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Journal articles on the topic 'GL'

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Published: 4 June 2021
Last updated: 1 August 2024

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1

Sun, Li, and Enlin Yang. "On the GL(r)×GL(r+s)×GL(s) convolution." Journal of Number Theory 134 (January 2014): 130–41. http://dx.doi.org/10.1016/j.jnt.2013.08.001.

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2

Sharma, Prahlad, and Will Sawin. "Subconvexity for GL(3)×GL(2) twists." Advances in Mathematics 404 (August 2022): 108420. http://dx.doi.org/10.1016/j.aim.2022.108420.

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3

KHAN, RIZWANUR. "Simultaneous non-vanishing of GL(3) × GL(2) and GL(2) L-functions." Mathematical Proceedings of the Cambridge Philosophical Society 152, no. 3 (December 12, 2011): 535–53. http://dx.doi.org/10.1017/s0305004111000806.

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AbstractFix g a Hecke–Maass form for SL3(). In the family of holomorphic newforms f of fixed weight and large prime level q, we find the average value of the product $L(\half,g\times f)L(\half,f)$. From this we derive a result on the simultaneous non-vanishing of these L-functions at the central point.
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4

Liu, Sheng-Chi. "Simultaneous nonvanishing of $GL(2) \times GL(2)$ and $GL(2)$ $L$-functions." Proceedings of the American Mathematical Society 142, no. 6 (March 7, 2014): 1953–64. http://dx.doi.org/10.1090/s0002-9939-2014-12066-1.

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5

Ishii, Taku, and Eric Stade. "Archimedean zeta integrals on GL n × GL m and SO2n+1 × GL m." Manuscripta Mathematica 141, no. 3-4 (September 28, 2012): 485–536. http://dx.doi.org/10.1007/s00229-012-0581-y.

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6

Wyser, Benjamin J., and Alexander Yong. "Polynomials for $$\mathrm{GL}_p\times \mathrm{GL}_q$$ GL p × GL q orbit closures in the flag variety." Selecta Mathematica 20, no. 4 (April 22, 2014): 1083–110. http://dx.doi.org/10.1007/s00029-014-0152-z.

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7

Wolfe, Rosalee. "Open GL." ACM SIGGRAPH Computer Graphics 32, no. 4 (November 1998): 29–31. http://dx.doi.org/10.1145/307710.307720.

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8

Everette, Sharon S. "Gl Distress." Gastroenterology Nursing 18, no. 6 (November 1995): 219–23. http://dx.doi.org/10.1097/00001610-199511000-00005.

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9

Castaño Giraldo, Gustavo Adolfo, Karim Chujfi Salazar, and Sergio Andrés Pineda Ramírez. "GL Ingenieros." Grafías, disciplinares de la UCPR, no. 23 (October 1, 2013): 39–52. http://dx.doi.org/10.31908/grafias.v0i23.1419.

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Por su complejidad e importancia, las organizaciones necesitan ser administradas con base en conocimiento técnico y en el seguimiento de los cambios que presenta su entorno. En este trabajo se hace énfasis en la administración financiera y en la gestión del talento humano para analizar algunas variables que intervienen en el funcionamiento de la organización GL Ingenieros S.A., que pertenece al sector de servicios eléctricos y actúa a nivel nacional.
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10

Farmer, David W., Sally Koutsoliotas, and Stefan Lemurell. "Maass Forms on GL(3) and GL(4)." International Mathematics Research Notices 2014, no. 22 (August 13, 2013): 6276–301. http://dx.doi.org/10.1093/imrn/rnt145.

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11

Kim, Henry H., and Freydoon Shahidi. "Functorial Products for GL 2 × GL 3 and the Symmetric Cube for GL 2." Annals of Mathematics 155, no. 3 (May 2002): 837. http://dx.doi.org/10.2307/3062134.

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12

Li, Shangzhi. "Overgroups in GL(U⊗ W) of certain subgroups of GL(U)⊗GL(W), I." Journal of Algebra 137, no. 2 (March 1991): 338–68. http://dx.doi.org/10.1016/0021-8693(91)90095-p.

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13

Flicker, Yuval Z. "Cusp Forms on GL(2n) with GL(n) × GL (n) Periods, and Simple Algebras." Mathematische Nachrichten 183, no. 1 (1997): 91–111. http://dx.doi.org/10.1002/mana.19971830107.

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14

Minchin, N. R., J. H. Hough, M. G. Burton, and T. Yamashita. "Near-infrared imaging polarimetry of bipolar nebulae - IV. GL 490, GL 2789 and GL 2136." Monthly Notices of the Royal Astronomical Society 251, no. 3 (August 1, 1991): 522–28. http://dx.doi.org/10.1093/mnras/251.3.522.

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15

Suprunenko, Irina, Alexander Kleshchev, and Jonathan Brundan. "Semisimple restrictions from GL(n) to GL(n-1)." Journal für die reine und angewandte Mathematik (Crelles Journal) 1998, no. 500 (July 1, 1998): 83–112. http://dx.doi.org/10.1515/crll.1998.072.

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16

Mukhin, Evgenii E., Vitaly O. Tarasov, and Alexander N. Varchenko. "Bispectral and $(\mathfrak{gl}_{N},\mathfrak{gl}_{M})$ dualities." Functional Analysis and Other Mathematics 1, no. 1 (November 15, 2007): 47–69. http://dx.doi.org/10.1007/s11853-007-0003-y.

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17

Harinck, Pascale, and Nicolas Jacquet. "Distributions propres invariantes sur la paire symétrique (gl(4,R),gl(2,R)×gl(2,R))." Journal of Functional Analysis 261, no. 9 (November 2011): 2362–436. http://dx.doi.org/10.1016/j.jfa.2011.06.012.

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18

Chan, Kei Yuen. "Homological branching law for $$({\mathrm {GL}}_{n+1}(F), {\mathrm {GL}}_n(F))$$: projectivity and indecomposability." Inventiones mathematicae 225, no. 1 (February 15, 2021): 299–345. http://dx.doi.org/10.1007/s00222-021-01033-5.

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AbstractLet F be a non-Archimedean local field. This paper studies homological properties of irreducible smooth representations restricted from $${\mathrm {GL}}_{n+1}(F)$$ GL n + 1 ( F ) to $${\mathrm {GL}}_n(F)$$ GL n ( F ) . A main result shows that each Bernstein component of an irreducible smooth representation of $${\mathrm {GL}}_{n+1}(F)$$ GL n + 1 ( F ) restricted to $${\mathrm {GL}}_n(F)$$ GL n ( F ) is indecomposable. We also classify all irreducible representations which are projective when restricting from $${\mathrm {GL}}_{n+1}(F)$$ GL n + 1 ( F ) to $${\mathrm {GL}}_n(F)$$ GL n ( F ) . A main tool of our study is a notion of left and right derivatives, extending some previous work joint with Gordan Savin. As a by-product, we also determine the branching law in the opposite direction.
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19

Plate, Aileen E., Jasmina Smajlović, Theodore S. Jardetzky, and Richard Longnecker. "Functional Analysis of Glycoprotein L (gL) from Rhesus Lymphocryptovirus in Epstein-Barr Virus-Mediated Cell Fusion Indicates a Direct Role of gL in gB-Induced Membrane Fusion." Journal of Virology 83, no. 15 (May 20, 2009): 7678–89. http://dx.doi.org/10.1128/jvi.00457-09.

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ABSTRACT Glycoprotein L (gL), which complexes with gH, is a conserved herpesvirus protein that is essential for Epstein-Barr virus (EBV) entry into host cells. The gH/gL complex has a conserved role in entry among herpesviruses, yet the mechanism is not clear. To gain a better understanding of the role of gL in EBV-mediated fusion, chimeric proteins were made using rhesus lymphocryptovirus (Rh-LCV) gL (Rh gL), which shares a high sequence homology with EBV gL but does not complement EBV gL in mediating fusion with B cells. A reduction in fusion activity was observed with chimeric gL proteins that contained the amino terminus of Rh gL, although they retained their ability to process and transport gH/gL to the cell surface. Amino acids not conserved within this region in EBV gL when compared to Rh gL were further analyzed, with the results mapping residues 54 and 94 as being functionally important for EBV-mediated fusion. All chimeras and mutants displayed levels of cell surface expression similar to that of wild-type gL and interacted with gH and gp42. Our data also suggest that the role of gL involves the activation or recruitment of gB with the gH/gL complex, as we found that reduced fusion of Rh gL, EBV/Rh-LCV chimeras, and gL point mutants could be restored by replacing EBV gB with Rh gB. These observations demonstrate a distinction between the role of gL in the processing and trafficking of gH to the cell surface and a posttrafficking role in cell-cell fusion.
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20

Schultz, Eric P., Jean-Marc Lanchy, Erin E. Ellerbeck, and Brent J. Ryckman. "Scanning Mutagenesis of Human Cytomegalovirus Glycoprotein gH/gL." Journal of Virology 90, no. 5 (December 9, 2015): 2294–305. http://dx.doi.org/10.1128/jvi.01875-15.

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ABSTRACTThe core, conserved function of the herpesvirus gH/gL is to promote gB-mediated membrane fusion during entry, although the mechanism is poorly understood. The human cytomegalovirus (HCMV) gH/gL can exist as either the gH/gL/gO trimer or the gH/gL/UL128/UL130/UL131 (gH/gL/UL128-131) pentamer. One model suggests that gH/gL/gO provides the core fusion role during entry into all cells within the broad tropism of HCMV, whereas gH/gL/UL128-131 acts at an earlier stage, by a distinct receptor-binding mechanism to enhance infection of select cell types, such as epithelial cells, endothelial cells, and monocytes/macrophages. To further study the distinct functions of these complexes, mutants with individual charged cluster-to-alanine (CCTA) mutations of gH and gL were combined to generate a library of 80 mutant gH/gL heterodimers. The majority of the mutant gH/gL complexes were unable to facilitate gB-mediated membrane fusion in transient-expression cell-cell fusion experiments. In contrast, these mutants supported the formation of gH/gL/UL128-131 complexes that could block HCMV infection in receptor interference experiments. These results suggest that receptor interactions with gH/gL/UL128-131 involve surfaces contained on the UL128-131 proteins but not on gH/gL. gH/gL/UL128-131 receptor interference could be blocked with anti-gH antibodies, suggesting that interference is a cell surface phenomenon and that anti-gH antibodies can block gH/gL/UL128-131 in a manner that is distinct from that for gH/gL/gO.IMPORTANCEInterest in the gH/gL complexes of HCMV (especially gH/gL/UL128-131) as vaccine targets has far outpaced our understanding of the mechanism by which they facilitate entry and contribute to broad cellular tropism. For Epstein-Barr virus (EBV), gH/gL and gH/gL/gp42 are both capable of promoting gB fusion for entry into epithelial cells and B cells, respectively. In contrast, HCMV gH/gL/gO appears to be the sole fusion cofactor that promotes gB fusion activity, whereas gH/gL/UL128-131 expands cell tropism through a distinct yet unknown mechanism. This study suggests that the surfaces of HCMV gH/gL are critical for promoting gB fusion but are dispensable for gH/gL/UL128-131 receptor interaction. This underscores the importance of gH/gL/gO in HCMV entry into all cell types and reaffirms the complex as a candidate target for vaccine development. The two functionally distinct forms of gH/gL present in HCMV make for a useful model with which to study the fundamental mechanisms by which herpesvirus gH/gL regulates gB fusion.
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21

Zhou, Momei, Jean-Marc Lanchy, and Brent J. Ryckman. "Human Cytomegalovirus gH/gL/gO Promotes the Fusion Step of Entry into All Cell Types, whereas gH/gL/UL128-131 Broadens Virus Tropism through a Distinct Mechanism." Journal of Virology 89, no. 17 (June 17, 2015): 8999–9009. http://dx.doi.org/10.1128/jvi.01325-15.

