Journal articles: 'G-cell'

1

Sawada, Mitsutaka, and Chris J. Dickinson. "The G Cell." Annual Review of Physiology 59, no. 1 (October 1997): 273–98. http://dx.doi.org/10.1146/annurev.physiol.59.1.273.

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Assmann, Sarah M. "Guard cell G proteins." Trends in Plant Science 1, no. 3 (March 1996): 73–74. http://dx.doi.org/10.1016/s1360-1385(96)89035-2.

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Clapham, David. "Cell Signalling.Noel G. Morgan." Quarterly Review of Biology 66, no. 1 (March 1991): 74. http://dx.doi.org/10.1086/417061.

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Amiot, L., B. Drénou, M. Onno, A. Bensussan, P. Le Bouteiller, G. Semana, B. Le Marchand, T. Lamy, and R. Fauchet. "HLA-G cell surface expression in hematopoietic cells." Human Immunology 47, no. 1-2 (April 1996): 144. http://dx.doi.org/10.1016/0198-8859(96)85476-0.

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Montagne, Kevin, Mutsuo Ogasawara, Jeonghyun Kim, Katsuko Furukawa, and Takashi Ushida. "GS1-18 HYDROSTATIC PRESSURE ACTIVATES HETEROTRIMERIC G PROTEINS IN CHONDROCYTE PROGENITOR CELLS(GS1: Cell and Tissue Biomechanics IV)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2015.8 (2015): 131. http://dx.doi.org/10.1299/jsmeapbio.2015.8.131.

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Nakamura, Fumio, Mariko Kato, Kimihiko Kameyama, Toshihide Nukada, Tatsuya Haga, Hiroyuki Kato, Tadaomi Takenawa, and Ushio Kikkawa. "Characterization of GFamily G Proteins G(G), G(G), and GExpressed in the Baculovirus-Insect Cell System." Journal of Biological Chemistry 270, no. 11 (March 17, 1995): 6246–53. http://dx.doi.org/10.1074/jbc.270.11.6246.

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R., Ali, Ahmad Fauzi M.N., Mutharasu D., and Zainal Z.A. "G-7 EFFECT OF CELL OPERATING TEMPERATURE ON THE PERFORMANCE OF AN INTERMEDIATE TEMPERATURE SOLID OXIDE FUEL CELL(Session: Fuel Cell/Magnet)." Proceedings of the Asian Symposium on Materials and Processing 2006 (2006): 133. http://dx.doi.org/10.1299/jsmeasmp.2006.133.

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Sun, Aining, Yanling Wu, Shengli Xue, Wu Depei, and Weirong Chang. "Mechanism of CAG Regimen Eliminating Human T Cell Acute Lymphoblastic Leukemia Cell Line, A3." Blood 112, no. 11 (November 16, 2008): 5051. http://dx.doi.org/10.1182/blood.v112.11.5051.5051.

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Abstract Objective To explore the mechanism of CAG regimen eliminating human T cell acute lymphoblastic leukemia cell line, A3 and evaluate the role played by G-CSF/G-CSFR system in this process. Methods The expression of G-CSFR on A3 cells was detected by flow cytometric analysis. Cell cycle parameters of A3 cells treated with different concentration of G-CSF(5ng/ml A10ng/ml A15ng/ml A20ng/ml G0ng/ml as control) were examined by propidium iodide staining. The inhibition and apoptosis rates of A3 cells caused by treatment with various combination of G-CSF, cytarabine (Ara-C), and aclarubicin (ACR) after incubation for 48h were analyzed by Cell Counting Kit (CCK-8) and AnnexinV staining, respectively. After incubation for 48 hours with G-CSF and PD98059(the specific inhibitor of MEK in Ras-MAPK signaling pathway), cell cycle and cell dynamic change were examined. Results The expression frenquency of G-CSFR on A3 cells was 94.2% which was comparable to that of KG-1 cells. The proportion of A3 cells in S-phase was elevated concomitantly with the increasing G-CSF concentrations within 0–20ng/ml, highest at 15ng/ml of G-CSF. After incubation with Ara-C and G-CSF for 48 hours, the proliferation of A3 cells was inhibited more significantly than incubation with incubation with Ara-C alone (P<0.05, Ara-C 10−5M and 10−6M) by CCK-8 assay. Incubated with Ara-C, ACR, and G-CSF for 48 hours, the apoptosis of A3 cells was increased than that treated with Ara-C and ACR. With the concentration of PD98059 increased gradually, the proportion of A3 cells in S-phase and OD values of A3 cells decreased, which was less than that of control group (p<0.05). Conclusion G-CSFR was expressed on A3 cells. G-CSF/G-CSFR system had a synergetic effect on eliminating A3 cells when administrated simultaneously with chemical agents by driving G0-phase cells into S-phase. Apoptosis was one of the mechanisms of CAG regimen eliminating A3 cells. The interaction between G-CSF and G-CSFR activates a series of signaling pathways which includes Ras-MAPK. The inhibition of MAPK phosphorylation by PD98059 contributed partially to the effect of G-CSF on A3 cells.

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Kudo, Tomoya, Hideaki Kigoshi, Takashi Hagiwara, Takahisa Takino, Masatoshi Yamazaki, and Satoru Yui. "Cathepsin G, a Neutrophil Protease, Induces Compact Cell-Cell Adhesion in MCF-7 Human Breast Cancer Cells." Mediators of Inflammation 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/850940.

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Cathepsin G is a serine protease secreted by activated neutrophils that play a role in the inflammatory response. Because neutrophils are known to be invading leukocytes in various tumors, their products may influence the characteristics of tumor cells such as the growth state, motility, and the adhesiveness between cells or the extracellular matrix. Here, we demonstrate that cathepsin G induces cell-cell adhesion of MCF-7 human breast cancer cells resulting from the contact inhibition of cell movement on fibronectin but not on type IV collagen. Cathepsin G subsequently induced cell condensation, a very compact cell colony, resulting due to the increased strength of E-cadherin-mediated cell-cell adhesion. Cathepsin G action is protease activity-dependent and was inhibited by the presence of serine protease inhibitors. Cathepsin G promotes E-cadherin/catenin complex formation and Rap1 activation in MCF-7 cells, which reportedly regulates E-cadherin-based cell-cell junctions. Cathepsin G also promotes E-cadherin/protein kinase D1 (PKD1) complex formation, and Go6976, the selective PKD1 inhibitor, suppressed the cathepsin G-induced cell condensation. Our findings provide the first evidence that cathepsin G regulates E-cadherin function, suggesting that cathepsin G has a novel modulatory role against tumor cell-cell adhesion.

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Blaschke, Angela, Cornelis Weijer, and Harry MacWilliams. "Dictyostelium discoideum: Cell-type proportioning, cell-differentiation preference, cell fate, and the behavior of anterior-like cells in Hs1/Hs2 and G+/G− mixtures." Differentiation 32, no. 1 (August 1986): 1–9. http://dx.doi.org/10.1111/j.1432-0436.1986.tb00549.x.

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Skinner, Amy M., Santhosh Chakkaramakkil Verghese, and Peter Kurre. "Cell- Cell Transmission of VSV-G Pseudotyped Lentivector Particles." PLoS ONE 8, no. 9 (September 10, 2013): e74925. http://dx.doi.org/10.1371/journal.pone.0074925.

