling in Cancer, 43–54. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Lee, Yuree, Teun Munnik, and Youngsook Lee. "Plant Phosphatidylinositol 3-Kinase." In Lipid Signaling in Plants, 95–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "Phosphatidylinositol 3-OH Kinase." In Encyclopedia of Signaling Molecules, 1369. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101026.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Schomburg, Dietmar, and Dörte Stephan. "1-Phosphatidylinositol 3-kinase." In Enzyme Handbook, 163–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59025-2_32.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Vogt, Peter K., Jonathan R. Hart, Marco Gymnopoulos, Hao Jiang, Sohye Kang, Andreas G. Bader, Li Zhao, and Adam Denley. "Phosphatidylinositol 3-Kinase: The Oncoprotein." In Current Topics in Microbiology and Immunology, 79–104. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_80.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Robert, Jacques. "La voie de la phosphatidylinositol-3-kinase." In Signalisation cellulaire et cancer, 59–69. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Salajegheh, Ali. "Phosphatidylinositol-4, 5-Bisphosphate 3-Kinase (PIK3Ca)." In Angiogenesis in Health, Disease and Malignancy, 241–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_37.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Salajegheh, Ali. "PIK3R2 (p85β) – Phosphatidylinositol 3-Kinase β-Subunit." In Angiogenesis in Health, Disease and Malignancy, 245–51. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_38.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Phosphatidylinositol 3-Kinases"

1

Ni, Qiang, Matthew Fosbrink, and Jin Zhang. "Illuminating the phosphatidylinositol 3-kinase/Akt pathway." In Biomedical Optics (BiOS) 2008, edited by Alexander P. Savitsky, Robert E. Campbell, and Robert M. Hoffman. SPIE, 2008. http://dx.doi.org/10.1117/12.765524.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Suga, K., Y. Uemura, T. Tsuijinaka, M. Sakon, J. Kambayashi, and T. Mori. "PROPERTIES OF PHOSPHATIDYLINOSITOL KINASE IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643807.

Full text
Abstract:
We have reported the specific 32P-labelling in phosphatidyl-inositol-4-monophosphate(PIP) of intact platelets upon addition of the agents which elevate intracellular cAMP (Thrombos.Res.44, 155,1986).This event may be catalyzed by the action of Pl-kinase, the properties of which has not been elucidatedyet.Thereby, attempts were made to assay and to characterize PI-kinase of human platelets.Fresh lysed platelets prelabelled with 32P in cold Tris-HCl buffer containing 2mM EGTA were incubated at 37 C in the presence of MgCl2 for designated times and the phospholipids were extracted and analyzed by thin layer chromatography.32P-labelling in PIP was gradually increased in consort with the decreased labelling in PI-4,5-bisphosphate.As the changes in the labelling was not affected by the presence of apyrase and as the radioactive inositol trisphosphate was not detected,it was suggested that the changes is due to the action of phoshomono-esterase rather than PI-kinase or phospholipase C.When 32P-ATP was added to non-labelled lysed platelets upon incubation, 32P was labelled only into PIP and the amount was markedly increased until 5min. after incubation.Since the labelling was strongly inhibited by apyrase,it likely reflects the activity of Pl-kinase. The activity of PI-kinase thus measured required Mg2+ strictly for the activity and the maximal activity was obtained in the presence of 30mM Mg2+ .In contrast,it was markedly inhibited in the presence of Ca2+ (as low as 2mM Ca2+ in the presence of 2mM EGTA),which was compatible.with our previous findings with intact platelets. The activity of A-kinase was not inhibited by a low concentration of Ca2+ .Furthermore,the activity was inhibited by cAMP or dbcAMP in a dose related manner and no enhancement of the activity Was obtained by the addition of catalytic subunit of A-kinase,though a significant reduction in the activity was observed in the presence of inhibitor protein to A-kinase. From these observations,the following conclusions were obtained; l)The activity of Pl-kinase in lysed platelets may be determined by pulse labelling with 32P-ATP. 2)It requires Mg2+ absolutely and is inhibited by a very low concentration of Ca2+. 3)Pl-kinase is activated by A-kinase but the activated enzyme is inhibited by cAMP, suggesting the presence of feedback mechanism.
APA, Harvard, Vancouver, ISO, and other styles
3

