Relevant bibliographies by topics / Gα15

Academic literature on the topic 'Gα15'

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Published: 11 March 2023

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Journal articles on the topic "Gα15"

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Davignon, I., M. D. Catalina, D. Smith, J. Montgomery, J. Swantek, J. Croy, M. Siegelman, and T. M. Wilkie. "Normal Hematopoiesis and Inflammatory Responses Despite Discrete Signaling Defects in Gα15 Knockout Mice." Molecular and Cellular Biology 20, no. 3 (February 1, 2000): 797–804. http://dx.doi.org/10.1128/mcb.20.3.797-804.2000.

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ABSTRACT Gα15 activates phospholipase Cβ in response to the greatest variety of agonist-stimulated heptahelical receptors among the four Gq class G-protein α subunits expressed in mammals. Gα15 is primarily expressed in hematopoietic cells in fetal and adult mice. We disrupted the Gα15 gene by homologous recombination in embryonic stem cells to identify its biological functions. Surprisingly, hematopoiesis was normal in Gα15−/− mice, Gα15−/−Gαq−/− double-knockout mice (which express only Gα11 in most hematopoietic cells), and Gα11−/− mice, suggesting functional redundancy in Gq class signaling. Inflammatory challenges, including thioglycolate-induced peritonitis and infection with Trichinella spiralis, stimulated similar responses in Gα15−/− adults and wild-type siblings. Agonist-stimulated Ca2+ release from intracellular stores was assayed to identify signaling defects in primary cultures of thioglycolate-elicited macrophages isolated from Gα15−/− mice. C5a-stimulated phosphoinositide accumulation and Ca2+ release was significantly reduced in Gα15−/− macrophages. Ca2+ signaling was abolished only in mutant cells pretreated with pertussis toxin, suggesting that the C5a receptor couples to both Gα15 and Gαi in vivo. Signaling evoked by other receptors coupled by Gq class α subunits appeared normal in Gα15−/− macrophages. Despite discrete signaling defects, compensation by coexpressed Gq and/or Gi class α subunits may suppress abnormalities in Gα15-deficient mice.
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Yule, David I., Christopher W. Baker, and John A. Williams. "Calcium signaling in rat pancreatic acinar cells: a role for Gαq, Gα11, and Gα14." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 1 (January 1, 1999): G271—G279. http://dx.doi.org/10.1152/ajpgi.1999.276.1.g271.

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Stimulus-secretion coupling in the pancreatic acinar cell is initiated by the secretagogues CCK and ACh and results in the secretion by exocytosis of the contents of zymogen granules. A key event in this pathway is the G protein-activated production of second messengers and the subsequent elevation of cytosolic-free Ca2+. The aim of this study was therefore to define the heterotrimeric G protein α-subunits present and participating in this pathway in rat pancreatic acinar cells. RT-PCR products were amplified from pancreatic acinar cell mRNA with primers specific for Gαq, Gα11, and Gα14 but were not amplified with primers specific for Gα15. The sequences of these PCR products confirmed them to be portions of the rat homologues of Gαq, Gα11, and Gα14. The pancreatic-derived cell line AR42J similarly expressed Gαq, Gα11, and Gα14; however, the Chinese hamster ovary (CHO) cell line only expressed Gα11 and Gαq. These data indicate that caution should be exercised when comparing signal transduction pathways between different cell types. The expression of these proteins in acinar cells was confirmed by immunoblotting samples of acinar membrane protein using specific antisera to the individual G protein α-subunits. The role of these proteins in Ca2+ signaling events was investigated by microinjecting a neutralizing antibody directed against a homologous sequence in Gαq, Gα11, and Gα14 into acinar cells and CHO cells. Ca2+ signaling was inhibited in acinar cells and receptor-bearing CHO cells in response to both physiological and supermaximal concentrations of agonists. The inhibition was >75% in both cell types. These data indicate a role for Gαq and/or Gα11 in intracellular Ca2+ concentration signaling in CHO cells, and in addition to Gαq and Gα11, Gα14 may also fulfill this role in rat pancreatic acinar cells.
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van den Bos, Esther, Benjamin Ambrosy, Markus Horsthemke, Stefan Walbaum, Anne C. Bachg, Nina Wettschureck, Giulio Innamorati, Thomas M. Wilkie, and Peter J. Hanley. "Knockout mouse models reveal the contributions of G protein subunits to complement C5a receptor–mediated chemotaxis." Journal of Biological Chemistry 295, no. 22 (April 24, 2020): 7726–42. http://dx.doi.org/10.1074/jbc.ra119.011984.