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Faradji, Floria, Sébastien Bloyer, Delphine Dardalhon-Cuménal, Neel B. Randsholt, and Frederique Peronnet. "Drosophila melanogasterCyclin G coordinates cell growth and cell proliferation." Cell Cycle 10, no. 5 (March 2011): 805–18. http://dx.doi.org/10.4161/cc.10.5.14959.

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13

Roush, W. "Cell Biology: Regulating G Protein Signaling." Science 271, no. 5252 (February 23, 1996): 1056–58. http://dx.doi.org/10.1126/science.271.5252.1056.

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Dhanasekaran, N., and M. V. V. S. Vara Prasad. "G Protein Subunits and Cell Proliferation." Neurosignals 7, no. 2 (1998): 109–17. http://dx.doi.org/10.1159/000014536.

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15

CUADRADO, A., M. NAVARRETE, and J. CANOVAS. "Regulation of G and G by cell size in higher plants." Cell Biology International Reports 10, no. 4 (April 1986): 223–30. http://dx.doi.org/10.1016/0309-1651(86)90068-8.

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16

Chaikot, Choochart, and Masakatsu Fukuda. "G-8 DEVELOPMENT OF LOW COBALT ALNICO-TYPE MAGNET(Session: Fuel Cell/Magnet)." Proceedings of the Asian Symposium on Materials and Processing 2006 (2006): 134. http://dx.doi.org/10.1299/jsmeasmp.2006.134.

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17

Matsumoto, Koji, Saburo Shikuwa, Yoshihisa Kawase, Masahiro Ito, Kazuko Shichijo, and Ichiro Sekine. "G Cell, D Cell and Parietal Cell in the Stomach of SHR." Japanese Heart Journal 29, no. 4 (1988): 565. http://dx.doi.org/10.1536/ihj.29.565.

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18

Rodriguez, Carlos O., Christine M. Stellrecht, and Varsha Gandhi. "Mechanisms for T-cell selective cytotoxicity of arabinosylguanine." Blood 102, no. 5 (September 1, 2003): 1842–48. http://dx.doi.org/10.1182/blood-2003-01-0317.

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AbstractNelarabine, prodrug of arabinosylguanine (ara-G), has demonstrated T-lymphoblastic antileukemic activity in cell lines and in the clinic. To investigate the mechanism for lineage-specific toxicity, the effects of ara-G were compared in CEM (T-lymphoblast), Raji (B-lymphoblast), and ML-1 (myeloid) cell lines. CEM cells were the most sensitive to ara-G–induced apoptosis and accumulated the highest levels of ara-G triphosphate (ara-GTP). However, compared with myeloid and B-lineage cell lines, CEM cells incorporated fewer ara-G molecules—which were at internucleotide positions in all 3 cell lines— into DNA. Ara-G induced an S-phase arrest in both Raji and ML-1, while in CEM the S-phase cells decreased with a concomitant increase in the sub-G1 population. Within 3 hours of ara-G treatment, the levels of soluble Fas ligand (sFasL) in the medium increased significantly in CEM cultures. In parallel, an induction of FasL gene expression was observed by real-time reverse transcriptase–polymerase chain reaction (RT-PCR). Pretreatment of CEM cells with a Fas antagonistic antibody inhibited ara-G–mediated cell death. These results demonstrate that high ara-GTP accumulation in T cells results in an S phase–dependent apoptosis induced by ara-G incorporation into DNA, which may lead to a T cell–specific signal for the induction and liberation of sFasL. Subsequently, the sFasL induces an apoptotic response in neighboring non–S-phase cells. In contrast, myeloid and B cells accumulated lower levels of ara-GTP and arrested in S phase, blocking any apoptotic signaling.

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Watson, E. L., C. Oliver, N. D'Silva, and C. M. Belton. "Localization of the G-protein G(o) in exocrine glands." Journal of Histochemistry & Cytochemistry 42, no. 1 (January 1994): 41–47. http://dx.doi.org/10.1177/42.1.7505300.

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The GTP-binding protein G(o) was localized immunohistochemically in the rat parotid gland and in other exocrine glands with specific G(o) antibodies. Immunohistochemical studies revealed that affinity-purified G(o alpha) polyclonal antibody (GO/85) immunoreacted primarily with duct cells of the rat parotid gland; immunoreactivity was also noted in duct cells of the rat submandibular, mouse parotid, and mouse submandibular glands. Light labeling of rat parotid and submandibular gland acinar cells was also noted. G(o alpha) antiserum (9072) differing in specificity for epitopes within G(o alpha) produced similar results. This antiserum also immunoreacted with rat submandibular duct cell secretory granule membranes. In contrast, in rat and mouse pancreas G(o alpha) antibodies immunoreacted primarily with islet cells. Duct cells were negative but there was light labeling of rat pancreatic acinar cells. The apparent duct specificity of G(o alpha) staining was further verified by demonstrating that G(o alpha) antibodies immunoreacted with HSG-PA cells, a human transformed salivary duct cell line. Specificity in immunohistochemical labeling of HSG-PA cells was confirmed by Western blot analysis. The results demonstrate that G(o) appears to be selectively expressed in the duct cells of rat parotid gland and other salivary glands. The selective enrichment of G(o) in duct cells suggests that this G-protein plays an important role in duct cell physiology.

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20

Kim, Tae Young, Hee Won Moon, Bora Oh, Sang Mee Hwang, Ja-Lok Ku, and Dong Soon Lee. "Expressions of G-CSF Receptor in Tumor Cells Might Stimulate the Proliferation of Malignant Cells Upon Treatment of G-CSF." Blood 114, no. 22 (November 20, 2009): 1009. http://dx.doi.org/10.1182/blood.v114.22.1009.1009.

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Abstract Abstract 1009 Poster Board I-31 We previously reported that the increased expression of G-CSFR in AML1/ETO+ AML cell, suggesting that cells with G-CSFR expression might easily proliferate in response to therapeutic G-CSF. To confirm the association of AML/ETO gene and increased expression of G-CSFR, we transfected AML1/ETO specific small interfering RNAs (siRNAs) to AML/ETO+ cell line and G-CSFR expression was decreased on transfection by siRNA AML1/ETO gene suggesting a strong association between AML1/ETO gene and G-CSFR up-regulation. To assess the effect of G-CSF on G-CSR expressing leukemic cells, we treated the most commonly used two forms of G-CSF on various leukemic cell lines. Both forms of G-CSF significantly stimulated the cell proliferation (40-80% increment compared to control) and the differentiation of AML1/ETO+ leukemic cells. Western blot showed marked increased signals of JAK2/STAT3 after treatment of G-CSF on AML/ETO+ Kasumi-1 cell line, while there was no increased signals in AML/ETO- CTV-1 cell line. To search the malignant tumors with increased G-CSFR, we screened the expressions of G-CSFR mRNA in 32 kinds of solid tumor cell lines and % kinds of leukemic cell lines, using real-time PCR. Among 32 kinds of solid tumor cell lines, 3 cell lines [hepatoblastoma (HepG2), squamous cell carcinoma of larynx (SNU-899), and breast carcinoma cell line (MCF 10A)] expressed G-CSFR mRNA and amount of G-CSFR expression of HepG2 cell was comparable to Kasumi-1 cell lines. In summary, association of G-CSFR and AML/ETO gene is strongly suggested. Expression of G-CSFR in some tumor cells is suspected, requiring pre-screening of G-CSFR expression before treatment of G-CSF. The present study shows that therapeutic G-CSF might stimulate the proliferation and differentiation of malignant cells with G-CSFR expression (AML/ETO+ AML cell and solid tumor cell lines) and we suggest the prescreening of G-CSFR expression primary tumor cells before treatment of G-CSF. Disclosures: No relevant conflicts of interest to declare.

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SIEPL, C., S. BODMER, E. HOFER, M. WRANN, K. FREI, and A. FONTANA. "Glioblastoma-Cell-Derived T-Cell Suppressor Factor (G-TsF) Sequence Analysis and Biologic Mechanism of G-TsF." Annals of the New York Academy of Sciences 540, no. 1 Advances in N (November 1988): 437–39. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27126.x.

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22

Joyner, Ronald W., Rajiv Kumar, David A. Golod, Ronald Wilders, Habo J. Jongsma, E. Etienne Verheijck, Lennart Bouman, William N. Goolsby, and Antoni C. G. Van Ginneken. "Electrical interactions between a rabbit atrial cell and a nodal cell model." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 6 (June 1, 1998): H2152—H2162. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h2152.

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Atrial activation involves interactions between cells with automaticity and slow-response action potentials with cells that are intrinsically quiescent with fast-response action potentials. Understanding normal and abnormal atrial activity requires an understanding of this process. We studied interactions of a cell with spontaneous activity, represented by a “real-time” simulation of a model of the rabbit sinoatrial (SA) node cell, simultaneously being electrically coupled via our “coupling clamp” circuit to a real, isolated atrial myocyte with variations in coupling conductance ( G c) or stimulus frequency. The atrial cells were able to be driven at a regular rate by a single SA node model (SAN model) cell. Critical G c for entrainment of the SAN model cell to a nonstimulated atrial cell was 0.55 ± 0.05 nS ( n = 7), and the critical G c that allowed entrainment when the atrial cell was directly paced at a basic cycle length of 300 ms was 0.32 ± 0.01 nS ( n = 7). For each atrial cell we found periodic phenomena of synchronization other than 1:1 entrainment when G c was between 0.1 and 0.3 nS, below the value required for frequency entrainment, when the atrial cell was directly driven at a basic cycle length of either 300 or 600 ms. In conclusion, the high input resistance of the atrial cells allows successful entrainment of nodal and atrial cells at low values of G c, but further uncoupling produces arrhythmic interactions.

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Mapara, MY, K. Bommert, RC Bargou, C. Leng, C. Beck, WD Ludwig, P. Gierschik, and B. Dorken. "G protein subunit G alpha 16 expression is restricted to progenitor B cells during human B-cell differentiation." Blood 85, no. 7 (April 1, 1995): 1836–42. http://dx.doi.org/10.1182/blood.v85.7.1836.bloodjournal8571836.

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Recently G alpha 16, a new guanosine triphosphate (GTP) binding protein alpha subunit has been described to be specifically expressed in human hematopoietic cells. Expression of G alpha 16 was observed in human cell lines of myelomonocytic and T-lymphocytic origin, but not in human B-cell lines Raji and IM9. We studied the expression of G alpha 16 in human B cells corresponding to different stages of B-cell differentiation by means of reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. The human Burkitt's lymphoma cell lines Raji, Ramos, BJAB, the lymphoblastoid cell line SKW6.4, and the plasmocytoma cell line U266 were devoid of G alpha 16. In contrast, G alpha 16 was detected in the human progenitor B cell lines Reh and Nalm-6. Using the mu+, k-cell line BLIN-1 (pre-B cell phenotype) and its derived subclone 1E8 (surface mu+, k+; B-cell phenotype) G alpha 16 expression was found to disappear on transition from pre-B to B-cell differentiation stage. The analysis of a broad panel of human neoplastic B lymphocytes ranging from progenitor B-acute lymphatic leukemia (pre-pre-B-ALL), common acute leukemias (cALL), pre-B-ALL, mature B-ALL to low grade B-cell lymphoma (chronic lymphocytic leukemia of B-cell type, leukemic centrocytic non-Hodgkins lymphoma [NHL], hairy cell leukemia) showed that G alpha 16 expression is limited to progenitor and pre-B-ALL cells. Therefore, we conclude that within B-cell differentiation, G alpha 16 is expressed solely during early B cell ontogeny and downregulated during differentiation. Thus, G alpha 16 might be an important regulator involved in signaling processes in progenitor B cells.

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Maloy, Kevin J., Christoph Burkhart, Tobias M. Junt, Bernhard Odermatt, Annette Oxenius, Luca Piali, Rolf M. Zinkernagel, and Hans Hengartner. "Cd4+ T Cell Subsets during Virus Infection." Journal of Experimental Medicine 191, no. 12 (June 19, 2000): 2159–70. http://dx.doi.org/10.1084/jem.191.12.2159.

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To analyze the antiviral protective capacities of CD4+ T helper (Th) cell subsets, we used transgenic T cells expressing an I-Ab–restricted T cell receptor specific for an epitope of vesicular stomatitis virus glycoprotein (VSV-G). After polarization into Th1 or Th2 effectors and adoptive transfer into T cell–deficient recipients, protective capacities were assessed after infection with different types of viruses expressing the VSV-G. Both Th1 and Th2 CD4+ T cells could transfer protection against systemic VSV infection, by stimulating the production of neutralizing immunoglobulin G antibodies. However, only Th1 CD4+ T cells were able to mediate protection against infection with recombinant vaccinia virus expressing the VSV-G (Vacc-IND-G). Similarly, only Th1 CD4+ T cells were able to rapidly eradicate Vacc-IND-G from peripheral organs, to mediate delayed-type hypersensitivity responses against VSV-G and to protect against lethal intranasal infection with VSV. Protective capacity correlated with the ability of Th1 CD4+ T cells to rapidly migrate to peripheral inflammatory sites in vivo and to respond to inflammatory chemokines that were induced after virus infection of peripheral tissues. Therefore, the antiviral protective capacity of a given CD4+ T cell is governed by the effector cytokines it produces and by its migratory capability.

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Li, Zhuo, Cher Hung, Reay G. Paterson, Frank Michel, Sandra Fuentes, Ryan Place, Yuan Lin, Robert J. Hogan, Robert A. Lamb, and Biao He. "Type II integral membrane protein, TM of J paramyxovirus promotes cell-to-cell fusion." Proceedings of the National Academy of Sciences 112, no. 40 (September 21, 2015): 12504–9. http://dx.doi.org/10.1073/pnas.1509476112.

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Paramyxoviruses include many important animal and human pathogens. Most paramyxoviruses have two integral membrane proteins: fusion protein (F) and attachment proteins hemagglutinin, hemagglutinin–neuraminidase, or glycoprotein (G), which are critical for viral entry into cells. J paramyxovirus (JPV) encodes four integral membrane proteins: F, G, SH, and transmembrane (TM). The function of TM is not known. In this work, we have generated a viable JPV lacking TM (JPV∆TM). JPV∆TM formed opaque plaques compared with JPV. Quantitative syncytia assays showed that JPV∆TM was defective in promoting cell-to-cell fusion (i.e., syncytia formation) compared with JPV. Furthermore, cells separately expressing F, G, TM, or F plus G did not form syncytia whereas cells expressing F plus TM formed some syncytia. However, syncytia formation was much greater with coexpression of F, G, and TM. Biochemical analysis indicates that F, G, and TM interact with each other. A small hydrophobic region in the TM ectodomain from amino acid residues 118 to 132, the hydrophobic loop (HL), was important for syncytial promotion, suggesting that the TM HL region plays a critical role in cell-to-cell fusion.

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Lonial, Sagar, Claire Torre, Amelia A. Langston, Stephanie McMillan, Ellie Hamilton, Christopher Flowers, Mary J. Lechowicz, and Edmund K. Waller. "A Randomized Trial To Evaluate the Impact of Cytokines (G-CSF or GM + G-CSF) on Dendritic Cell and T-Cell Content and Function When Mobilizing Normal Donors for Allogeneic Progenitor Cell Transplant." Blood 106, no. 11 (November 16, 2005): 1960. http://dx.doi.org/10.1182/blood.v106.11.1960.1960.

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Abstract Introduction: Optimal cellular immunity following allogeneic HPC transplant is a tenuous balance between effective anti-tumor immunity and the avoidance of life threatening GvHD. The events necessary for potentially curative GvL are related to tumor burden, T-cell content, NK cell content, and dendritic cell content. Our group previously demonstrated that DC content following allogeneic BMT can impact EFS (Waller et al, Blood 2001), and that cytokines used during mobilization impact DC content of the autologous graft (Lonial et al, BBMT 2004). The current trial was designed with the hypothesis that the use of G + GM-CSF will result in fewer tolerogenic DC2 cells within the graft, and increased Th1 phenotype among the mobilized T-cells. Methods: 40 normal donors were randomized to receive G-CSF alone (7.5 mcg/kg BID) or G-CSF (7.5mcg/kg qd) and GM-CSF (7.5 mcg/kg qd) for 5 days or longer if additional apheresis were necessary. Side effects between the 2 cytokine regimens were documented using a questionnaire that was administered within 2 weeks of successful collection. Graft content was evaluated using multi-color flow cytometry, and pre-mobilization blood was collected to test for T-cell and DC content as well as T-cell function. T-cell proliferation was assessed using thymidine incorporation assays following mitogen exposure, and T-cell activation profile was assessed using ELISA assays of secreted cytokines following mitogen stimulation. DC1 (myeloid DC) were defined as Lin-/HLA-DR+/CD11C+/CD123−, while DC2 (lymphoid DC) were defined as Lin-/HLA-DR+/CD11C−/CD123+. Results: 18 patients received G+GM-CSF and 22 patients received G-CSF alone. All 40 donors were successfully mobilized, though more patients in the G-CSF arm required multiple days of collection (mean number of collections 1.5 G-CSF vs 1.0 G+GM-CSF, p=0.01). Donors mobilized with G-CSF alone had a higher overall cell count (765e8/ml compared with 615e8/ml for G+GM-CSF, p=0.04), though the CD34 content of the grafts were comparable. Again, there was a significant reduction in delivered DC2 content of graft mobilized with G+GM-CSF when compared with G-CSF alone (5.1e6/kg compared with 2.85e6/kg, p=0.001), with a trend towards fewer DC1 cells as well (2.6e6/kg vs 1.7e6/kg, p=0.05). Overall, the DC1:DC2 ratio favors DC1 among donors mobilized with G+GM-CSF. Additionally, grafts collected with G-CSF alone had nearly twice the total T-cell content of grafts mobilized with G+GM-CSF (420e6/kg vs 220e6/kg, p=0.0001). The reduction in total T-cells was evenly distributed between CD4 and CD8 cells with similar magnitude of reduction in both subsets amongst those receiving G+GM-CSF. Interestingly, grafts collected from the recipients of G+GM-CSF produced more IL-2 at rest, and secreted significantly more IL-12 in response to mitogen. Toxicity between the 2 arms were similar with 1 patient in the G+GM-CSF arm having to stop growth factors due to bone pain and fever. Conclusion: The combination of G+GM-CSF mobilizes fewer DC2 cells as well as 40–50% fewer T-cells, and is more likely to result in a successful single PBSC collection than the use of G-CSF alone. Preliminary data suggests that the combination of G+GM-CSF shifts T-cells towards a Th1 phenotype, despite fewer overall T-cells. Further laboratory evaluation of the graft, survival, and GvHD data following transplant will also be presented.

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Waller, Edmund K., Brent R. Logan, Mingwei Fei, Stephanie J. Lee, Dennis Confer, Alan Howard, Shanmuganathan Chandrakasan, Claudio Anasetti, Shanelle M. Fernando, and Cynthia R. Giver. "Kinetics of immune cell reconstitution predict survival in allogeneic bone marrow and G-CSF–mobilized stem cell transplantation." Blood Advances 3, no. 15 (July 25, 2019): 2250–63. http://dx.doi.org/10.1182/bloodadvances.2018029892.

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Abstract The clinical utility of monitoring immune reconstitution after allotransplant was evaluated using data from Blood and Marrow Transplant Clinical Trials Network BMT CTN 0201 (NCT00075816), a multicenter randomized study of unrelated donor bone marrow (BM) vs granulocyte colony-stimulating factor (G-CSF)–mobilized blood stem cell (G-PB) grafts. Among 410 patients with posttransplant flow cytometry measurements of immune cell subsets, recipients of G-PB grafts had faster T-cell reconstitution than BM recipients, including more naive CD4+ T cells and T-cell receptor excision circle–positive CD4+ and CD8+ T cells at 3 months, consistent with better thymic function. Faster reconstitution of CD4+ T cells and naive CD4+ T cells at 1 month and CD8+ T cells at 3 months predicted more chronic graft-versus-host disease (GVHD) but better survival in G-PB recipients, but consistent associations of T-cell amounts with GVHD or survival were not seen in BM recipients. In contrast, a higher number of classical dendritic cells (cDCs) in blood samples at 3 months predicted better survival in BM recipients. Functional T-cell immunity measured in vitro by cytokine secretion in response to stimulation with cytomegalovirus peptides was similar when comparing blood samples from BM and G-PB recipients, but the degree to which acute GVHD suppressed immune reconstitution varied according to graft source. BM, but not G-PB, recipients with a history of grades 2-4 acute GVHD had lower numbers of B cells, plasmacytoid dendritic cells, and cDCs at 3 months. Thus, early measurements of T-cell reconstitution are predictive cellular biomarkers for long-term survival and response to GVHD therapy in G-PB recipients, whereas more robust DC reconstitution predicted better survival in BM recipients.

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Urosevic, Mirjana, Joerg Willers, Beatrix Mueller, Werner Kempf, Guenter Burg, and Reinhard Dummer. "HLA-G protein up-regulation in primary cutaneous lymphomas is associated with interleukin-10 expression in large cell T-cell lymphomas and indolent B-cell lymphomas." Blood 99, no. 2 (January 15, 2002): 609–17. http://dx.doi.org/10.1182/blood.v99.2.609.

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Abstract Primary cutaneous lymphomas (CLs) constitute a spectrum of diseases characterized by a clonal accumulation of lymphocytes in the skin. Most CLs display a Th2 cytokine profile, including expression of interleukin-10 (IL-10). Because the up-regulation of HLA-G, a nonclassical class Ib molecule inducible by IL-10, might account for the immunescape of the malignant clone, HLA-G and IL-10 expression has been investigated in 45 cases of primary CL (10 of B-cell and 35 of T-cell origin) with quantitative polymerase chain reaction (PCR) and immunohistochemistry. HLA-G message was present in all cutaneous B-cell (CBCL) and T-cell (CTCL) lymphomas evaluated. Immunohistochemistry revealed HLA-G protein expression in 23 (51%) of 45 cases (7 of 10 CBCL, 16 of 35 CTCL). While in CBCL mostly indolent types displayed HLA-G positivity, in CTCL HLA-G expression was associated with high-grade histology and advanced stage of the disease. Except for neoplastic and infiltrating lymphocytes, other cells such as macrophages and dendritic cells showed HLA-G immunoreactivity. Furthermore, IL-10 protein expression was demonstrated in 16 (73%) of 22 HLA-G+ cases, which correlated with HLA-G protein presence (P < .001). HLA-G up-regulation together with IL-10 expression in CL might additionally contribute to the evasion of immunosurveillance and facilitate the transition from low- to high-grade lymphomas.

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Knust, Elisabeth. "G Protein Signaling and Asymmetric Cell Division." Cell 107, no. 2 (October 2001): 125–28. http://dx.doi.org/10.1016/s0092-8674(01)00534-7.

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Karagöz, Bülent, Abdullah Haholu, Alpaslan Özgün, Oguz Bilgi, Tolga Tunçel, Levent Emirzeoglu, Serkan Çelik, and Dilaver Demirel. "HLA-G in Testicular Germ Cell Tumors." Oncology Research and Treatment 37, no. 5 (2014): 3. http://dx.doi.org/10.1159/000362377.

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Millner, P. A. "Heterotrimeric G-proteins in plant cell signaling." New Phytologist 151, no. 1 (July 2001): 165–74. http://dx.doi.org/10.1046/j.1469-8137.2001.00172.x.

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Kwan, Chi Pong, and Guido N. J. Tytgat. "Antral G-cell hyperplasia: a vanishing disease?" European Journal of Gastroenterology & Hepatology 7, no. 11 (November 1995): 1099–103. http://dx.doi.org/10.1097/00042737-199511000-00014.

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Dhanasekaran, N., Siu-Tai Tsim, Jonathan M. Dermott, and Djamila Onesime. "Regulation of cell proliferation by G proteins." Oncogene 17, no. 11 (September 1998): 1383–94. http://dx.doi.org/10.1038/sj.onc.1202242.

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Karagoz, Bulent, Abdullah Haholu, Alpaslan Ozgun, Oguz Bilgi, Tolga Tuncel, Levent Emirzeoglu, Serkan Celik, and Dilaver Demirel. "HLA-G in testis germ cell tumors." Journal of Clinical Oncology 32, no. 15_suppl (May 20, 2014): e15620-e15620. http://dx.doi.org/10.1200/jco.2014.32.15_suppl.e15620.

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Landry, Y., M. Mousli, T. Fischer, and C. Bronner. "Neuropeptides, G-proteins and mast cell secretion." Neuropeptides 22, no. 1 (May 1992): 39. http://dx.doi.org/10.1016/0143-4179(92)90436-z.

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Gukovskaya, Anna S. "G proteins in T cell signal transduction." Immunology Letters 31, no. 1 (January 1992): 1–9. http://dx.doi.org/10.1016/0165-2478(92)90002-6.

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Dolphin, Annette C. "Role of G-proteins in cell signalling." Journal of Molecular and Cellular Cardiology 22 (May 1990): S125. http://dx.doi.org/10.1016/0022-2828(90)91895-e.

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Siepl, C., S. Bodmer, E. Hofer, M. Wrann, and A. Fontana. "The glioblastoma cell derived T cell suppressor factor (G-TsF): Sequence analysis and biological mechanism of G-TsF." Journal of Neuroimmunology 16, no. 1 (September 1987): 161–62. http://dx.doi.org/10.1016/0165-5728(87)90380-8.

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Takaishi, Kenji, Takuya Sasaki, Hirokazu Kotani, Hideo Nishioka, and Yoshimi Takai. "Regulation of Cell–Cell Adhesion by Rac and Rho Small G Proteins in MDCK Cells." Journal of Cell Biology 139, no. 4 (November 17, 1997): 1047–59. http://dx.doi.org/10.1083/jcb.139.4.1047.

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The Rho small G protein family, consisting of the Rho, Rac, and Cdc42 subfamilies, regulates various cell functions, such as cell shape change, cell motility, and cytokinesis, through reorganization of the actin cytoskeleton. We show here that the Rac and Rho subfamilies furthermore regulate cell–cell adhesion. We prepared MDCK cell lines stably expressing each of dominant active mutants of RhoA (sMDCK-RhoDA), Rac1 (sMDCK-RacDA), and Cdc42 (sMDCK-Cdc42DA) and dominant negative mutants of Rac1 (sMDCK-RacDN) and Cdc42 (sMDCK-Cdc42DN) and analyzed cell adhesion in these cell lines. The actin filaments at the cell–cell adhesion sites markedly increased in sMDCK-RacDA cells, whereas they apparently decreased in sMDCK-RacDN cells, compared with those in wild-type MDCK cells. Both E-cadherin and β-catenin, adherens junctional proteins, at the cell–cell adhesion sites also increased in sMDCK-RacDA cells, whereas both of them decreased in sMDCK-RacDN cells. The detergent solubility assay indicated that the amount of detergent-insoluble E-cadherin increased in sMDCK-RacDA cells, whereas it slightly decreased in sMDCK-RacDN cells, compared with that in wild-type MDCK cells. In sMDCK-RhoDA, -Cdc42DA, and -Cdc42DN cells, neither of these proteins at the cell–cell adhesion sites was apparently affected. ZO-1, a tight junctional protein, was not apparently affected in any of the transformant cell lines. Electron microscopic analysis revealed that sMDCK-RacDA cells tightly made contact with each other throughout the lateral membranes, whereas wild-type MDCK and sMDCK-RacDN cells tightly and linearly made contact at the apical area of the lateral membranes. These results suggest that the Rac subfamily regulates the formation of the cadherin-based cell– cell adhesion. Microinjection of C3 into wild-type MDCK cells inhibited the formation of both the cadherin-based cell–cell adhesion and the tight junction, but microinjection of C3 into sMDCK-RacDA cells showed little effect on the localization of the actin filaments and E-cadherin at the cell–cell adhesion sites. These results suggest that the Rho subfamily is necessary for the formation of both the cadherin-based cell– cell adhesion and the tight junction, but not essential for the Rac subfamily-regulated, cadherin-based cell– cell adhesion.

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LeMaoult, Joel, Julien Caumartin, Marina Daouya, Benoit Favier, Solene Le Rond, Alvaro Gonzalez, and Edgardo D. Carosella. "Immune regulation by pretenders: cell-to-cell transfers of HLA-G make effector T cells act as regulatory cells." Blood 109, no. 5 (October 31, 2006): 2040–48. http://dx.doi.org/10.1182/blood-2006-05-024547.

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Abstract Trogocytosis is the uptake of membrane fragments from one cell by another and has been described for immune cells in mice and humans. Functional consequences of trogocytosis are emerging, but a dramatic immune function has still to be associated with it. Here we show that some resting, and most activated, CD4+ and CD8+ T cells acquire immunosuppressive HLA-G1 from antigen-presenting cells (APCs) in a few minutes. Acquisition of HLA-G through membrane transfers does not change the real nature of the T cells but immediately reverses their function from effectors to regulatory cells. These regulatory cells can inhibit allo-proliferative responses through HLA-G1 that they acquired. These data demonstrate that trogocytosis of HLA-G1 leads to instant generation of a new type of regulatory cells, which act through cell-surface molecules they temporarily display but do not express themselves. Such regulatory cells whose existence is most likely limited in space and time might constitute an “emergency” immune suppression mechanism used by HLA-G–expressing tissues to protect themselves against immune aggression. In addition, T cells acquire from HLA-G–expressing APCs their HLA-G–dependent capability to induce the slower differentiation of regulatory cells that act independently of HLA-G. These data re-emphasize the significance of HLA-G expression in normal and pathologic situations.

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Lonial, Sagar, Claire Torre, Michelle Hicks, Stephanie Mcmillan, Amelia A. Langston, Christopher R. Flowers, Mary J. Lechowicz, and Edmund K. Waller. "A Randomized Trial to Evaluate the Impact of Cytokines on Dendritic Cell, T-Cell and T-Cell Function When Mobilizing Normal Donors for Allogeneic Progenitor Cell Transplant: An Interim Analysis." Blood 104, no. 11 (November 16, 2004): 2854. http://dx.doi.org/10.1182/blood.v104.11.2854.2854.

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Abstract Introduction:Optimal cellular immunity following allogeneic HPC transplant represents a balance between the induction of sufficient anti-tumor immunity to eradicate residual cancer cells without the induction of life-threatening GvHD. Dendritic cells are potent APCs with the ability to regulate immune responses. Our group has previously reported that increased numbers of donor DC2 result in inferior EFS following allo BMT (Waller et al, Blood 2001), and that myeloid cytokines used for mobilization modulate the DC content of the auto graft (Lonial et al, BBMT in press). The current trial was designed to evaluate the impact of different cytokine combinations on DC content and T-cell function in normal donors mobilized with either G-CSF or the combination of G-CSF + GM-CSF. Methods: 32 normal donors were randomized to mobilization with G-CSF (7.5 mcg/kg BID) or the combination of GM-CSF (7.5 mcg/kg qAM) + G-CSF (7.5 mcg/kg qPM) until completion of the stem cell collection. Side effects between the 2 regimens were documented using a questionnaire filled out by the donors within 2 weeks of stem cell collection. DC, T-cell, and other cell subsets were measured from the graft using flow cytometry. T-cell function was evaluated by measuring T-cell proliferation in response to PMA, Con A, PHA, and PWM. Cytokines (IL2, IL4, IL10,IL12, TNF, and INF) secreted in response to antigens were measured by ELISA. DC1 (myeloid DC) were defined as Lin-/HLA-DR+/CD11c+/CD123- while DC2 (lymphoid DC) were defined as Lin-/HLA-DR+/CD11c-/CD123+. Results: 28 patients have been successfully collected to date (G-CSF n=15, GM+G-CSF n=13). No donor has failed to mobilize in either group. Among the 15 donors mobilized with G-CSF alone, 5 required multiple days of apheresis as compared with 1 of 13 donors who received GM+G-CSF who required multiple days of apheresis (p=0.06). There was no difference in baseline values of T-cells or DC subsets in the peripheral blood prior to cytokine administration. Grafts collected with GM-CSF+ G-CSF contained significantly fewer DC2 cells and T-cells (median DC2 dose of 2.1 x 10E6/kg and CD3 dose of 197x 10E6/kg) compared with grafts from donors who received G-CSF alone (median DC2 dose of 3.8 x 10E6/kg (p=.01) and CD3 dose of 320 x 10E6/kg (p=0.001)). There was no difference in the content of CD34+ or DC1 in the grafts, nor in the ratio of CD4:CD8 T-cells between grafts collected with the 2 cytokine combinations. T-cell proliferation and cytokine secretion in response to mitogens was not different between grafts collected from the two groups. To date, there is no difference in the frequency of GvHD or relapse between the patients transplanted with the grafts collected from the 2 cytokine cohorts. Conclusions: The addition of GM-CSF to the mobilization regimen results in significantly fewer DC2 cells and T-cells in the blood HPC graft which could impact immune function and GvL following allogeneic HPC transplant. Clinical outcomes and further analysis of TH1/TH2 polarization of T-cells in grafts collected with either G-CSF or G-CSF+GM-CSF are in progress..

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Kiuchi, Tai, Tomoaki Nagai, Kazumasa Ohashi, and Kensaku Mizuno. "Measurements of spatiotemporal changes in G-actin concentration reveal its effect on stimulus-induced actin assembly and lamellipodium extension." Journal of Cell Biology 193, no. 2 (April 18, 2011): 365–80. http://dx.doi.org/10.1083/jcb.201101035.

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To understand the intracellular role of G-actin concentration in stimulus-induced actin assembly and lamellipodium extension during cell migration, we developed a novel technique for quantifying spatiotemporal changes in G-actin concentration in live cells, consisting of sequential measurements of fluorescent decay after photoactivation (FDAP) of Dronpa-labeled actin. Cytoplasmic G-actin concentrations decreased by ∼40% immediately after cell stimulation and thereafter the cell area extended. The extent of stimulus-induced G-actin loss and cell extension correlated linearly with G-actin concentration in unstimulated cells, even at concentrations much higher than the critical concentration of actin filaments, indicating that cytoplasmic G-actin concentration is a critical parameter for determining the extent of stimulus-induced G-actin assembly and cell extension. Multipoint FDAP analysis revealed that G-actin concentration in lamellipodia was comparable to that in the cell body. We also assessed the cellular concentrations of free G-actin, profilin- and thymosin-β4–bound G-actin, and free barbed and pointed ends of actin filaments by model fitting of jasplakinolide-induced temporal changes in G-actin concentration.

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Miller, Jeffrey S., Felipe Prosper, and Valarie McCullar. "Natural Killer (NK) Cells Are Functionally Abnormal and NK Cell Progenitors Are Diminished in Granulocyte Colony-Stimulating Factor–Mobilized Peripheral Blood Progenitor Cell Collections." Blood 90, no. 8 (October 15, 1997): 3098–105. http://dx.doi.org/10.1182/blood.v90.8.3098.

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Abstract Granulocyte colony-stimulating factor (G-CSF)–mobilized peripheral blood progenitor cell (PBPC) collections are increasingly emerging as the graft of choice in many centers for autologous transplantation, and with increasing frequency for allogeneic transplantation. However, the role of myeloid cytokines in lymphoid function, lymphoid progenitors, and immune-mediated antitumor responses is not known. We studied PBPC collections from normal donors mobilized with G-CSF (10 μg/kg). CD56+/CD3− natural killer (NK) cells sorted from PBPC products exhibited a diminished ability to kill tumor targets, were less responsive in acquiring increased cytolysis with interleukin-2 (IL-2), and proliferated less than NK cells from normal unprimed peripheral blood. This abnormality was not explained by a change in phenotype of NK cells normally circulating in the blood after G-CSF administration. We could not demonstrate any direct suppressive effect on normal unprimed NK cell proliferation or cytotoxicity by culture with pharmacologic concentrations of G-CSF. We next evaluated the effects of G-CSF on CD34+ NK cell progenitors. CD34+/CD2+, CD34+/CD7+, and CD34+/CD10+ progenitors were markedly diminished in G-CSF–mobilized PBPC products. CD34+ cells cultured in limiting dilution assays showed a sixfold decrease in NK cell progenitors when derived from G-CSF–mobilized CD34+ PBPCs compared with CD34+ cells derived from unprimed marrow. The finding of decreased NK cell function, inhibited proliferation, and diminished cloning frequency after treatment with G-CSF could be mimicked in vitro by culture of primitive marrow progenitors (CD34+, lineage-negative, HLA-DR−) on stromal layers in the presence of exogenous G-CSF. The findings presented here show that G-CSF administration to normal donors decreases NK cell function and the relative frequency of NK cell progenitors within the CD34+ progenitor population. Overcoming this diminished lymphoid capacity may be important to facilitate early posttransplant immunotherapy. Our in vitro model will be used in future studies to determine the mechanism of the G-CSF–induced suppression of NK cell progenitors, which may occur early in the differentiation process.

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Donahue, Robert E., Ping Jin, Aylin C. Bonifacino, Mark E. Metzger, Jiaqiang Ren, Ena Wang, and David F. Stroncek. "Plerixafor (AMD3100) and granulocyte colony-stimulating factor (G-CSF) mobilize different CD34+ cell populations based on global gene and microRNA expression signatures." Blood 114, no. 12 (September 17, 2009): 2530–41. http://dx.doi.org/10.1182/blood-2009-04-214403.

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Abstract Plerixafor (AMD3100) and granulocyte colony-stimulating factor (G-CSF) mobilize peripheral blood stem cells by different mechanisms. A rhesus macaque model was used to compare plerixafor and G-CSF–mobilized CD34+ cells. Three peripheral blood stem cell concentrates were collected from 3 macaques treated with G-CSF, plerixafor, or plerixafor plus G-CSF. CD34+ cells were isolated by immunoselection and were analyzed by global gene and microRNA (miR) expression microarrays. Unsupervised hierarchical clustering of the gene expression data separated the CD34+ cells into 3 groups based on mobilization regimen. Plerixafor-mobilized cells were enriched for B cells, T cells, and mast cell genes, and G-CSF–mobilized cells were enriched for neutrophils and mononuclear phagocyte genes. Genes up-regulated in plerixafor plus G-CSF–mobilized CD34+ cells included many that were not up-regulated by either agent alone. Two hematopoietic progenitor cell miR, miR-10 and miR-126, and a dendritic cell miR, miR-155, were up-regulated in G-CSF–mobilized CD34+ cells. A pre-B-cell acute lymphocytic leukemia miR, miR-143-3p, and a T-cell miR, miR-143-5p, were up-regulated in plerixafor plus G-CSF–mobilized cells. The composition of CD34+ cells is dependent on the mobilization protocol. Plerixafor-mobilized CD34+ cells include more B-, T-, and mast cell precursors, whereas G-CSF–mobilized cells have more neutrophil and mononuclear phagocyte precursors.

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Migliaccio, G., A. R. Migliaccio, B. L. Kreider, G. Rovera, and J. W. Adamson. "Selection of lineage-restricted cell lines immortalized at different stages of hematopoietic differentiation from the murine cell line 32D." Journal of Cell Biology 109, no. 2 (August 1, 1989): 833–41. http://dx.doi.org/10.1083/jcb.109.2.833.

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Erythropoietin (Epo), granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor- (G-CSF) dependent cell lines have been derived from the murine hematopoietic cell line 32D with a selection strategy involving the culture of the cells in FBS-deprived medium supplemented only with pure recombinant Epo, GM-CSF, or G-CSF. The cells retain the diploid karyotype of the original 32D clone, do not grow in the absence of exogenous growth factor, and do not induce tumors when injected into syngeneic recipients. The morphology of the Epo-dependent cell lines (32D Epo1, -2, and -3) was heterogeneous and evolved with passage. The percent of differentiated cells also was a function of the cell line investigated. Benzidine-positive cells ranged from 1-2% (32D Epo3) to 50-60% (32D Epo1). These erythroid cells expressed carbonic anhydrase I and/or globin mRNA but not carbonic anhydrase II. The GM-CSF- and G-CSF-dependent cell lines had predominantly the morphology of undifferentiated myeloblasts or metamyelocytes, respectively. The GM-CSF-dependent cell lines were sensitive to either GM-CSF or interleukin-3 (IL-3) but did not respond to G-CSF. The G-CSF-dependent cell lines grew to a limited extent in IL-3 but did not respond to GM-CSF. These results indicate that the cell line 32D, originally described as predominantly a basophil/mast cell line, has retained the capacity to give rise to cells which proliferate and differentiate in response to Epo, GM-CSF, and/or G-CSF. These cells represent the first nontransformed cell lines which can be maintained in growth factors other than IL-3 and which differentiate in the presence of physiologic signals. As such, they may represent a model to study the molecular mechanisms underlying the process of hematopoietic differentiation, as well as sensitive targets for bioassays of specific growth factors.

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Lee, K. H., T. Kinashi, K. Tohyama, K. Tashiro, N. Funato, K. Hama, and T. Honjo. "Different stromal cell lines support lineage-selective differentiation of the multipotential bone marrow stem cell clone LyD9." Journal of Experimental Medicine 173, no. 5 (May 1, 1991): 1257–66. http://dx.doi.org/10.1084/jem.173.5.1257.

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An interleukin 3-dependent multipotential stem cell clone, LyD9, has been shown to generate mature B lymphocytes, macrophages, and neutrophils by coculture with primary bone marrow stromal cells. We report here that coculture with the cloned stromal cell lines PA6 and ST2 can support differentiation of LyD9 cells predominantly into granulocyte/macrophage colony-stimulating factor (GM-CSF)- and granulocyte (G)-CSF-responsive cells, respectively. However, these stromal cell lines were unable to support lymphopoiesis of LyD9 cells. The GM-CSF-dependent line, L-GM, which was derived from LyD9 cells cocultured with PA6 stromal cells, could differentiate into macrophages and granulocytes in the presence of GM-CSF. The L-GM line can further differentiate predominantly into neutrophils by coculture with ST2 stromal cells. The G-CSF-dependent line, L-G, which was derived from LyD9 cells cocultured with ST2 stromal cells, differentiated into neutrophils in response to G-CSF. Although the stromal cell-supported differentiation of LyD9 cells required the direct contact between LyD9 and stromal cells, a small fraction of LyD9 cells that were pretreated with 5-azacytidine could differentiate into neutrophils and macrophages without direct contact with stromal cells. These results indicate that different stromal cell lines support lineage-selective differentiation of the LyD9 stem cell and that 5-azacytidine treatment can bypass the requirement of direct contact with stromal cells, albeit with a lower frequency.

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Villota, Hernán, Sebastian Pizarro, Francisco Gajardo, Álvaro Delgadillo, Fabián Cortés-Mancera, and Giuliano Bernal. "Ruthenium Complex Induce Cell Death in G-415 Gallbladder Cancer Cells." Journal of Gastrointestinal Cancer 51, no. 2 (August 13, 2019): 571–78. http://dx.doi.org/10.1007/s12029-019-00278-x.

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Mark, Tomer, David Jayabalan, Roger N. Pearse, Jessica Stern, Jessica Furst, April Rambo, John Harpel, et al. "Cyclophosphamide Overcomes the Suppressive Effect of LenalidomideTherapy on Stem Cell Collection in Preparation for Autologous Stem Cell Transplantation for Multiple Myeloma." Blood 110, no. 11 (November 16, 2007): 3024. http://dx.doi.org/10.1182/blood.v110.11.3024.3024.