Trautmann, Marcel, Magdalene Cyra, Christian Bertling, Ilka Isfort, Bianca Altvater, Claudia Rossig, Susanne Hafner, et al. "Abstract 3939: Activation of phosphatidylinositol-3′-kinase/Akt signaling in myxoid liposarcoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3939.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Troxell, ML, D. Ang, A. Warrick, C. Beadling, and CL Corless. "Abstract P2-08-03: Phosphatidylinositol-3-kinase mutations are common in lobular neoplasia." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p2-08-03.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Geletu, Mulu, Samantha Greer, and Leda Raptis. "Abstract 31: Activated phosphatidylinositol-3 kinase: An oncogene that increases gap junctional, intercellular communication." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-31.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Rapp, Judit, Vivien Telek, Tunde Minier, László Czirják, Timea Berki, and Diana Simon. "THU0326 ANALYSIS OF PHOSPHATIDYLINOSITOL 3-KINASE PATHWAY IN B CELL ACTIVATION OF SYSTEMIC SCLEROSIS PATIENTS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7499.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Anders, CK, B. Adamo, AM Deal, CA Livasy, H. Meng, E. Burrows, K. Fritchie, et al. "Abstract P1-14-01: Phosphatidylinositol 3-Kinase (PI3K) Pathway Activation in Breast Cancer Brain Metastases." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p1-14-01.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Troxell, ML, AL Brunner, K. Montgomery, SX Zhu, T. Neff, A. Warrick, C. Beadling, CL Corless, and RB West. "P2-06-04: Phosphatidylinositol-3-Kinase Pathway Mutations Are Common in Breast Columnar Cell Lesions." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p2-06-04.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Choi, Youn Jin, Yoo Yeon Jung, and Jing Jing Liu. "Abstract 338: Inhibition of phosphatidylinositol 3-kinase signaling antagonizes paclitaxel-mediated resistance in cervical cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-338.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Choi, Youn Jin, Yoo Yeon Jung, and Jing Jing Liu. "Abstract 338: Inhibition of phosphatidylinositol 3-kinase signaling antagonizes paclitaxel-mediated resistance in cervical cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-338.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Phosphatidylinositol 3-Kinases"

1

Balajee, A. S., J. A. Meador, and Y. Su. Cellular response to low dose radiation: Role of phosphatidylinositol-3 kinase like kinases. Office of Scientific and Technical Information (OSTI), March 2011. http://dx.doi.org/10.2172/1009811.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Hutchinson, John N., and William Muller. The Role of Phosphatidylinositol 3' -OH Kinase Signaling in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396742.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Parker, Amanda P., Barbara S. Beckman, and Matthew Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada409382.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Parker, Amanda, Barbara Beckman, and Matthew E. Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada431891.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hansen, Peter J., and Amir Arav. Embryo transfer as a tool for improving fertility of heat-stressed dairy cattle. United States Department of Agriculture, September 2007. http://dx.doi.org/10.32747/2007.7587730.bard.

Full text
Abstract:
The overall objective of the current proposal is to develop procedures to improve the pregnancy rate achieved following transfer of fresh or cryopreserved embryos produced in the laboratory into heat-stress recipients. The overall hypothesis is that pregnancy rate in heat-stressed lactating cows can be improved by use of embryo transfer and that additional gains in pregnancy rate can be achieved through development of procedures to cryopreserve embryos, select embryos most likely to establish and maintain pregnancy after transfer, and to enhance embryo competence for post-transfer survival through manipulation of culture conditions. The original specific objectives were to 1) optimize procedures for cryopreservation (Israel/US), 2) develop procedures for identifying embryos with the greatest potential for development and survival using the remote monitoring system called EmbryoGuard (Israel), 3) perform field trials to test the efficacy of cryopreservation and the EmbryoGuard selection system for improving pregnancy rates in heat-stressed, lactating cows (US/Israel), 4) test whether selection of fresh or frozen-thawed blastocysts based on measurement of group II caspase activity is an effective means of increasing survival after cryopreservation and post-transfer pregnancy rate (US), and 5) identify genes in blastocysts induced by insulin-like growth factor-1 (IGF-1) (US). In addition to these objectives, additional work was carried out to determine additional cellular determinants of embryonic resistance to heat shock. There were several major achievements. Results of one experiment indicated that survival of embryos to freezing could be improved by treating embryos with cytochalasin B to disrupt the cytoskeleton. An additional improvement in the efficacy of embryo transfer for achieving pregnancy in heat-stressed cows follows from the finding that IGF-1 can improve post-transfer survival of in vitro produced embryos in the summer but not winter. Expression of several genes in the blastocyst was regulated by IGF-1 including IGF binding protein-3, desmocollin II, Na/K ATPase, Bax, heat shock protein 70 and IGF-1 receptor. These genes are likely candidates 1) for developing assays for selection of embryos for transfer and 2) as marker genes for improving culture conditions for embryo production. The fact that IGF-1 improved survival of embryos in heat-stressed recipients only is consistent with the hypothesis that IGF-1 confers cellular thermotolerance to bovine embryos. Other experiments confirmed this action of IGF-1. One action of IGF-1, the ability to block heat-shock induced apoptosis, was shown to be mediated through activation of the phosphatidylinositol 3-kinase pathway. Other cellular determinants of resistance of embryos to elevated temperature were identified including redox status of the embryo and the ceramide signaling pathway. Developmental changes in embryonic apoptosis responses in response to heat shock were described and found to include alterations in the capacity of the embryo to undergo caspase-9 and caspase-3 activation as well as events downstream from caspase-3 activation. With the exception of IGF-1, other possible treatments to improve pregnancy rate to embryo transfer were not effective including selection of embryos for caspase activity, treatment of recipients with GnRH.and bilateral transfer of twin embryos. In conclusion, accomplishments achieved during the grant period have resulted in methods for improving post-transfer survival of in vitro produced embryos transferred into heat-stressed cows and have lead to additional avenues for research to increase embryo resistance to elevated temperature and improve survival to cryopreservation. In addition, embryo transfer of vitrified IVF embryos increased significantly the pregnancy rate in repeated breeder cows.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Phosphatidylinositol 3-Kinases' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography