PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 18524170-8 2008 In addition, primed splenocytes produced a CD8+ IFNgamma response to gB. gb 69-71 CD8a molecule Homo sapiens 43-46 18474550-2 2008 The most conserved component of their entry machinery is glycoprotein B (gB), yet how gB functions is unclear. gb 73-75 glycoprotein B Murid gammaherpesvirus 4 57-71 19122386-6 2008 Because gB is essential for HSV-1 to infect cells, we analyzed function of PILRalpha in HSV-1 infection. gb 8-10 paired immunoglobin like type 2 receptor alpha Homo sapiens 75-84 18524170-8 2008 In addition, primed splenocytes produced a CD8+ IFNgamma response to gB. gb 69-71 interferon gamma Homo sapiens 48-56 17554016-3 2007 In the present study, I found that the PRV gB generated in human colon carcinoma LoVo cells, which lack the ubiquitous protease furin, remained in the uncleaved form and the virus replicated in these cells without cell fusion. gb 43-45 furin, paired basic amino acid cleaving enzyme Homo sapiens 128-133 18358807-4 2008 Our results demonstrate that cellular receptors for both gB and gD are required for HSV-1 infection and that PILRalpha plays an important role in HSV-1 infection as a coreceptor that associates with gB. gb 199-201 paired immunoglobin like type 2 receptor alpha Homo sapiens 109-118 17913800-9 2007 Furthermore, blocking gB internalization or impairing gB recycling to the cell surface, using drugs or a transdominant negative form of Rab11, significantly reduced cell-cell fusion. gb 22-24 RAB11A, member RAS oncogene family Homo sapiens 136-141 17913800-9 2007 Furthermore, blocking gB internalization or impairing gB recycling to the cell surface, using drugs or a transdominant negative form of Rab11, significantly reduced cell-cell fusion. gb 54-56 RAB11A, member RAS oncogene family Homo sapiens 136-141 17686835-7 2007 In cells expressing the dominant negative form of Vps4, the site of intracellular gB accumulation was altered; part of gB accumulated as an endoglycosidase H-sensitive immature form at a calreticulin-positive compartment, indicating that gB traffic was dependent on a functional MVB pathway. gb 82-84 vacuolar protein sorting 4 homolog A Homo sapiens 50-54 17686835-7 2007 In cells expressing the dominant negative form of Vps4, the site of intracellular gB accumulation was altered; part of gB accumulated as an endoglycosidase H-sensitive immature form at a calreticulin-positive compartment, indicating that gB traffic was dependent on a functional MVB pathway. gb 119-121 vacuolar protein sorting 4 homolog A Homo sapiens 50-54 17686835-7 2007 In cells expressing the dominant negative form of Vps4, the site of intracellular gB accumulation was altered; part of gB accumulated as an endoglycosidase H-sensitive immature form at a calreticulin-positive compartment, indicating that gB traffic was dependent on a functional MVB pathway. gb 119-121 vacuolar protein sorting 4 homolog A Homo sapiens 50-54 17947836-9 2007 Then, in both groups HbA1c after 12 months of Gb increased, and after 18 reduced (A: 9.2, and 8.8, B 9.1 and 8.5 respectively). gb 46-48 hemoglobin subunit alpha 1 Homo sapiens 21-25 17418502-5 2008 The distribution of the gB genotype of the CMV was: gB1 38,70%; gB2 25,80%; gB3 16,12% and gB4 19,35%. gb 24-26 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 52-55 18034158-3 2007 Glycoprotein B (gB) is the most conserved component of the herpesvirus entry machinery and its N terminus (gB-NT) is a common neutralization target. gb 16-18 glycoprotein B Murid gammaherpesvirus 4 0-14 17554016-4 2007 The uncleaved gB was converted into its subunits after furin digestion. gb 14-16 furin, paired basic amino acid cleaving enzyme Homo sapiens 55-60 17554016-8 2007 These results indicate that PRV gB is cleaved by furin and that the cleavage is dispensable for virus replication in vitro. gb 32-34 furin, paired basic amino acid cleaving enzyme Homo sapiens 49-54 14722275-6 2004 Interferon regulatory factor 3 (IRF3), a key transcriptional regulator of cellular interferon responses, is activated by CMV virions and soluble gB. gb 145-147 interferon regulatory factor 3 Homo sapiens 0-30 17348031-7 2007 CASA predicts the correct sign and order of magnitude of the stability change for 81% of the mutations, compared to 97% with the best GB. gb 134-136 casein alpha s1 Homo sapiens 0-4 17309289-9 2007 Tested against PB results, our GB method has an average unsigned relative error of only 0.6% for a representative set of 55 proteins and of 0.4% and 0.3%, respectively, for folded and unfolded conformations of cytochrome b562 sampled in molecular dynamics simulations. gb 31-33 mitochondrially encoded cytochrome b Homo sapiens 210-222 16216889-0 2005 Endogenous human cytomegalovirus gB is presented efficiently by MHC class II molecules to CD4+ CTL. gb 33-35 CD4 molecule Homo sapiens 90-93 16216889-5 2005 Human CD4+ T cells specific for gB were both highly abundant in blood and cytolytic in vivo. gb 32-34 CD4 molecule Homo sapiens 6-9 16216889-6 2005 gB-specific CD4+ T cell clones recognized gB that was expressed in glial, endothelial, and epithelial cells, but not exogenous gB that was fed to these cells. gb 0-2 CD4 molecule Homo sapiens 12-15 16216889-6 2005 gB-specific CD4+ T cell clones recognized gB that was expressed in glial, endothelial, and epithelial cells, but not exogenous gB that was fed to these cells. gb 42-44 CD4 molecule Homo sapiens 12-15 16216889-6 2005 gB-specific CD4+ T cell clones recognized gB that was expressed in glial, endothelial, and epithelial cells, but not exogenous gB that was fed to these cells. gb 42-44 CD4 molecule Homo sapiens 12-15 15767408-3 2005 A linear domain of gB designated AD-1 (antigenic domain 1) represents a dominant antibody binding site on this protein. gb 19-21 amyloid beta precursor protein Homo sapiens 33-37 15767408-4 2005 AD-1 from clinical isolates of HCMV exhibits little sequence variation, suggesting that AD-1 plays an essential role in gB structure or function. gb 120-122 amyloid beta precursor protein Homo sapiens 0-4 15767408-4 2005 AD-1 from clinical isolates of HCMV exhibits little sequence variation, suggesting that AD-1 plays an essential role in gB structure or function. gb 120-122 amyloid beta precursor protein Homo sapiens 88-92 15767408-5 2005 We investigated this possibility by examining the role of AD-1 in early steps of gB synthesis. gb 81-83 amyloid beta precursor protein Homo sapiens 58-62 15767408-6 2005 Our results from studies using eukaryotic cells indicated that amino acid (aa) 635 of the gB sequence represented the carboxyl-terminal limit of this domain and that deletion of aa 560 to 640 of the gB sequence resulted in loss of AD-1 expression. gb 199-201 amyloid beta precursor protein Homo sapiens 231-235 15767408-7 2005 AD-1 was shown to be required for oligomerization of gB. gb 53-55 amyloid beta precursor protein Homo sapiens 0-4 15767408-8 2005 Mutation of cysteine at either position 573 or 610 in AD-1 resulted in loss of its reactivity with AD-1-specific monoclonal antibodies and gB oligomerization. gb 139-141 amyloid beta precursor protein Homo sapiens 54-58 15767408-9 2005 Infectious virus could not be recovered from HCMV bacterial artificial chromosomes following introduction of these mutations into the HCMV genome, suggesting that AD-1 was an essential structural domain required for gB function in the replicative cycle of HCMV. gb 216-218 amyloid beta precursor protein Homo sapiens 163-167 17142766-9 2006 HBD3 bound both gB and heparan sulfate, but hBD1 and hBD2 bound neither. gb 16-18 defensin beta 103B Homo sapiens 0-4 16830864-11 2006 The LDH-B mRNA expression in GB was detected during all periods of the study (after embryonic d 12). gb 29-31 lactate dehydrogenase B Gallus gallus 4-9 16830864-12 2006 These observations suggest that GB expressed only LDH-B and that GB cells are not lactate-producing cells, like astrocyte, but rather are lactate-consuming cells, similar to neurons in CNS. gb 32-34 lactate dehydrogenase B Gallus gallus 50-55 16504488-3 2006 GA and GB were up to 4- and 22-fold elevated, respectively, in total and regional (cerebellum, hippocampus, cortex) brain extracts derived from SSADH(-/-) mice. gb 7-9 aldhehyde dehydrogenase family 5, subfamily A1 Mus musculus 144-149 15878864-4 2005 We now report that gB can activate the vascular endothelial growth factor receptor 3 (VEGFR-3) on the surface of microvascular endothelial cells and trigger receptor signaling, which can modulate endothelial migration and proliferation. gb 19-21 fms related receptor tyrosine kinase 4 Homo sapiens 39-84 15878864-4 2005 We now report that gB can activate the vascular endothelial growth factor receptor 3 (VEGFR-3) on the surface of microvascular endothelial cells and trigger receptor signaling, which can modulate endothelial migration and proliferation. gb 19-21 fms related receptor tyrosine kinase 4 Homo sapiens 86-93 15878864-6 2005 These functional changes in the endothelium may contribute to the pathogenesis of Kaposi"s sarcoma and suggest that interventions that inhibit gB activation of VEGFR-3 could be useful in the treatment of this neoplasm. gb 143-145 fms related receptor tyrosine kinase 4 Homo sapiens 160-167 15470476-6 2005 Coadministration of the gB and IL-12 genes also elevated the serum level of interferon-gamma. gb 24-26 interferon gamma Mus musculus 76-92 15302848-3 2004 Few naive gB-specific T cells express Ly49 or CD94/NKG2 receptors. gb 10-12 killer cell lectin like receptor A1, pseudogene Homo sapiens 38-42 15302848-3 2004 Few naive gB-specific T cells express Ly49 or CD94/NKG2 receptors. gb 10-12 killer cell lectin like receptor D1 Homo sapiens 46-50 15302848-3 2004 Few naive gB-specific T cells express Ly49 or CD94/NKG2 receptors. gb 10-12 killer cell lectin like receptor C1 Homo sapiens 51-55 15302848-4 2004 Following acute infection of C57BL/6 mice with either HSV-1 or a recombinant influenza virus that encodes the gB determinant, gB-specific T cells showed a dramatic upregulation of CD94/NKG2 receptors. gb 110-112 killer cell lectin like receptor D1 Homo sapiens 180-184 15302848-4 2004 Following acute infection of C57BL/6 mice with either HSV-1 or a recombinant influenza virus that encodes the gB determinant, gB-specific T cells showed a dramatic upregulation of CD94/NKG2 receptors. gb 110-112 killer cell lectin like receptor C1 Homo sapiens 185-189 15302848-4 2004 Following acute infection of C57BL/6 mice with either HSV-1 or a recombinant influenza virus that encodes the gB determinant, gB-specific T cells showed a dramatic upregulation of CD94/NKG2 receptors. gb 126-128 killer cell lectin like receptor D1 Homo sapiens 180-184 15302848-4 2004 Following acute infection of C57BL/6 mice with either HSV-1 or a recombinant influenza virus that encodes the gB determinant, gB-specific T cells showed a dramatic upregulation of CD94/NKG2 receptors. gb 126-128 killer cell lectin like receptor C1 Homo sapiens 185-189 15302848-5 2004 Moreover, gB-specific CD8 T cells that expressed CD94/NKG2 receptors were also found to express another NK receptor, KLRG1. gb 10-12 killer cell lectin like receptor D1 Homo sapiens 49-53 15302848-5 2004 Moreover, gB-specific CD8 T cells that expressed CD94/NKG2 receptors were also found to express another NK receptor, KLRG1. gb 10-12 killer cell lectin like receptor C1 Homo sapiens 54-58 15302848-5 2004 Moreover, gB-specific CD8 T cells that expressed CD94/NKG2 receptors were also found to express another NK receptor, KLRG1. gb 10-12 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 3 Homo sapiens 104-115 15302848-5 2004 Moreover, gB-specific CD8 T cells that expressed CD94/NKG2 receptors were also found to express another NK receptor, KLRG1. gb 10-12 killer cell lectin like receptor G1 Homo sapiens 117-122 15302848-6 2004 We established that while Ag-stimulated gB-specific CD8 T cells primarily express inhibitory isoforms of CD94/NKG2 receptors, these cells remain capable of producing gammaIFN upon peptide stimulation. gb 40-42 killer cell lectin like receptor D1 Homo sapiens 105-109 15302848-6 2004 We established that while Ag-stimulated gB-specific CD8 T cells primarily express inhibitory isoforms of CD94/NKG2 receptors, these cells remain capable of producing gammaIFN upon peptide stimulation. gb 40-42 killer cell lectin like receptor C1 Homo sapiens 110-114 15302848-7 2004 While peak CD94/NKG2 expression on gB-specific cells was reached 2-3 days following infection, it remained elevated beyond 60 days post-infection with either HSV-1 or a gB-expressing recombinant influenza virus. gb 35-37 killer cell lectin like receptor D1 Homo sapiens 11-15 15302848-7 2004 While peak CD94/NKG2 expression on gB-specific cells was reached 2-3 days following infection, it remained elevated beyond 60 days post-infection with either HSV-1 or a gB-expressing recombinant influenza virus. gb 35-37 killer cell lectin like receptor C1 Homo sapiens 16-20 15307021-3 2004 The distribution of gB genotypes was as follows: gB1, 28.9% of patients; gB2, 19.6%; gB3, 23.7%; gB4, 2.0%; and mixed infection, 25.8%. gb 20-22 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 49-52 15307021-3 2004 The distribution of gB genotypes was as follows: gB1, 28.9% of patients; gB2, 19.6%; gB3, 23.7%; gB4, 2.0%; and mixed infection, 25.8%. gb 20-22 gamma-aminobutyric acid type B receptor subunit 2 Homo sapiens 73-76 14722275-6 2004 Interferon regulatory factor 3 (IRF3), a key transcriptional regulator of cellular interferon responses, is activated by CMV virions and soluble gB. gb 145-147 interferon regulatory factor 3 Homo sapiens 32-36 12741063-1 2003 The authors have conducted electron microscopic and ultracytochemical studies of blood lymphocytes of healthy individuals containing Gall bodies (GB) which are typical for CD4+ cell subpopulation. gb 146-148 CD4 molecule Homo sapiens 172-175 11504538-7 2001 Heparin, a gB-specific inhibitor of virus-induced cell fusion, inhibited both wild-type gB and gB(syn3)-mediated cell fusion. gb 11-13 synapsin III Homo sapiens 98-102 11875308-8 2002 Plasma ACE activity was 100% higher in the BN-Gb than in the Lewis-Gb rats (P < 0.05). gb 46-48 angiotensin I converting enzyme Rattus norvegicus 7-10 11875308-9 2002 Ang II plasma levels were higher in the BN-sham than in the Lewis-sham rats (255 +/- 22 versus 161 +/- 16 pg/ml, P < 0.05), increased in both Gb groups and correlated significantly with SBP (r = 0.58, P < 0.01). gb 145-147 angiotensinogen Rattus norvegicus 0-6 11777979-3 2002 Preferential expression of the activation marker CD25 by tetramer-positive cells in draining popliteal nodes but not spleen suggested that gB-specific T cells were initially activated within the lymph node. gb 139-141 interleukin 2 receptor subunit alpha Homo sapiens 49-53 11773401-3 2002 Here we report on the construction of a viral mutant in which the recognition site of gB for the cellular endoprotease furin was destroyed. gb 86-88 furin, paired basic amino acid cleaving enzyme Homo sapiens 119-124 11752458-6 2001 HCMV infection causes the redistribution of the induced viperin from its normal endoplasmic reticulum association, first to the Golgi apparatus and then to cytoplasmic vacuoles containing gB and pp28. gb 188-190 radical S-adenosyl methionine domain containing 2 Homo sapiens 56-63 11562944-6 2001 The best GB/ACE implementation uses a set of atomic Voronoi volumes reported recently, obtained by averaging over a large database of crystallographic protein structures. gb 9-11 angiotensin I converting enzyme Homo sapiens 12-15 11562944-8 2001 This GB/ACE parameterization yields stable trajectories on the 0.5-1-ns time scale that deviate moderately (approximately 1.5-2.5 A) from the X-ray structure, reproduce approximately the surface distribution of charged, polar, and hydrophobic groups, and reproduce accurately backbone flexibility as measured by amide NMR-order parameters. gb 5-7 angiotensin I converting enzyme Homo sapiens 8-11 10627549-5 2000 Computer algorithm predictions of gB"s secondary structure indicate that the furin-recognized cleavage site falls within an exposed loop. gb 34-36 furin, paired basic amino acid cleaving enzyme Homo sapiens 77-82 11038377-2 2000 The immunodominant region on gB is the antigenic domain 1 (AD-1), a complex structure that requires a minimal continuous sequence of more than 75 amino acids (aa 552-635) for antibody binding. gb 29-31 amyloid beta precursor protein Homo sapiens 39-57 11038377-2 2000 The immunodominant region on gB is the antigenic domain 1 (AD-1), a complex structure that requires a minimal continuous sequence of more than 75 amino acids (aa 552-635) for antibody binding. gb 29-31 amyloid beta precursor protein Homo sapiens 59-63 11007483-5 2000 Instead, GB acts upstream to regulates NE activity by inactivating alpha1-proteinase inhibitor (alpha1-PI). gb 9-11 elastase, neutrophil expressed Mus musculus 39-41 11007483-6 2000 Excess NE produces lesions in GB -/- mice without cleaving alpha1-PI. gb 30-32 elastase, neutrophil expressed Mus musculus 7-9 10925295-8 2000 In contrast to the gB-specific CD8+ T cell population within the PLN, the entire gB-specific CD8+ T cell population within the spleen was CD25-. gb 81-83 interleukin 2 receptor subunit alpha Homo sapiens 138-142 10821670-7 2000 Here we show that this gB fragment forms beta-pleated sheets, self-assembles into fibrils that are thioflavin-positive and ultrastructurally indistinguishable from A beta, accelerates the formation of A beta fibrils in vitro, and is toxic to primary cortical neurons at doses comparable to those of A beta. gb 23-25 amyloid beta precursor protein Homo sapiens 164-170 10821670-7 2000 Here we show that this gB fragment forms beta-pleated sheets, self-assembles into fibrils that are thioflavin-positive and ultrastructurally indistinguishable from A beta, accelerates the formation of A beta fibrils in vitro, and is toxic to primary cortical neurons at doses comparable to those of A beta. gb 23-25 amyloid beta precursor protein Homo sapiens 201-207 10821670-7 2000 Here we show that this gB fragment forms beta-pleated sheets, self-assembles into fibrils that are thioflavin-positive and ultrastructurally indistinguishable from A beta, accelerates the formation of A beta fibrils in vitro, and is toxic to primary cortical neurons at doses comparable to those of A beta. gb 23-25 amyloid beta precursor protein Homo sapiens 201-207 10482621-5 1999 gB colocalized with clathrin-coated vesicles containing the transferrin receptor in the early endocytic/recycling pathway, indicating that gB traffics in this pathway. gb 0-2 transferrin Homo sapiens 60-71 10766304-3 2000 The ANGpath virus, which also has a syn3 mutation in the C-terminal endodomain of gB (Val for Ala at residue 855) is pathogenic for adult mice (39), but can be made nonpathogenic by replacing the gBANGpath gene by the corresponding gBKOS sequence (21). gb 82-84 synapsin III Mus musculus 36-40 10516079-3 1999 The study of distinct HHV-7-positive human samples showed preferential associations of some gB alleles with some alleles of two other genes, distantly located on the HHV-7 genome, coding for the phosphoprotein p100 (p100) and the major capsid protein (MCP). gb 92-94 major capsid protein Human betaherpesvirus 7 230-250 10516079-3 1999 The study of distinct HHV-7-positive human samples showed preferential associations of some gB alleles with some alleles of two other genes, distantly located on the HHV-7 genome, coding for the phosphoprotein p100 (p100) and the major capsid protein (MCP). gb 92-94 major capsid protein Human betaherpesvirus 7 252-255 10482621-5 1999 gB colocalized with clathrin-coated vesicles containing the transferrin receptor in the early endocytic/recycling pathway, indicating that gB traffics in this pathway. gb 139-141 transferrin Homo sapiens 60-71 10696431-7 1999 Increasing IFN quantities caused a reduction in a stepwise manner of plaque numbers as well as a suppression of pp38 and gB expression in the CVI988- and HVT-infected cells, respectively. gb 121-123 interferon Gallus gallus 11-14 10208930-5 1999 gB DNA-immunized mice cleared virus less rapidly (5 days), and the incidence of lesions was 10 and 25% in BALB/c and muK/O mice, respectively. gb 0-2 mitogen-activated protein kinase kinase kinase 12 Mus musculus 117-120 10207084-3 1999 Cells incubated with a purified, soluble form of gB resulted in the transcriptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2"-5" oligoadenylate synthetase and an IFN-stimulated gene product of 54 kDa) to a comparable level as virions or IFN. gb 49-51 interferon alpha 1 Homo sapiens 100-103 10207084-3 1999 Cells incubated with a purified, soluble form of gB resulted in the transcriptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2"-5" oligoadenylate synthetase and an IFN-stimulated gene product of 54 kDa) to a comparable level as virions or IFN. gb 49-51 SPARC related modular calcium binding 1 Homo sapiens 121-124 10207084-3 1999 Cells incubated with a purified, soluble form of gB resulted in the transcriptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2"-5" oligoadenylate synthetase and an IFN-stimulated gene product of 54 kDa) to a comparable level as virions or IFN. gb 49-51 interferon induced protein with tetratricopeptide repeats 2 Homo sapiens 129-134 10207084-3 1999 Cells incubated with a purified, soluble form of gB resulted in the transcriptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2"-5" oligoadenylate synthetase and an IFN-stimulated gene product of 54 kDa) to a comparable level as virions or IFN. gb 49-51 interferon alpha 1 Homo sapiens 184-187 10207084-3 1999 Cells incubated with a purified, soluble form of gB resulted in the transcriptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2"-5" oligoadenylate synthetase and an IFN-stimulated gene product of 54 kDa) to