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Abstract Multiple Myeloma (MM) therapy has evolved over recent years to include powerful new therapeutic agents. The goal for most patients with MM, however, still remains high-dose chemotherapy followed by autologous stem cell transplantations as this procedure has been proven to have a therapeutic benefit. Therefore, the selection of an induction therapy must take into consideration the potential impact on the ability to collect enough stem cells for future transplantation. Recent studies have discussed difficulty in collecting stem cells in patients receiving lenalidomide-based induction therapy using filgastrim (G-CSF) in preparation for autologous stem cell transplantation in MM. It also has been recommended that the duration of lenalidomide induction therapy be limited to 4–6 cycles, since longer treatment time can hinder collection yields. We sought to determine if the addition of cyclophosphamide (CTX) to G-CSF as a mobilization regimen could rescue the ability to collect adequate stem cells for at least two autologous stem cell transplants for patients who had induction therapy with the BiRD (Biaxin® [clarithromycin]/Revlimid® [lenalidomide]/dexamethasone) regimen. BiRD therapy is as follows for each 28-day cycle: Clarithromycin 500mg po BID for days 1–28, Lenalidomide 25mg po daily for days 1–21, and Dexamethasone 40mg po weekly on days 1, 8, 15, and 21. All patients had either Stage II or III MM by Salmon-Durie criteria and were treatment naïve. Patients were advised to undergo stem cell collection after either maximum disease response or disease plateau had been achieved. Prior to stem cell mobilization, BiRD therapy was held for a minimum of 14 days. Stem cell collection was performed after either G-CSF alone at a dose 10 mcg/kg/day for 5–10 consecutive days until a total of 10 × 106/kg CD34+ stem cells had been collected or with the addition of cyclophosphamide (CTX) at a dose of 3g/m2 once prior to the initiation of G-CSF therapy. A total of 28 patients underwent stem cell collection. Stem cell mobilization was attempted with G-CSF alone in 9 instances and with CTX+G-CSF in 20 instances (1 patient underwent mobilization with both G-CSF alone and CTX+G-CSF). In comparison to the G-CSF monotherapy, CTX+G-CSF yielded a significantly greater stem cell collection (mean CD34+ cells collected: 3.78 × 106/kg vs. 32.33 × 106/kg, P < 0.0001). Only 33% of patients who attempted stem cell mobilization with G-CSF alone obtained sufficient CD34+ cell yield vs. 100% of the patients mobilized with CTX+G-CSF (P < 0.0001). The extent of BiRD therapy prior to stem cell mobilization ranged from 2–27 cycles. The number of cycles of BiRD did not significantly impact the success rate of stem cell collection (P = 0.14). In conclusion, the patients mobilized with CTX+G-CSF had a higher number of CD34+ cells collected and were all able collect enough stem cells for two autologous transplants. There was no association with the duration of BiRD therapy and successful CD34+ cell collection. We therefore recommend continuing lenalidomide-based induction therapy until desired tumor reduction goal is achieved and using the CTX in addition to G-CSF to ensure successful stem cell harvest prior to autologous transplantation.

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Stepan, Vinzenz M., Dieter F. Krametter, Masashi Matsushima, Andrea Todisco, John Delvalle, and Chris J. Dickinson. "Glycine-extended gastrin regulates HEK cell growth." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 2 (August 1, 1999): R572—R581. http://dx.doi.org/10.1152/ajpregu.1999.277.2.r572.

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Posttranslational processing of progastrin to a carboxy terminally amidated form (G-NH2) is essential for its effect on gastric acid secretion and other biological effects mediated by gastrin/CCK-B receptors. The immediate biosynthetic precursor of G-NH2, glycine-extended gastrin (G-Gly), does not stimulate gastric acid secretion at physiological concentrations but is found in high concentrations during development. G-NH2 and G-Gly have potent growth stimulatory effects on gastrointestinal tissues, and G-NH2 can stimulate proliferation of human kidney cells. Thus we sought to explore the actions of G-NH2 and G-Gly on the human embryonic kidney cell line HEK 293. HEK 293 cells showed specific binding sites for 125I-labeled Leu15-G17-NH2and125I-Leu15-G2—17-Gly. Both G-NH2 and G-Gly induced a dose-dependent increase in [3H]thymidine incorporation, and both peptides together significantly increased [3H]thymidine incorporation above the level of either peptide alone. G-NH2 and G-Gly were detected by radioimmunoassay in serum-free conditioned media. Antibodies directed against G-NH2 and G-Gly lead to a significant reduction in [3H]thymidine incorporation. G-NH2 but not G-Gly increased intracellular Ca2+concentration. We conclude that G-NH2 and G-Gly act cooperatively via distinct receptors to stimulate the growth of a nongastrointestinal cell line (HEK 293) in an autocrine fashion.

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Mangor, J. T., S. A. Monsma, M. C. Johnson, and G. W. Blissard. "A GP64-Null Baculovirus Pseudotyped with Vesicular Stomatitis Virus G Protein." Journal of Virology 75, no. 6 (March 15, 2001): 2544–56. http://dx.doi.org/10.1128/jvi.75.6.2544-2556.2001.

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ABSTRACT The Autographa californica multiple nucleopolyhedrovirus (AcMNPV) GP64 protein is an essential virion protein that is involved in both receptor binding and membrane fusion during viral entry. Genetic studies have shown that GP64-null viruses are unable to move from cell to cell and this results from a defect in the assembly and production of budded virions (BV). To further examine requirements for virion budding, we asked whether a GP64-null baculovirus, vAc64−, could be pseudotyped by introducing a heterologous viral envelope protein (vesicular stomatitis virus G protein [VSV-G]) into its membrane and whether the resulting virus was infectious. To address this question, we generated a stably transfected insect Sf9 cell line (Sf9VSV-G) that inducibly expresses the VSV-G protein upon infection with AcMNPV Sf9VSV-G and Sf9 cells were infected with vAc64−, and cells were monitored for infection and for movement of infection from cell to cell. vAc64− formed plaques on Sf9VSV-G cells but not on Sf9 cells, and plaques formed on Sf9VSV-G cells were observed only after prolonged intervals. Passage and amplification of vAc64− on Sf9VSV-G cells resulted in pseudotyped virus particles that contained the VSV-G protein. Cell-to-cell propagation of vAc64− in the G-expressing cells was delayed in comparison to wild-type (wt) AcMNPV, and growth curves showed that pseudotyped vAc64− was generated at titers of approximately 106 to 107 infectious units (IU)/ml, compared with titers of approximately 108 IU/ml for wt AcMNPV. Propagation and amplification of pseudotyped vAc64− virions in Sf9VSV-G cells suggests that the VSV-G protein may either possess the signals necessary for baculovirus BV assembly and budding at the cell surface or may otherwise facilitate production of infectious baculovirus virions. The functional complementation of GP64-null viruses by VSV-G protein was further demonstrated by identification of a vAc64−-derived virus that had acquired the G gene through recombination with Sf9VSV-G cellular DNA. GP64-null viruses expressing the VSV-G gene were capable of productive infection, replication, and propagation in Sf9 cells.

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Journal articles on the topic 'G-cell'

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