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ABSTRACTInteraction between gH/gL and the fusion protein gB is likely a conserved feature of the entry mechanism for all herpesviruses. Human cytomegalovirus (HCMV) gH/gL can be bound by gO or by the set of proteins UL128, UL130, and UL131, forming gH/gL/gO and gH/gL/UL128-131. The mechanisms by which these complexes facilitate entry are poorly understood. Mutants lacking UL128-131 replicate well on fibroblasts but fail to enter epithelial/endothelial cells, and this has led to the general assumption that gH/gL/UL128-131 promotes gB-mediated fusion on epithelial/endothelial cells whereas gH/gL/gO provides this function on fibroblasts. This was challenged by observations that gO-null mutants were defective on all of these cell types, suggesting that entry into epithelial/endothelial cells requires both of the gH/gL complexes, but the severe replication defect of the gO mutants precluded detailed analysis. We previously reported that the ratio of gH/gL/gO and gH/gL/UL128-131 in the virion envelope varied dramatically among HCMV strains. Here, we show that strains not only differ in the ratio, but also vary in the total amount of gH/gL in the virion. Cell-type-specific particle-to-PFU ratios of HCMV strains that contained different amounts of gH/gL/gO and gH/gL/UL128-131 were determined. Infection of both fibroblasts and epithelial cells was generally correlated with the abundance of gH/gL/gO, but not with that of gH/gL/UL128-131. The low infectivity of virions rich in gH/gL/UL128-131 but low in gH/gL/gO could be overcome by treatment with the chemical fusogen polyethylene glycol (PEG), strongly arguing that gH/gL/gO provides the conserved herpesvirus gH/gL entry function of promoting gB-mediated fusion for entry into all cell types, whereas gH/gL/UL128-131 acts through a distinct mechanism to allow infection of select cell types.IMPORTANCEThe functions of HCMV gH/gL complexes in entry are unclear. Unlike the well-studied Epstein-Barr virus (EBV), where gH/gL and gH/gL/gp42 complexes both seem capable of promoting gB fusion during entry into different cell types, our studies here suggest that for HCMV, gH/gL/gO promotes gB fusion on all cell types, whereas gH/gL/UL128-131 broadens virus tropism through a distinct, as yet unknown mechanism. To our knowledge, this is the first suggestion of a herpesvirus gH/gL that does not act by promoting gB fusion, which might make HCMV a useful model to study the fundamental mechanisms by which herpesvirus gH/gL regulates gB fusion. Moreover, gH/gL/UL128-131 is a candidate vaccine target. Our findings help to explain the cell-type-dependent virus neutralization exhibited by anti-gH/gL/UL128-131 antibodies and underscore the importance of gH/gL/gO as another important part of vaccine or therapeutic strategies.
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22

Ciferri, Claudio, Sumana Chandramouli, Danilo Donnarumma, Pavel A. Nikitin, Michael A. Cianfrocco, Rachel Gerrein, Adam L. Feire, et al. "Structural and biochemical studies of HCMV gH/gL/gO and Pentamer reveal mutually exclusive cell entry complexes." Proceedings of the National Academy of Sciences 112, no. 6 (January 26, 2015): 1767–72. http://dx.doi.org/10.1073/pnas.1424818112.

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Human cytomegalovirus (HCMV) is a major cause of morbidity and mortality in transplant patients and the leading viral cause of birth defects after congenital infection. The glycoprotein complexes gH/gL/gO and gH/gL/UL128/UL130/UL131A (Pentamer) are key targets of the human humoral response against HCMV and are required for HCMV entry into fibroblasts and endothelial/epithelial cells, respectively. We expressed and characterized soluble forms of gH/gL, gH/gL/gO, and Pentamer. Mass spectrometry and mutagenesis analysis revealed that gL-Cys144 forms disulfide bonds with gO-Cys351 in gH/gL/gO and with UL128-Cys162 in the Pentamer. Notably, Pentamer harboring the UL128-Cys162Ser/gL-Cys144Ser mutations had impaired syncytia formation and reduced interference of HCMV entry into epithelial cells. Electron microscopy analysis showed that HCMV gH/gL resembles HSV gH/gL and that gO and UL128/UL130/UL131A bind to the same site at the gH/gL N terminus. These data are consistent with gH/gL/gO and Pentamer forming mutually exclusive cell entry complexes and reveal the overall location of gH/gL-, gH/gL/gO-, and Pentamer-specific neutralizing antibody binding sites. Our results provide, to our knowledge, the first structural view of gH/gL/gO and Pentamer supporting the development of vaccines and antibody therapeutics against HCMV.
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23

Yano, Yuristella, Katia R. Cesar, Magali Araujo, Adilson C. Rodrigues, Lucia C. Andrade, and Antonio J. Magaldi. "Aquaporin 2 expression increased by glucagon in normal rat inner medullary collecting ducts." American Journal of Physiology-Renal Physiology 296, no. 1 (January 2009): F54—F59. http://dx.doi.org/10.1152/ajprenal.90367.2008.

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It is well known that Glucagon (Gl) is released after a high protein diet and participates in water excretion by the kidney, principally after a protein meal. To study this effect in in vitro perfused inner medullary collecting ducts (IMCD), the osmotic water permeability (Pf; μm/s) at 37°C and pH 7.4 in normal rat IMCDs ( n = 36) perfused with Ringer/HCO3 was determined. Gl (10−7 M) in absence of Vasopressin (AVP) enhanced the Pf from 4.38 ± 1.40 to 11.16 ± 1.44 μm/s ( P < 0.01). Adding 10−8, 10−7, and 10−6 M Gl, the Pf responded in a dose-dependent manner. The protein kinase A inhibitor H8 blocked the Gl effect. The specific Gl inhibitor, des-His1-[Glu9] glucagon (10−7 M), blocked the Gl-stimulated Pf but not the AVP-stimulated Pf. There occurred a partial additional effect between Gl and AVP. The cAMP level was enhanced from the control 1.24 ± 0.39 to 59.70 ± 15.18 fm/mg prot after Gl 10−7 M in an IMCD cell suspension. The immunoblotting studies indicated an increase in AQP2 protein abundance of 27% (cont 100.0 ± 3.9 vs. Gl 127.53; P = 0.0035) in membrane fractions extracted from IMCD tubule suspension, incubated with 10−6 M Gl. Our data showed that 1) Gl increased water absorption in a dose-dependent manner; 2) the anti-Gl blocked the action of Gl but not the action of AVP; 3) Gl stimulated the cAMP generation; 4) Gl increased the AQP2 water channel protein expression, leading us to conclude that Gl controls water absorption by utilizing a Gl receptor, rather than a AVP receptor, increasing the AQP2 protein expression.
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24

Weiss, Jillian Todd. "GL vs. BT." Journal of Bisexuality 3, no. 3-4 (April 12, 2003): 25–55. http://dx.doi.org/10.1300/j159v03n03_02.

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25

Waye, Jerome D. "Upper Gl bleeding." Gastrointestinal Endoscopy 50, no. 5 (November 1999): 730. http://dx.doi.org/10.1016/s0016-5107(99)80040-6.

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26

Nango, M., M. Maekawa, K. Murakami, and H. Yoshida. "CPS GL 799." Colloid & Polymer Science 269, no. 1 (January 1991): 70–76. http://dx.doi.org/10.1007/bf00654661.

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27

WILKINSON, MARY M. "Inpatient Gl Nursing." Gastroenterology Nursing 14, no. 4 (February 1992): 215–18. http://dx.doi.org/10.1097/00001610-199202000-00014.

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28

ZHUANG, Lingzi. "GL-impsing Bodish." Cahiers de Linguistique Asie Orientale 51, no. 2 (October 10, 2022): 139–74. http://dx.doi.org/10.1163/19606028-bja10024.

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Abstract A heretofore unrecognized prefix **g- is reconstructed for Proto-Bodish as an agentive transitivization prefix. This prefix is fossilized before liquids in at least 9 Tamangic verbs, and preserved as a root preinitial in at least 39 Tibetan verbs. The semantic value of agentive transitivization is characterized as an increase in the level of Agent involvement, and/or in the Agent’s conscious effort in performing the action. I describe a newly-documented suffix -wʌ in Sikleś Gurung (Tamangic) which innovatively grammaticalize this meaning category. The reconstruction of **g- lends support to the notional Bodish subgroup by grounding it in a shared innovation.
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29

Balkanova, O., G. Bhowmik, D. Frolenkov, and N. Raulf. "Mixed moment of GL(2) and GL(3)L‐functions." Proceedings of the London Mathematical Society 121, no. 2 (December 5, 2019): 177–219. http://dx.doi.org/10.1112/plms.12312.

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30

De Leo, Stefano, and Khaled Abdel-Khalek. "Octonionic representations of GL(8,R) and GL(4,C)." Journal of Mathematical Physics 38, no. 2 (February 1997): 582–98. http://dx.doi.org/10.1063/1.531879.

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31

Parashar, Deepak. "On the biparametric quantum deformation of GL(2)⊗GL(1)." Journal of Mathematical Physics 42, no. 11 (November 2001): 5431–43. http://dx.doi.org/10.1063/1.1407280.

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32

Sun, Qingfeng. "Averages of shifted convolution sums for GL(3)×GL(2)." Journal of Number Theory 182 (January 2018): 344–62. http://dx.doi.org/10.1016/j.jnt.2017.07.005.

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33

Xu, Zhao. "The second moment of GL(3) × GL(2) L-functions at special points from GL(3) forms." Frontiers of Mathematics in China 15, no. 5 (October 2020): 1071–88. http://dx.doi.org/10.1007/s11464-020-0860-y.

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34

van Dijk, G. "Harmonic analysis on the finite symmetric space GL(n, K)GL(1, K) × GL(n − 1, K)." Indagationes Mathematicae 6, no. 2 (June 1995): 153–66. http://dx.doi.org/10.1016/0019-3577(95)91240-v.

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35

Cui, Xinle, Zhouhong Cao, Shuishu Wang, Michael Flora, Stuart P. Adler, Michael A. McVoy, and Clifford M. Snapper. "Immunization of Rabbits with Recombinant Human Cytomegalovirus Trimeric versus Monomeric gH/gL Protein Elicits Markedly Higher Titers of Antibody and Neutralization Activity." International Journal of Molecular Sciences 20, no. 13 (June 28, 2019): 3158. http://dx.doi.org/10.3390/ijms20133158.

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Congenital human cytomegalovirus (HCMV) infection and HCMV infection of immunosuppressed patients cause significant morbidity and mortality, and vaccine development against HCMV is a major public health priority. HCMV envelope glycoproteins gB, gH, and gL, which constitute the core fusion machinery, play critical roles in HCMV fusion and entry into host cells. HCMV gB and gH/gL have been reported to elicit potent neutralizing antibodies. Recently, the gB/gH/gL complex was identified in the envelope of HCMV virions, and 16–50% of the total gH/gL bound to gB, forming the gB/gH/gL complex. These findings make the gB/gH/gL a unique HCMV vaccine candidate. We previously reported the production of HCMV trimeric gB and gH/gL heterodimers, and immunization with a combination of trimeric gB and gH/gL heterodimers elicited strong synergistic HCMV-neutralizing activity. To further improve the immunogenicity of gH/gL, we produced trimeric gH/gL. Rabbits immunized with HCMV trimeric gH/gL induced up to 38-fold higher serum titers of gH/gL-specific IgG relative to HCMV monomeric gH/gL, and elicited ~10-fold higher titers of complement-dependent and complement-independent HCMV-neutralizing activity for both epithelial cells and fibroblasts. HCMV trimeric gH/gL in combination with HCMV trimeric gB would be a novel promising HCMV vaccine candidate that could induce highly potent neutralizing activities.
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36

Klyachkin, Yuri M., Krista D. Stoops, and Robert J. Geraghty. "Herpes simplex virus type 1 glycoprotein L mutants that fail to promote trafficking of glycoprotein H and fail to function in fusion can induce binding of glycoprotein L-dependent anti-glycoprotein H antibodies." Journal of General Virology 87, no. 4 (April 1, 2006): 759–67. http://dx.doi.org/10.1099/vir.0.81563-0.

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The herpes simplex virus type 1 (HSV-1) glycoproteins H (gH) and L (gL) form a heterodimer and efficient expression of gH at the virion or cell surface is dependent upon gL. Five carboxy-terminal deletion mutants of gL were created and their ability to interact with and mediate cell-surface expression of gH, to promote binding of gL-dependent anti-gH antibodies and to contribute to cell fusion was analysed. All of the gL mutants bound gH, but only two mutants, containing the amino-terminal 161 or 168 aa of gL, mediated cell-surface expression of gH, and only gL161 and gL168 functioned in cell fusion. The binding of gL to gH, therefore, was not sufficient to ensure gH cell-surface expression and it was not possible to separate the gH-trafficking role of gL from gL function in fusion. Co-expression of gH with any gL mutant conferred binding of the anti-gH mAbs 53S and LP11. If the acquisition of 53S and LP11 binding to gH reflects a gL-induced conformational change, such a change is not sufficient to mediate trafficking of the gH–gL heterodimer.
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37

Unlu, Serhan, Christopher Haddad, Danai Dima, Tariq Kewan, Olisaemeka Ogbue, Waled Bahaj, Carlos Bravo-Perez, et al. "Somatic Genetic Rescue Involving CSF3R and Other Novel Phosphothyrosine Kinase Receptor Mutations Occurring in Myeloid Malignancies." Blood 142, Supplement 1 (November 28, 2023): 3219. http://dx.doi.org/10.1182/blood-2023-187151.

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Somatic gene rescue (SGR), via acquisition and selection of somatic (SM) genetic hits, neutralizes functional defects resulting from hypomorphic germline (GL) mutations. However, this process may be maladaptive and lead to the development of leukemia. Acquisition of SM gain-of-function CSF3R mutations in the context of severe congenital neutropenia (SCN) illustrates such a scenario. Here, we further explored this and similar mechanisms in a cohort of 7121 adults with myeloid neoplasia and bone marrow failure (AML=1473, MDS=2248, other=3400). CSF3R mutations were found in 97 patients. In total, there were 37 and 56 patients with SM and GL mutations, respectively; biallelic GL and SM were 4. Among SM alterations, 18 were pathogenic or likely pathogenic including 8 nonsense truncating variants in class III isoform specific region of the cytoplasmic domain and 10 classical missense mutations in the juxtamembrane region, previously defined in the context of post-SCN AML and CNL. We thus hypothesized that these CSF3R SM mutations may also represent SGR in adult patients harboring hypomorphic GL variants and investigated the presence of SCN-associated alterations ( ELANE, WAS, GFI1) and in other phosphothyrosine kinase receptors (PTKR) such as CSF1R, CSF2RA, CSF2RB, FLT3 and KIT. Indeed, we found biallelic WAS p.D264H GL and CSF3R p.A119T SM in a patient with aplastic anemia (AA). Biallelic CSF3R were present in 4 patients: a) p.Q749X GL withp.M696T SM, b) E835K GL with p.T618I SM, c) p.Y752X GL withp.Q754E SM and d) biallelic p.Y752X GL with p.Q754E GL configuration with T615A SM. Compound heterozygous configuration of CSF3R SM included CSF1R SM variants( CSF3R p.M696T SM & CSF1R p.R294Q GL in a 64 year old. patient with MPN, CSF3R p.M696T SM & CSF1R c.1626+3G&gt;A GL in a 61 year old patient with MDS) and CSF2RB ( CSF3R p.T618I SM & CSF2RB p.V890I GL in a 69 year old female patient with AML with leukopenia). When we analyzed the remaining 66 GL CSF3R variants in 56 carriers (in addition to the aforementioned biallelic combinations), we identified 9 compound heterozygous mutants involving CSF1R SM (n=1), CSF2RA (n=1), CSF2RB (n=3), FLT3(TKD/ITD, n=4/1). Specifically, we found the following configurations and disease associations: a) CSF3R p.V372E GL CSF2RB p.P842L SM in a 49 yo. AA patient who subsequently developed AML with FLT3 TKD, b) MDS patients with CSF3R p.E149 GL CSF1R p.G413S SM, c) CSF3R p.R440Q GL& CSF2RA p.R164Q SM and d) CSF3R p.E405K GL& CSF2RB c.1152+6G&gt;A SM and e) AML patients with CSF3R p.E405K GL& CSF2RB p.R432C SM; f) CSF3R p.L619S GLandg,h)2 AML cases with CSF3R p.E808K GL of which all 3 acquired compound heterozygosity with FLT3 TKD, i) CSF3R p.E808K GL CSF3R p.E835K GL in a 71 year old patient with MDS with FLT3 ITD AML. In addition to FLT3 GOF mutations, the most common SM hits observed in CSF3R GLcarriers were ASXL1 (n=12), TET2 (n=12), and SF3B1 (n=12). Identification of somatic and GL alterations in PTKR genes other than CSF3R, led us to systematically analyze these genes as targets of GL and SM CSF3R alterations. In total, we identified 72 GL and 73 SM CSF1R variants, 7 SM and 19 GL CSF2RA and 47 GL and 69 SM CSFR2B. Among these, we found 3 patients with compound heterozygous CSF2RB SM CSF3R GL, one with CSF2RB GL CSF3R GLas described above. We also identified one patient with CSF2RA SM CSF3R GL . Finally, we identified two patients with CSF1R GL and CSF3R SM, and one with CSF1R SM CSF3R GLmutations. In summary, our study provides evidence for a tremendous complexity of interaction between less penetrant GL alterations of receptor genes and somatic GOF mutations, which may in some instances, correspond to the result of SGR. It is likely that the degree of LOF corresponds to the selection pressure for somatic rescue lesions.
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38

Fan, Qing, Erick Lin, and Patricia G. Spear. "Insertional Mutations in Herpes Simplex Virus Type 1 gL Identify Functional Domains for Association with gH and for Membrane Fusion." Journal of Virology 83, no. 22 (September 2, 2009): 11607–15. http://dx.doi.org/10.1128/jvi.01369-09.