a comparable level as virions or IFN. gb 49-51 interferon alpha 1 Homo sapiens 184-187 10207084-7 1999 Together these data indicate that a principal means by which cytomegalovirus induces intracellular signaling and activation of the interferon-responsive pathway is via an interaction of gB with an as yet unidentified, likely novel cellular receptor that interfaces with the IFN signaling pathway. gb 186-188 interferon alpha 1 Homo sapiens 131-141 10207084-7 1999 Together these data indicate that a principal means by which cytomegalovirus induces intracellular signaling and activation of the interferon-responsive pathway is via an interaction of gB with an as yet unidentified, likely novel cellular receptor that interfaces with the IFN signaling pathway. gb 186-188 interferon alpha 1 Homo sapiens 274-277 9310835-2 1997 We have previously shown that C57BL/6 mice mount a gB-specific, Kb-restricted CTL response which is dominated by a TCRBV10+ population and a TCRBV8S1+ subpopulation, both containing highly conserved CDR3 elements. gb 51-53 cerebellar degeneration-related 3 Mus musculus 199-203 10078607-4 1999 Mice immunized with the gB plasmid predominantly produced IgG2a gB-specific antibody, while the gB680 plasmid raised mostly IgG1 anti-gB antibody. gb 24-26 immunoglobulin heavy variable V1-9 Mus musculus 58-63 9620078-6 1998 Partial sequence analysis revealed that this new gB genotype is closely related to gB3, and it was therefore named gB3". gb 49-51 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 83-86 9620078-6 1998 Partial sequence analysis revealed that this new gB genotype is closely related to gB3, and it was therefore named gB3". gb 49-51 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 115-118 9620078-12 1998 A new gB variant, gB3", was found in the ocular samples of 4 of 27 patients, but not in the blood samples tested. gb 6-8 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 18-21 9747890-4 1998 Immunisation with the gB-peptide resulted in the generation of gB-specific CTL that showed a similar TCRBV10 bias to that observed after HSV-1 infection. gb 22-24 T cell receptor beta, variable 10 Mus musculus 101-108 9747890-5 1998 When the gB-determinant was expressed as a part of a fusion protein, immunised mice again exhibited the TCRBV10 bias with the junctional sequence conservation in the responding CTL. gb 9-11 T cell receptor beta, variable 10 Mus musculus 104-111 9747890-7 1998 Analysis of the TCRBV usage of variant specific CTL lines showed that substitutions at the TCR-contact positions 4, 6 and 7 of the gB-peptide resulted in a loss of the TCRBV10 bias. gb 131-133 T cell receptor beta, variable 10 Mus musculus 168-175 9747890-8 1998 These results suggest that the TCRBV10 bias seen in gB-specific CTL after HSV-1 infection is due to antigenic selection by the minimal peptide and is determined by residues proposed to contact the TCR beta-chain CDR3. gb 52-54 T cell receptor beta, variable 10 Mus musculus 31-38 9747890-8 1998 These results suggest that the TCRBV10 bias seen in gB-specific CTL after HSV-1 infection is due to antigenic selection by the minimal peptide and is determined by residues proposed to contact the TCR beta-chain CDR3. gb 52-54 T cell receptor beta chain Mus musculus 197-205 9747890-8 1998 These results suggest that the TCRBV10 bias seen in gB-specific CTL after HSV-1 infection is due to antigenic selection by the minimal peptide and is determined by residues proposed to contact the TCR beta-chain CDR3. gb 52-54 cerebellar degeneration-related 3 Mus musculus 212-216 9573262-8 1998 Coimmunoprecipitation experiments revealed that the cysteine mutations resulted in gB misfolding and retention by the molecular chaperones calnexin, calreticulin, and Grp78 in the ER. gb 83-85 calnexin Homo sapiens 139-147 9573262-8 1998 Coimmunoprecipitation experiments revealed that the cysteine mutations resulted in gB misfolding and retention by the molecular chaperones calnexin, calreticulin, and Grp78 in the ER. gb 83-85 heat shock protein family A (Hsp70) member 5 Homo sapiens 167-172 9151851-2 1997 Indirect immunofluorescence followed by flow cytometric analysis revealed specific binding of gB-Fc to the membrane of SupT1 cells but not to other CD4+ T-lymphoblastoid cell lines, such as Jurkat or PM1, clearly indicating that gB-Fc did not bind to the CD4 molecule. gb 94-96 transmembrane