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G protein–coupled receptor signaling is required for the navigation of immune cells along chemoattractant gradients. However, chemoattractant receptors may couple to more than one type of heterotrimeric G protein, each of which consists of a Gα, Gβ, and Gγ subunit, making it difficult to delineate the critical signaling pathways. Here, we used knockout mouse models and time-lapse microscopy to elucidate Gα and Gβ subunits contributing to complement C5a receptor-mediated chemotaxis. Complement C5a-mediated chemokinesis and chemotaxis were almost completely abolished in macrophages lacking Gnai2 (encoding Gαi2), consistent with a reduced leukocyte recruitment previously observed in Gnai2−/− mice, whereas cells lacking Gnai3 (Gαi3) exhibited only a slight decrease in cell velocity. Surprisingly, C5a-induced Ca2+ transients and lamellipodial membrane spreading were persistent in Gnai2−/− macrophages. Macrophages lacking both Gnaq (Gαq) and Gna11 (Gα11) or both Gna12 (Gα12) and Gna13 (Gα13) had essentially normal chemotaxis, Ca2+ signaling, and cell spreading, except Gna12/Gna13-deficient macrophages had increased cell velocity and elongated trailing ends. Moreover, Gnaq/Gna11-deficient cells did not respond to purinergic receptor P2Y2 stimulation. Genetic deletion of Gna15 (Gα15) virtually abolished C5a-induced Ca2+ transients, but chemotaxis and cell spreading were preserved. Homozygous Gnb1 (Gβ1) deletion was lethal, but mice lacking Gnb2 (Gβ2) were viable. Gnb2−/− macrophages exhibited robust Ca2+ transients and cell spreading, albeit decreased cell velocity and impaired chemotaxis. In summary, complement C5a-mediated chemotaxis requires Gαi2 and Gβ2, but not Ca2+ signaling, and membrane protrusive activity is promoted by G proteins that deplete phosphatidylinositol 4,5-bisphosphate.
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Feild, John A., James J. Foley, Tania T. Testa, Parvathi Nuthulaganti, Catherine Ellis, Henry M. Sarau, and Robert S. Ames. "Cloning and characterization of a rabbit ortholog of human Gα16 and mouse Gα15." FEBS Letters 460, no. 1 (October 22, 1999): 53–56. http://dx.doi.org/10.1016/s0014-5793(99)01317-4.

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GAUDREAU, Rémi, Christian Le GOUILL, Salim MÉTAOUI, Stéphane LEMIRE, Jana STANKOVÀ, and Marek ROLA-PLESZCZYNSKI. "Signalling through the leukotriene B4 receptor involves both αi and α16, but not αq or α11 G-protein subunits." Biochemical Journal 335, no. 1 (October 1, 1998): 15–18. http://dx.doi.org/10.1042/bj3350015.

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COS-7 cells transfected with the leukotriene (LT) B4 receptor (BLTR) cDNA were unable to produce LTB4-induced inositol phosphates (IPs) in spite of the presence of endogenous Gαi, Gαq and Gα11 proteins. Co-transfection of BLTR with Gα16, however, resulted in high levels of IP production, which were 17-, 10- and 6-fold higher than with co-transfected Gα11, Gαq and Gα14, respectively. Co-transfection of BLTR with phospholipase C (PLC) β2, on the other hand, resulted in efficient IP production and co-transfection of BLTR with both Gα16 and PLCβ2 resulted in a greater than additive response.
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Rafa-Zabłocka, Katarzyna, Agnieszka Zelek-Molik, Beata Tepper, Piotr Chmielarz, Grzegorz Kreiner, Michał Wilczkowski, and Irena Nalepa. "Chronic restraint stress induces changes in the cerebral Galpha 12/13 and Rho-GTPase signaling network." Pharmacological Reports 73, no. 4 (June 11, 2021): 1179–87. http://dx.doi.org/10.1007/s43440-021-00294-4.

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Abstract Background Evidence indicates that Gα12, Gα13, and its downstream effectors, RhoA and Rac1, regulate neuronal morphology affected by stress. This study was aimed at investigating whether repeated stress influences the expression of proteins related to the Gα12/13 intracellular signaling pathway in selected brain regions sensitive to the effects of stress. Furthermore, the therapeutic impact of β(1)adrenergic receptors (β1AR) blockade was assessed. Methods Restraint stress (RS) model in mice (2 h/14 days) was used to assess prolonged stress effects on the mRNA expression of Gα12, Gα13, RhoA, Rac1 in the prefrontal cortex (PFC), hippocampus (HIP) and amygdala (AMY). In a separate study, applying RS model in rats (3–4 h/1 day or 14 days), we evaluated stress effects on the expression of Gα12, Gα11, Gαq, RhoA, RhoB, RhoC, Rac1/2/3 in the HIP. Betaxolol (BET), a selective β1AR antagonist, was introduced (5 mg/kg/p.o./8–14 days) in the rat RS model to assess the role of β1AR in stress effects. RT-qPCR and Western Blot were used for mRNA and protein assessments, respectively. Results Chronic RS decreased mRNA expression of Gα12 and increased mRNA for Rac1 in the PFC of mice. In the mice AMY, decreased mRNA expression of Gα12, Gα13 and RhoA was observed. Fourteen days of RS exposure increased RhoA protein level in the rats’ HIP in the manner dependent on β1AR activity. Conclusions Together, these results suggest that repeated RS affects the expression of genes and proteins known to be engaged in neural plasticity, providing potential targets for further studies aimed at unraveling the molecular mechanisms of stress-related neuropsychiatric diseases.
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Cho, Min Kyung, Won Dong Kim, Sung Hwan Ki, Jong-Ik Hwang, Sangdun Choi, Chang Ho Lee, and Sang Geon Kim. "Role of Gα12 and Gα13 as Novel Switches for the Activity of Nrf2, a Key Antioxidative Transcription Factor." Molecular and Cellular Biology 27, no. 17 (June 25, 2007): 6195–208. http://dx.doi.org/10.1128/mcb.02065-06.

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ABSTRACT Gα12 and Gα13 function as molecular regulators responding to extracellular stimuli. NF-E2-related factor 2 (Nrf2) is involved in a protective adaptive response to oxidative stress. This study investigated the regulation of Nrf2 by Gα12 and Gα13. A deficiency of Gα12, but not of Gα13, enhanced Nrf2 activity and target gene transactivation in embryo fibroblasts. In mice, Gα12 knockout activated Nrf2 and thereby facilitated heme catabolism to bilirubin and its glucuronosyl conjugations. An oligonucleotide microarray demonstrated the transactivation of Nrf2 target genes by Gα12 gene knockout. Gα12 deficiency reduced Jun N-terminal protein kinase (JNK)-dependent Nrf2 ubiquitination required for proteasomal degradation, and so did Gα13 deficiency. The absence of Gα12, but not of Gα13, increased protein kinase C δ (PKC δ) activation and the PKC δ-mediated serine phosphorylation of Nrf2. Gα13 gene knockout or knockdown abrogated the Nrf2 phosphorylation induced by Gα12 deficiency, suggesting that relief from Gα12 repression leads to the Gα13-mediated activation of Nrf2. Constitutive activation of Gα13 promoted Nrf2 activity and target gene induction via Rho-mediated PKC δ activation, corroborating positive regulation by Gα13. In summary, Gα12 and Gα13 transmit a JNK-dependent signal for Nrf2 ubiquitination, whereas Gα13 regulates Rho-PKC δ-mediated Nrf2 phosphorylation, which is negatively balanced by Gα12.
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McNeil Coffield, V., Whitney S. Helms, Qi Jiang, and Lishan Su. "Gα13 Mediates a Signal That Is Essential for Proliferation and Survival of Thymocyte Progenitors." Journal of Experimental Medicine 200, no. 10 (November 8, 2004): 1315–24. http://dx.doi.org/10.1084/jem.20040944.

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G protein signaling via the Gα12 family (Gα12 and Gα13) has not been well studied in T cells. To investigate whether Gα12 and Gα13 are involved in thymopoiesis, we expressed the regulator of G protein signaling domain of p115RhoGEF to inhibit Gα12 and Gα13 during thymopoiesis. Fetal thymus organ cultures seeded with p115ΔDH-expressing progenitor cells showed impaired thymopoiesis with a block at the CD4−CD8−CD44−CD25+ (DN3) stage. Using Gα13 or Gα12 minigenes, we demonstrated that Gα13, but not Gα12, is required for thymopoiesis. T progenitor cells expressing p115ΔDH showed reduced proliferation and increased cell death. T cell receptor stimulation of the fetal thymus organ cultures did not rescue the block. Overexpression of the antiapoptotic gene Bcl2 rescued the defect in DN3 cells and partially rescued T cell development. Therefore, Gα13-mediated signaling is necessary in early thymocyte proliferation and survival.
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Tutunea-Fatan, Elena, Jasper C. Lee, Bradley M. Denker, and Lakshman Gunaratnam. "Heterotrimeric Gα12/13 proteins in kidney injury and disease." American Journal of Physiology-Renal Physiology 318, no. 3 (March 1, 2020): F660—F672. http://dx.doi.org/10.1152/ajprenal.00453.2019.

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Gα12 and Gα13 are ubiquitous members of the heterotrimeric guanine nucleotide-binding protein (G protein) family that play central and integrative roles in the regulation of signal transduction cascades within various cell types in the kidney. Gα12/Gα13 proteins enable the kidney to adapt to an ever-changing environment by transducing stimuli from cell surface receptors and accessory proteins to effector systems. Therefore, perturbations in Gα12/Gα13 levels or their activity can contribute to the pathogenesis of various renal diseases, including renal cancer. This review will highlight and discuss the complex and expanding roles of Gα12/Gα13 proteins on distinct renal pathologies, with emphasis on more recently reported findings. Deciphering how the different Gα12/Gα13 interaction networks participate in the onset and development of renal diseases may lead to the discovery of new therapeutic strategies.
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Luo, W., L. R. Latchney, and D. J. Culp. "G protein coupling to M1 and M3muscarinic receptors in sublingual glands." American Journal of Physiology-Cell Physiology 280, no. 4 (April 1, 2001): C884—C896. http://dx.doi.org/10.1152/ajpcell.2001.280.4.c884.

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Rat sublingual gland M1 and M3 muscarinic receptors each directly activate exocrine secretion. To investigate the functional role of coreceptor expression, we determined receptor-G protein coupling. Although membrane proteins of 40 and 41 kDa are ADP-ribosylated by pertussis toxin (PTX), and 44 kDa proteins by cholera toxin (CTX), both carbachol-stimulated high-affinity GTPase activity and the GTP-induced shift in agonist binding are insensitive to CTX or PTX. Carbachol enhances photoaffinity labeling ([α-32P]GTP-azidoaniline) of only 42-kDa proteins that are subsequently tractable to immunoprecipitation by antibodies specific for Gαq or Gα11 but not Gα12 or Gα13. Carbachol-stimulated photoaffinity labeling as well as phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis is reduced 55% and 60%, respectively, by M1 receptor blockade with m1-toxin. Gαq/11-specific antibody blocks carbachol-stimulated PIP2 hydrolysis. We also provide estimates of the molar ratios of receptors to Gαq and Gα11. Although simultaneous activation of M1 and M3receptors is required for a maximal response, both receptor subtypes are coupled to Gαq and Gα11 to stimulate exocrine secretion via redundant mechanisms.
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Dissertations / Theses on the topic "Gα15"

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Chauvet, Sylvain. "Les protéines Gα12 et Gα13 dans la mucoviscidose : Rôle dans la dégradation de la protéine CFTR mutée F508del et dans le contrôle des jonctions intercellulaires." Phd thesis, Université de Grenoble, 2011. http://tel.archives-ouvertes.fr/tel-00684255.

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70% des mutations identifiées sur le gène responsable de la mucoviscidose correspondent à la délétion de la phénylalanine en position 508 (F508del) de la protéine CFTR (Cystic Fibrosis Transmembrane conductance Regulator). Cette mutation est responsable, à 37°C, d'un mauvais repliement, du blocage et de la dégradation rapide de CFTR au niveau du réticulum endoplasmique (RE), et par conséquent de l'absence de sécrétion des ions Cl- au niveau de la membrane apicale des cellules épithéliales. Deux conséquences principales de cette mutation sont un épaississement important du mucus bronchique et une diminution de l'intégrité de la barrière luminale de l'épithélium bronchique. Ces deux phénomènes participent à l'invasion et à l'infection du tissu pulmonaire par des bactéries pathogènes comme Pseudomonas aeruginosa, exacerbant l'inflammation et la destruction tissulaire au niveau des poumons. L'objectif de cette étude a été de déterminer le rôle de deux protéines appartenant à la famille des protéines G hétérotrimériques, Gα12 et Gα13, dans la dégradation de la protéine CFTR-F508del ainsi que dans le contrôle des complexes jonctionnels au niveau de l'épithélium bronchique sain et mucoviscidosique. Nos travaux démontrent pour la première fois que dans la mucoviscidose, l'expression des protéines Gα12 et Gα13 est faible. Nous avons aussi montré que Gα12, et non Gα13, est impliquée dans le contrôle de la dégradation de la protéine CFTR-F508del via les protéines chaperonnes Calnexine et HSP90, et dans la formation et le maintien des jonctions cellulaires bronchiques via E-cadhérine et ZO-1 de manière inverse par rapport à l'épithélium rénale. Ces travaux placent donc Gα12 comme un acteur non négligeable de la maladie de la mucoviscidose.
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Zanini, Sara. "FUNCTIONAL ANALYSIS OF Gα15 EXPRESSION IN PANCREATIC CANCER." Doctoral thesis, 2014. http://hdl.handle.net/11562/711365.

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Il tumore al pancreas ( PaCa ) è la quarta causa di morte per cancro negli Stati Uniti con un tasso complessivo di sopravvivenza a 5 anni del 3-5 % che porta a una stima di 227.000 morti all'anno in tutto il mondo. Ad oggi non sono disponibili terapie efficaci. La chirurgia è l'unico trattamento potenzialmente curativo; tuttavia poiché la maggior parte delle lesioni sono tardivamente diagnosticate esso si traduce in un trattamento palliativo nella maggior parte dei casi. Pertanto, l'identificazione di nuovi fattori coinvolti nel processo di tumorigenesi potrebbe contribuire a chiarire la biologia molecolare del cancro del pancreas e ad individuare nuovi marcatori e/o target farmacologici. G15 è una proteina G eterotrimerica con la sua subunità α appartenente alla famiglia Gαq/11. Nei tessuti adulti Gα15 è selettivamente espressa in tipi cellulari immaturi che presentano maggiori potenzialità di rinnovamento cellulare. Gα15 si accoppia promiscuamente ad un'ampia varietà di recettori accoppiati a proteine G (GPCR ) associati alla fosfolipasi C e mostra un'eccezionale resistenza al meccanismo della desensitizzazione β-arrestina dipendente. Sulla base delle caratteristiche peculiari di Gα15 abbiamo ipotizzato che la proteina potrebbe favorire la crescita tumorale se espressa al di fuori del suo contesto cellulare. La nostra attenzione è stata rivolta all'espressione nel PaCa alla luce dei risultati preliminari che hanno evidenziato un' espressione significativa di Gα15 in biopsie umane di PaCa xenotrapiantate in topi. Nella presente tesi dimostriamo che Gα15 non è espresso nel pancreas normale. Uno screening di diverse linee cellulari di PaCa mediante analisi PCR basata su TaqMan hanno dimostrato l'espressione ectopica di trascritti di mRNA di Gα15 in un significativo gruppo di linee cellulari. Tali risultati sono stati ulteriormente confermati mediante immunoblot . Inoltre, Gα15 supporta la stimolazione di PKD1 poiché la sua deplezione in linee cellulari di PaCa riduce l'attivazione tonica di PKD1. In aggiunta, la sua deplezione inibisce notevolmente la resistenza alla mancanza di sostanze nutritive e la crescita ancoraggio-indipendente . Sulla base del fatto che l'endoderma embrionale dà origine a tutto il tubo digerente, l'espressione ectopica di Gα15 è stata studiata anche nelle neoplasie neuroendocrine del piccolo intestino. I risultati emersi nel PaCa sono stati confermati anche in queste neoplasie. Solo un sottoinsieme di campioni tumorali dei pazienti e linee cellulari di neoplasie neuroendocrine del piccolo intestino esprime Gα15 che è assente nella mucosa normale e nelle cellule enterocromaffini normali. E' stato anche dimostrato che un maggior livello di espressione di Gα15 potrebbe essere predittivo di una peggiore sopravvivenza. Nel loro insieme , i nostri risultati suggeriscono che Gα15 supporta la trasformazione neoplastica nel pancreas e, eventualmente, in altri organi del tratto digestivo e quindi potrebbe offrire un nuovo potenziale bersaglio per la terapia del PaCa.
Pancreatic cancer (PaCa) is the fourth leading cause of cancer death in the USA with overall 5-year survival rate of only 3-5% that leads to an estimated 227000 deaths per year worldwide. To date no effective therapies are available. Surgery is the only potentially curative treatment; however because the majority of lesions are lately diagnosed it results in a palliative treatment in the majority of cases. Therefore, the identification of new factors involved in the tumorigenesis process could help to enlighten the molecular biology of pancreatic cancer and to identify new marker and/or pharmacological target. G15 is a heterotrimeric G protein with its α subunit belonging to the Gαq/11 family. In adult tissues it is selectively expressed in immature cell lineages that feature higher cell renewal potential. It promiscuously couples a wide variety of G protein-coupled receptors (GPCRs) to phospholipase C and shows an exceptional resistance to β-arrestin desensitization. Based on the peculiar characteristics of Gα15, we hypothesized that it might promote tumour growth if expressed out of its natural cell context. Our attention has been drawn toward PaCa since previous results revealed significant expression of Gα15 in human tumour PaCa biopsies xenografted in mice. Here we show that Gα15 is not expressed in normal pancreas. A screening of several PaCa cell lines by TaqMan PCR analysis demonstrated ectopic expression of Gα15 mRNA in a significant subset of cases, as confirmed also by immunoblot. Moreover, Gα15 supports stimulation of PKD1 since its depletion in PaCa cell lines reduced the tonic activation of PKD1. In addition, its depletion dramatically inhibited resistance to the lack of nutrients and anchorage-independent growth. Based on the fact that embryonic endoderm gives rise to the whole digestive tube, Gα15 ectopic expression was investigated also in small intestinal neuroendocrine neoplasia (SI-NENs). The results emerged for PaCa were confirmed also in SI-NENs: only a subset of patient tumour samples and SI-NENs cell lines expressed Gα15 that is absent in normal mucosa and normal enterochromaffin cells. Moreover, a higher Gα15 expression could be predictive of a worse survival. Taken together, our findings suggest that Gα15 supports neoplastic transformation in pancreas and possibly in other organs of the digestive tract and therefore could offer novel potential target for the therapy of PaCa.
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Fahimi-Vahid, Mercedeh [Verfasser]. "Untersuchungen zur Beteiligung von Gα12 [G-alpha-12], Gα13-Proteinen [G-alpha-13-Proteinen] an der Aktivierung der Phospholipase D in Kardiomyozyten der neonatalen Ratten / vorgelegt von Mercedeh Fahimi-Vahid." 2004. http://d-nb.info/970526733/34.

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Liu, Yi-Ching, and 柳依青. "Expression of Gα12 in oral squamous cell carcinoma." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/52690522087536223361.

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Jiang, Shin-Hua, and 江欣樺. "The Studies of the Gα11 Pseudogene in Leukemia Cell Line K562 Differentiation." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/15035953741852029744.

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碩士
大葉大學
分子生物科技學系碩士班
101
Heterotrimeric guanine nucleotide-binding proteins (G-protein) have been demonstrated to play integral role in the transduction of extracellular signals from cell membrane receptor (G-protein-coupled receptors, GPCR) to intracellular effectors proteins. G proteins regulate critical processes such as cell growth, differentiation and development. Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder of hematopoietic stem cells, that has acquired a Philadelphia (Ph) chromosome encoding the BCR–ABL oncogenic fusion protein, which has lost its differentiation activity. Therefore, in recent years, some scholars proposed differentiation therapy, by treating appropriate inducers to induced advanced or aggressive malignant cells maturation and differentiation into mature cells. K562 is the first human immortalized myelogenous leukaemia cell line and belonging undifferentiated pluripotent hematopoietic progenitor cells. K562 cell can be differentiated into erythrocytic or megakaryocytic lineages upon different inducers treatments and was used as a model cell line to study the relationship between the blood cell differentiation and signal transduction. In this report, three different inducers, huangqi (Astragalus membranaceus) and chemicals Hemin and HMBA were used to induce K562 cell differentiation. Two erythroid markers, β-globin or γ-globin, and two megakaryocyte markers CD41 and CD61 are used to monitor the differentiation process. In former report, the Gα11 pseudogene was induced by the huangqi administration. In this study, in promoter activity assay the pseudogene promoter activity increased by two fold when the presence of 1.5 mg / ml of huangqi extract. However, under the influence of the three-inducing agent, the Gα11 pseudogene were up-regulated in the HMBA-induced K562 cell, but we failed to detect significant changing of cell differentiation markers. It may be the consequence of fetal bovine serum used in cell culture which led to change cell characters and low transfection efficiency of the genes. Currently, re-transfection with higher amount of expression plasmid in K562 cells, and select stable clones are on going. I expect the performance of the proper Gα proteins function will change cell fate. In conclusion, understand the G protein function in cell differentiation, can provide the information need for future differentiation therapy of leukemia.
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Schütz, Vera [Verfasser]. "Charakterisierung des L-Typ Ca2+-Stroms im linken Ventrikel des Herzens von Gα11-defizienten [G-alpha-11-defizienten] Mäusen / vorgelegt von Vera Schütz." 2011. http://d-nb.info/1011708388/34.

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Book chapters on the topic "Gα15"

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "Gα12." In Encyclopedia of Signaling Molecules, 847. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100598.

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Gutkind, J. Silvio, Omar A. Coso, and Ningzhi Xu. "Gα12- and Gα13-Subunits of Heterotrimeric G-Proteins A Novel Family of Oncogenes." In G Proteins, Receptors, and Disease, 101–17. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1802-9_6.

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"Gα12 and Gα13." In Encyclopedia of Signaling Molecules, 2316. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_105117.

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Tanabe, Shihori, Barry Kreutz, Nobuchika Suzuki, and Tohru Kozasa. "Regulation of RGS-RhoGEFs by Gα12 and Gα13 Proteins." In Methods in Enzymology, 285–94. Elsevier, 2004. http://dx.doi.org/10.1016/s0076-6879(04)90018-3.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "Gα13." In The Gene Knockout FactsBook, 366–67. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50203-9.

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Dermott, Jonathan M., and N. Dhanasekaran. "Determining Cellular Role of Gα12." In G Protein Pathways, Part B: G Proteins and their Regulators, 298–309. Elsevier, 2002. http://dx.doi.org/10.1016/s0076-6879(02)44722-2.

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Hart, Matthew J., William Roscoe, and Gideon Bollag. "Activation of Rho GEF activity by Gα13." In Methods in Enzymology, 61–71. Elsevier, 2000. http://dx.doi.org/10.1016/s0076-6879(00)25431-1.

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Mao, Junhao, and Dianqing Wu. "Functional Interaction of Gα13 with p115RhoGEF Determined with Transcriptional Reporter System." In Methods in Enzymology, 404–10. Elsevier, 2002. http://dx.doi.org/10.1016/s0076-6879(02)45033-1.

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Conference papers on the topic "Gα15"

1

Scarlett, Kisha, Elshaddai White, Christopher Coke, Jada Carter, LaToya Bryant, and Cimona V. Hinton. "Abstract 2512: Agonist-induced heterodimerization between CXCR4 and CB2 inhibits Gα13/RhoA-mediated cell migration." 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.am2018-2512.

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Ha, Ji Hee, Danny Dhanasekaran, Jeremy Ward, Yoon Mi Yang, Sang Geon Kim, and Lakshmi Varadarajalu. "Abstract 3020: The gep protooncogene Gα12 mediates LPA-stimulated activation of CREB in ovarian cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3020.

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Goodwin, AT, B. Hinz, and G. Jenkins. "S77 The G proteins Gαq/11 and Gα12/13 drive unique myofibroblast functions to promote pulmonary fibrosis." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.82.

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Chaim, Olga M., Jinhui Ma, Jacqueline Lara, Frank Furnari, Shigeki Myamoto, and Joan H. Brown. "Abstract A19: Regulation of glioblastoma tumor growth and stem cell properties through Gα12 and tissue factor, upstream and downstream players in YAP signaling." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-a19.

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You might also be interested in the extended bibliographies on the topic 'Gα15' for particular source types:
Journal articles
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