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ABSTRACT Glycoprotein L (gL) is one of four glycoproteins required for the entry of herpes simplex virus (HSV) into cells and for virus-induced cell fusion. This glycoprotein oligomerizes with gH to form a membrane-bound heterodimer but can be secreted when expressed without gH. Twelve unique gL linker-insertion mutants were generated to identify regions critical for gH binding and gH/gL processing and regions essential for cell fusion and viral entry. All gL mutants were detected on the cell surface in the absence of gH, suggesting incomplete cleavage of the signal peptide or the presence of a cell surface receptor for secreted gL. Coexpression with gH enhanced the levels of cell surface gL detected by antibodies for all gL mutants except those that were defective in their interactions with gH. Two insertions into a conserved region of gL abrogated the binding of gL to gH and prevented gH expression on the cell surface. Three other insertions reduced the cell surface expression of gH and/or altered the properties of gH/gL heterodimers. Altered or absent interaction of gL with gH was correlated with reduced or absent cell fusion activity and impaired complementation of virion infectivity. These results identify a conserved domain of gL that is critical for its binding to gH and two noncontiguous regions of gL, one of which contains the conserved domain, that are critical for the gH/gL complex to perform its role in membrane fusion.
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39

Ryckman, Brent J., Marie C. Chase, and David C. Johnson. "Human Cytomegalovirus TR Strain Glycoprotein O Acts as a Chaperone Promoting gH/gL Incorporation into Virions but Is Not Present in Virions." Journal of Virology 84, no. 5 (December 23, 2009): 2597–609. http://dx.doi.org/10.1128/jvi.02256-09.

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ABSTRACT Human cytomegalovirus (HCMV) produces the following two gH/gL complexes: gH/gL/gO and gH/gL/UL128-131. Entry into epithelial and endothelial cells requires gH/gL/UL128-131, and we have provided evidence that gH/gL/UL128-131 binds saturable epithelial cell receptors to mediate entry. HCMV does not require gH/gL/UL128-131 to enter fibroblasts, and laboratory adaptation to fibroblasts results in mutations in the UL128-131 genes, abolishing infection of epithelial and endothelial cells. HCMV gO-null mutants produce very small plaques on fibroblasts yet can spread on endothelial cells. Thus, one prevailing model suggests that gH/gL/gO mediates infection of fibroblasts, while gH/gL/UL128-131 mediates entry into epithelial/endothelial cells. Most biochemical studies of gO have involved the HCMV lab strain AD169, which does not assemble gH/gL/UL128-131 complexes. We examined gO produced by the low-passage clinical HCMV strain TR. Surprisingly, TR gO was not detected in purified extracellular virus particles. In TR-infected cells, gO remained sensitive to endoglycosidase H, suggesting that the protein was not exported from the endoplasmic reticulum (ER). However, TR gO interacted with gH/gL in the ER and promoted export of gH/gL from the ER to the Golgi apparatus. Pulse-chase experiments showed that a fraction of gO remained bound to gH/gL for relatively long periods, but gO eventually dissociated or was degraded and was not found in extracellular virions or secreted from cells. The accompanying report by P. T. Wille et al. (J. Virol., 84:2585-2596, 2010) showed that a TR gO-null mutant failed to incorporate gH/gL into virions and that the mutant was unable to enter fibroblasts and epithelial and endothelial cells. We concluded that gO acts as a molecular chaperone, increasing gH/gL ER export and incorporation into virions. It appears that gO competes with UL128-131 for binding onto gH/gL but is released from gH/gL, so that gH/gL (lacking UL128-131) is incorporated into virions. Thus, our revised model suggests that both gH/gL and gH/gL/UL128-131 are required for entry into epithelial and endothelial cells.
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40

Cairns, Tina M., Lisa S. Friedman, Huan Lou, J. Charles Whitbeck, Marie S. Shaner, Gary H. Cohen, and Roselyn J. Eisenberg. "N-Terminal Mutants of Herpes Simplex Virus Type 2 gH Are Transported without gL but Require gL for Function." Journal of Virology 81, no. 10 (March 7, 2007): 5102–11. http://dx.doi.org/10.1128/jvi.00097-07.

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ABSTRACT Glycoprotein H (gH) is conserved among all herpesviruses and is essential for virus entry and cell fusion along with gL, gB, and, in most alphaherpesviruses, gD. Within the gH/gL heterodimer, it is thought that gH accounts for the fusion function and gL acts as a chaperone for the folding and transport of gH. Here, we found that the N terminus of gH2 contains important elements involved in both its folding and its transport. Our conclusions are based on the phenotypes of a series of gH deletion mutants in which the signal sequence (residues 1 to 18) was retained and N-terminal residues were removed up to the number indicated. The first mutant, gH2Δ29 (deletion of residues 19 to 28), like wild-type (WT) gH, required gL for both transport and function. To our surprise, two other mutants (gH2Δ64 and gH2Δ72) were transported to the cell surface independent of gL but were nonfunctional, even when complexed with gL. Importantly, a fourth mutant (gH2Δ48) was transported independent of gL but was functional only when complexed with gL. Using a panel of monoclonal antibodies against gH2, we found that when gH2Δ48 was expressed alone, its antigenic structure differed from that of gH2Δ48/gL or gH2-WT/gL. Mutation of gH2 residue R39, Y41, W42, or D44 allowed gL-independent transport of gH. Our results also show that gL is not merely required for gH transport but is also necessary for the folding and function of the complex. Since gH2Δ64/gL and gH2Δ72/gL were nonfunctional, we hypothesized that residues critical for gH/gL function lie within this deleted region. Additional mutagenesis identified L66 and L72 as important for function. Together, our results highlight several key gH residues: R39, Y41, W42, and D44 for gH transport and L66 and L72 for gH/gL structure and function.
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41

Fricke, Thomas, Anna K. Großkopf, Armin Ensser, Marija Backovic, and Alexander S. Hahn. "Antibodies Targeting KSHV gH/gL Reveal Distinct Neutralization Mechanisms." Viruses 14, no. 3 (March 5, 2022): 541. http://dx.doi.org/10.3390/v14030541.

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Kaposi’s sarcoma herpesvirus (KSHV) is associated with a significant disease burden, in particular in Sub-Sahara Africa. A KSHV vaccine would be highly desirable, but the mechanisms underlying neutralizing antibody responses against KSHV remain largely unexplored. The complex made of glycoproteins H and L (gH/gL) activates gB for the fusion of viral and cellular membranes in all herpesviruses. KSHV gH/gL also interacts with cellular Eph family receptors. To identify optimal antigens for vaccination and to elucidate neutralization mechanisms, we primed mice with recombinantly expressed, soluble gH/gL (gHecto/gL) that was either wildtype (WT), lacking defined glycosylation sites or bearing modified glycosylation, followed by boosts with WT gHecto/gL. We also immunized with a gL-gHecto fusion protein or a gHecto-ferritin/gL nanoparticle. Immune sera neutralized KSHV and inhibited EphA2 receptor binding. None of the regimens was superior to immunization with WT gHecto/gL with regard to neutralizing activity and EphA2 blocking activity, the gL-gHecto fusion protein was equally effective, and the ferritin construct was inferior. gH/gL-targeting sera inhibited gB-mediated membrane fusion and inhibited infection also independently from receptor binding and gL, as demonstrated by neutralization of a novel KSHV mutant that does not or only marginally incorporate gL into the gH/gL complex and infects through an Eph-independent route.
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42

Gianni, Tatiana, Raffaele Massaro, and Gabriella Campadelli-Fiume. "Dissociation of HSV gL from gH by αvβ6- or αvβ8-integrin promotes gH activation and virus entry." Proceedings of the National Academy of Sciences 112, no. 29 (July 8, 2015): E3901—E3910. http://dx.doi.org/10.1073/pnas.1506846112.

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Herpes simplex virus (HSV) is an important human pathogen. It enters cells through an orchestrated process that requires four essential glycoproteins, gD, gH/gL, and gB, activated in cascade fashion by receptor-binding and signaling. gH/gL heterodimer is conserved across theHerpesviridaefamily. HSV entry is enabled by gH/gL interaction with αvβ6- or αvβ8-integrin receptors. We report that the interaction of virion gH/gL with integrins resulted in gL dissociation and its release in the medium. gL dissociation occurred if all components of the entry apparatus—receptor-bound gD and gB—were present and was prevented if entry was blocked by a neutralizing monoclonal antibody to gH or by a mutation in gH. We propose that (i) gL dissociation from gH/gL is part of the activation of HSV glycoproteins, critical for HSV entry; and (ii) gL is a functional inhibitor of gH and maintains gH in an inhibited form until receptor-bound gD and integrins signal to gH/gL.
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43

Gianni, Tatiana, Arianna Cerretani, Rebecca DuBois, Stefano Salvioli, Scott S. Blystone, Felix Rey, and Gabriella Campadelli-Fiume. "Herpes Simplex Virus Glycoproteins H/L Bind to Cells Independently of αVβ3 Integrin and Inhibit Virus Entry, and Their Constitutive Expression Restricts Infection." Journal of Virology 84, no. 8 (February 10, 2010): 4013–25. http://dx.doi.org/10.1128/jvi.02502-09.

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ABSTRACT Herpes simplex virus (HSV) fusion with cells requires the gD, gB, and gH/gL glycoprotein quartet. gD serves as a receptor binding glycoprotein. gB and gH/gL execute fusion in an as-yet-unclear manner. To better understand the role of gH/gL in HSV entry, we produced a soluble version of gH/gL carrying a One-STrEP tag (gHt.st/gL). Previous findings implicated integrins as possible ligands to gH/gL (C. Parry et al., J. Gen. Virol. 86:7-10, 2005). We report that (i) gHt.st/gL bound a number of cells in a dose-dependent manner at concentrations similar to those required for the binding of soluble gB or gD. (ii) gHt.st/gL inhibited HSV entry at the same concentrations required for binding. It also inhibited cell-cell fusion in transfected cells. (iii) The absence of β3 integrin did not prevent the binding of gHt.st/gL to CHO cells and infection inhibition. Conversely, integrin-negative K562 cells did not acquire the ability to bind gHt.st/gL when hyperexpressing αVβ3 integrin. (iv) Constitutive expression of wild-type gH/gL (wt-gH/gL) restricted infection in all of the cell lines tested, a behavior typical of glycoproteins which bind cellular receptors. The extent of restriction broadly paralleled the efficiency of gH/gL transfection. RGD motif mutant gH/gL could not be differentiated from wt-gH with respect to restriction of infection. Cumulatively, the present results provide several lines of evidence that HSV gH/gL interacts with a cell surface cognate protein(s), that this protein is not necessarily an αVβ3 integrin, and that this interaction is required for the process of virus entry/fusion.
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44

He, Jie, Hazelman Norhafis, and Lin Qin. "Responses of Green Leaves and Green Pseudobulbs of CAM Orchid Cattleya laeliocattleya Aloha Case to Drought Stress." Journal of Botany 2013 (July 16, 2013): 1–9. http://dx.doi.org/10.1155/2013/710539.

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This study examined the responses of green leaves (GL) and green pseudobulbs (GPSB) of CAM orchid Cattleya laeliocattleya Aloha Case to drought stress. After being subjected to drought stress, the decrease in water content (WC) was much greater in GPSB than in GL, indicating that GPSB facilitated a slow reduction in the WC of GL. This finding was further supported by the result of relative water content (RWC) of GL, which started to decrease only after 3 weeks of drought stress. Decreases of midday Fv/Fm ratios of GL occurred in all plants. However, the degrees of decrease were much greater in drought-stressed GL than in well-watered GL. Reduced Fv/Fm ratio (<0.8) at early morning was observed in drought-stressed GL after 3 weeks of treatments. Decreases in total chlorophyll (Chl) content, electron transport rate (ETR), photochemical quenching, qP, and nonphotochemical quenching, qN, were severer in GPSB than in GL after drought treatment. CAM acidity was significantly lower in both GL and GPSB after 2 weeks of drought treatment compared to well-watered plants. However, decrease of CAM acidity was smaller in GL than in GPSB. These results suggest that both GL and GPSB of CAM orchid Cattleya plantswere susceptible to drought stress.
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45

Neretin, Yu A. "The Fourier Transform on the Group $$\mathrm {GL}_2({\mathbb R })$$ GL 2 ( R ) and the Action of the Overalgebra $$\mathfrak {gl}_4$$ gl 4." Journal of Fourier Analysis and Applications 25, no. 2 (December 4, 2017): 488–505. http://dx.doi.org/10.1007/s00041-017-9589-8.

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46

Liu, Sheng-Chi. "Determination of GL(3) cusp forms by central values of GL(3)×GL(2) L-functions, level aspect." Journal of Number Theory 131, no. 8 (August 2011): 1397–408. http://dx.doi.org/10.1016/j.jnt.2011.01.014.