protein 11 Homo sapiens 200-203 9266998-7 1997 It is suggested that a bicistronic transcript of 8 kb encoded by ORFs UL55 and UL54 is involved in biosynthesis of early HCMV gB. gb 126-128 envelope glycoprotein B Human betaherpesvirus 5 70-74 9266998-7 1997 It is suggested that a bicistronic transcript of 8 kb encoded by ORFs UL55 and UL54 is involved in biosynthesis of early HCMV gB. gb 126-128 DNA polymerase catalytic subunit Human betaherpesvirus 5 79-83 9151851-2 1997 Indirect immunofluorescence followed by flow cytometric analysis revealed specific binding of gB-Fc to the membrane of SupT1 cells but not to other CD4+ T-lymphoblastoid cell lines, such as Jurkat or PM1, clearly indicating that gB-Fc did not bind to the CD4 molecule. gb 94-96 CD4 molecule Homo sapiens 255-258 9151851-7 1997 Although the CD4 antigen is a critical component of the receptor for the T-lymphotropic HHV-7, these findings suggest that heparin-like molecules also play an important role in HHV-7-cell surface interactions required for infection and that gB represents one of the HHV-7 envelope proteins involved in the adsorption of virus-to-cell surface proteoglycans. gb 241-243 CD4 molecule Homo sapiens 13-16 8892927-8 1996 Analysis of protein complexes formed by gB and molecular chaperones in the ER showed that calnexin and calreticulin, lectin-like chaperones, bound equal amounts of uncleaved wild-type gB, gB deltaI, and gB KNPm, but the glucose-regulated proteins 78 (BiP) and 94 formed stable complexes only with the mutated forms, causing their retention in the ER. gb 40-42 calnexin Homo sapiens 90-98 8943404-6 1996 Here we examine the contribution of the TCR alpha-chain to the gB-specific CTL diversity. gb 63-65 T cell receptor alpha chain Mus musculus 40-49 8943404-7 1996 The TCR alpha-chains from different TCRBV10-positive gB-specific CTL clones were found to exhibit extensive sequence variation. gb 53-55 T cell receptor alpha chain Mus musculus 4-13 8943404-7 1996 The TCR alpha-chains from different TCRBV10-positive gB-specific CTL clones were found to exhibit extensive sequence variation. gb 53-55 T cell receptor beta, variable 10 Mus musculus 36-43 8892927-8 1996 Analysis of protein complexes formed by gB and molecular chaperones in the ER showed that calnexin and calreticulin, lectin-like chaperones, bound equal amounts of uncleaved wild-type gB, gB deltaI, and gB KNPm, but the glucose-regulated proteins 78 (BiP) and 94 formed stable complexes only with the mutated forms, causing their retention in the ER. gb 40-42 calreticulin Homo sapiens 103-115 8892927-8 1996 Analysis of protein complexes formed by gB and molecular chaperones in the ER showed that calnexin and calreticulin, lectin-like chaperones, bound equal amounts of uncleaved wild-type gB, gB deltaI, and gB KNPm, but the glucose-regulated proteins 78 (BiP) and 94 formed stable complexes only with the mutated forms, causing their retention in the ER. gb 184-186 calnexin Homo sapiens 90-98 8892927-8 1996 Analysis of protein complexes formed by gB and molecular chaperones in the ER showed that calnexin and calreticulin, lectin-like chaperones, bound equal amounts of uncleaved wild-type gB, gB deltaI, and gB KNPm, but the glucose-regulated proteins 78 (BiP) and 94 formed stable complexes only with the mutated forms, causing their retention in the ER. gb 184-186 calreticulin Homo sapiens 103-115 8642648-3 1996 Pulse-chase experiments demonstrate that the 160-kDa gB precursor was transiently associated with calnexin, a membrane-bound chaperone, in the ER. gb 53-55 calnexin Homo sapiens 98-106 8918549-4 1996 In contrast, the precursor of gB showed prolonged association with calnexin. gb 30-32 calnexin Homo sapiens 67-75 8822632-3 1996 Giant cell formation by ANGpath was attributed to a mutation that alters the codon GCC (in KOS and strain 17 sequences) to GTC (in ANGpath sequence) changing the amino acid 854 in the same (syn3) region of the gB molecule. gb 210-212 guanylate cyclase 2c Mus musculus 83-86 8822632-3 1996 Giant cell formation by ANGpath was attributed to a mutation that alters the codon GCC (in KOS and strain 17 sequences) to GTC (in ANGpath sequence) changing the amino acid 854 in the same (syn3) region of the gB molecule. gb 210-212 synapsin III Mus musculus 190-194 8642648-7 1996 Both forms of the gB precursor could bind to calnexin. gb 18-20 calnexin Homo