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47

McKee, Mark, Haiwei Sun, and Yangbo Ye. "Improved subconvexity bounds for $GL(2)\times GL(3)$ and $GL(3)$ $L$-functions by weighted stationary phase." Transactions of the American Mathematical Society 370, no. 5 (December 14, 2017): 3745–69. http://dx.doi.org/10.1090/tran/7159.

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48

Kato, Kakuki, Asako Horiba, Hiroaki Hayashi, Hajime Mizukami, and Kazuyoshi Terasaka. "Characterization of Triterpene Saponin Glycyrrhizin Transport by Glycyrrhiza glabra." Plants 11, no. 9 (May 5, 2022): 1250. http://dx.doi.org/10.3390/plants11091250.

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Glycyrrhizin (GL), a triterpene compound produced by Glycyrrhiza species, is a crucial pharmacologically active component of crude drugs. In contrast to the biosynthesis of GL in plants, little is known about GL transport and accumulation in plants. The transport mechanism of GL was characterized using cultured cells of Glycyrrhiza glabra. Cultured cells of G. glabra efficiently incorporated exogenously supplied GL. Proton pump inhibitors, such as probenecid and niflumic acid, as well as a protonophore (carbonylcyanide m-chlorophenylhydrazone), markedly inhibited GL uptake by cultured cells, whereas vanadate exhibited a moderate inhibition. Furthermore, GL transport by G. glabra tonoplast vesicles is dependent not on a H+-electrochemical gradient but MgATP and is markedly inhibited by vanadate. These results suggest that GL uptake by cultured cells is mediated by a H+-symporter in the plasma membrane and an ATP-binding cassette transporter, which has high specificity for the aglycone structure of GL on the tonoplast.
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49

Ryckman, Brent J., Barb L. Rainish, Marie C. Chase, Jamie A. Borton, Jay A. Nelson, Michael A. Jarvis, and David C. Johnson. "Characterization of the Human Cytomegalovirus gH/gL/UL128-131 Complex That Mediates Entry into Epithelial and Endothelial Cells." Journal of Virology 82, no. 1 (October 17, 2007): 60–70. http://dx.doi.org/10.1128/jvi.01910-07.

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ABSTRACT The entry of human cytomegalovirus (HCMV) into biologically relevant epithelial and endothelial cells involves endocytosis followed by low-pH-dependent fusion. This entry pathway is facilitated by the HCMV UL128, UL130, and UL131 proteins, which form one or more complexes with the virion envelope glycoprotein gH/gL. gH/gL/UL128-131 complexes appear to be distinct from the gH/gL/gO complex, which likely facilitates entry into fibroblasts. In order to better understand the assembly and protein-protein interactions of gH/gL/UL128-131 complexes, we generated HCMV mutants lacking UL128-131 proteins and nonreplicating adenovirus vectors expressing gH, gL, UL128, UL130, and UL131. Our results demonstrate that UL128, UL130, and UL131 can each independently assemble onto gH/gL scaffolds. However, the binding of individual UL128-131 proteins onto gH/gL can significantly affect the binding of other proteins; for example, UL128 increased the binding of both UL130 and UL131 to gH/gL. Direct interactions between gH/UL130, UL130/UL131, gL/UL128, and UL128/UL130 were also observed. The export of gH/gL complexes from the endoplasmic reticulum (ER) to the Golgi apparatus and cell surface was dramatically increased when all of UL128, UL130, and UL131 were coexpressed with gH/gL (with or without gO expression). Incorporation of gH/gL complexes into the virion envelope requires transport beyond the ER. Thus, we concluded that UL128, UL130, and UL131 must all bind simultaneously onto gH/gL for the production of complexes that can function in entry into epithelial and endothelial cells.
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50

Peng, Tao, Manuel Ponce de Leon, Michael J. Novotny, Hongbin Jiang, John D. Lambris, Gary Dubin, Patricia G. Spear, Gary H. Cohen, and Roselyn J. Eisenberg. "Structural and Antigenic Analysis of a Truncated Form of the Herpes Simplex Virus Glycoprotein gH-gL Complex." Journal of Virology 72, no. 7 (July 1, 1998): 6092–103. http://dx.doi.org/10.1128/jvi.72.7.6092-6103.1998.

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ABSTRACT The herpes simplex virus (HSV) gH-gL complex is essential for virus infectivity and is a major antigen for the host immune system. The association of gH with gL is required for correct folding, cell surface trafficking, and membrane presentation of the complex. Previously, a mammalian cell line was constructed which produces a secreted form of gHt-gL complex lacking the transmembrane and cytoplasmic tail regions of gH. gHt-gL retains a conformation similar to that of its full-length counterpart in HSV-infected cells. Here, we examined the structural and antigenic properties of gHt-gL. We first determined its stoichiometry and carbohydrate composition. We found that the complex consists of one molecule each of gH and gL. The N-linked carbohydrate (N-CHO) site on gL and most of the N-CHO sites on gH are utilized, and both proteins also contain O-linked carbohydrate and sialic acid. These results suggest that the complex is processed to the mature form via the Golgi network prior to secretion. To determine the antigenically active sites of gH and gL, we mapped the epitopes of a panel of gH and gL monoclonal antibodies (MAbs), using a series of gH and gL C-terminal truncation variant proteins produced in transiently transfected mammalian cells. Sixteen gH MAbs (including H6 and 37S) reacted with the N-terminal portion of gH between amino acids 19 and 276. One of the gH MAbs, H12, reacted with the middle portion of gH (residues 476 to 678). Nine gL MAbs (including 8H4 and VIII 62) reacted with continuous epitopes within the C-terminal portion of gL, and this region was further mapped within amino acids 168 to 178 with overlapping synthetic peptides. Finally, plasmids expressing the gH and gL truncations were employed in cotransfection assays to define the minimal regions of both gH and gL required for complex formation and secretion. The first 323 amino acids of gH and the first 161 amino acids of gL can form a stable secreted hetero-oligomer with gL and gH792, respectively, while gH323-gL168 is the smallest secreted hetero-oligomer. The first 648 amino acids of gH are required for reactivity with MAbs LP11 and 53S, indicating that a complex of gH648-gL oligomerizes into the correct conformation. The data suggest that both antigenic activity and oligomeric structure require the amino-terminal portions of gH and gL.
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