sapiens 45-53 8642648-8 1996 The kinetics of the conversion from the fully reduced to the oxidized form coincided with that of dissociation of the 160-kDa gB precursor from calnexin, suggesting that the two steps are closely related. gb 126-128 calnexin Homo sapiens 144-152 8057463-12 1994 Conversely, cloned DNA fragments containing the mutant A4B UL45 gene transferred the loss of cell-cell fusion to other gB syn mutants, rendering them UL45 negative and nonsyncytial. gb 119-121 membrane protein UL45 Human alphaherpesvirus 1 59-63 7844520-4 1995 Deletion of hd2, but not that of hd1, caused loss of membrane anchoring of the gB molecule, resulting in secretion of the respective gB form into the culture medium. gb 79-81 histone deacetylase 2 Homo sapiens 12-15 7844520-4 1995 Deletion of hd2, but not that of hd1, caused loss of membrane anchoring of the gB molecule, resulting in secretion of the respective gB form into the culture medium. gb 133-135 histone deacetylase 2 Homo sapiens 12-15 7844520-6 1995 Our observations indicate that hd2 is essential as well as sufficient for membrane anchoring of the HCMV gB molecule. gb 105-107 histone deacetylase 2 Homo sapiens 31-34 9049391-3 1995 In this report we detected, using the recombinants 27/III and K-7, that an amino acid exchange from Ala to Val at aa position 854 of gB is the main determinant for FFWO activity of strains ANG, ANG path and recombinant K-7. gb 133-135 RBPJ pseudogene 4 Homo sapiens 62-65 9049391-3 1995 In this report we detected, using the recombinants 27/III and K-7, that an amino acid exchange from Ala to Val at aa position 854 of gB is the main determinant for FFWO activity of strains ANG, ANG path and recombinant K-7. gb 133-135 angiogenin Homo sapiens 189-192 9049391-3 1995 In this report we detected, using the recombinants 27/III and K-7, that an amino acid exchange from Ala to Val at aa position 854 of gB is the main determinant for FFWO activity of strains ANG, ANG path and recombinant K-7. gb 133-135 angiogenin Homo sapiens 194-197 9049391-3 1995 In this report we detected, using the recombinants 27/III and K-7, that an amino acid exchange from Ala to Val at aa position 854 of gB is the main determinant for FFWO activity of strains ANG, ANG path and recombinant K-7. gb 133-135 RBPJ pseudogene 4 Homo sapiens 219-222 8057463-13 1994 We conclude that normal UL45 expression is required to allow cell fusion induced by gB syn mutants and that the nonessential UL45 protein may play an important role as a mediator of fusion events during HSV-1 infection. gb 84-86 membrane protein UL45 Human alphaherpesvirus 1 24-28 8113751-13 1994 Analysis of immune sera revealed that those from donors with PBMC proliferative responses always contained antibodies reactive with B cell epitopes on both the N-terminal gp93 and C-terminal gp55 portions of gB. gb 208-210 neuroplastin Homo sapiens 191-195 7871762-0 1994 Glycoprotein B of bovine herpesvirus type 4: its phylogenetic relationship to gB equivalents of the herpesviruses. gb 78-80 glycoprotein B Bovine gammaherpesvirus 4 0-14 8178437-2 1994 The genomic locations of these genes coincide with that of the gB gene of serotype 1 MDV (gB-1). gb 63-65 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 90-94 8113751-14 1994 In contrast, many of the sera from donors with low gB-specific proliferative responses had gp55-specific antibodies but lacked antibodies to gp93. gb 51-53 neuroplastin Homo sapiens 91-95 2164374-6 1990 Further analysis using competition assays revealed that these sera can be classified into at least two groups: (i) that contain gB-reactive antibodies reactive to intact gB or tgB (772); (ii) that contain antibodies that recognize all forms of gB-derivatives tested. gb 128-130 pro-platelet basic protein Homo sapiens 176-179 8226541-6 1993 Intravascular NO attenuated the response to angiotensin II more (P < 0.001) in GB- (with and without plasma) than in blood- (hematocrit = 41 and 5%) perfused lungs (75.6 +/- 6.4 and 70.9 +/- 4.8% vs. 22.2 +/- 2.4 and 39.4 +/- 7.6%). gb 82-84 angiotensinogen Rattus norvegicus 44-58 1651591-6 1991 The glucose-regulated proteins GRP78 and GRP94, which are resident proteins of the ER, associated with partially glycosylated, faster-migrating forms of gB but not with the fully processed, more slowly migrating product. gb 153-155 heat shock protein family A (Hsp70) member 5 Homo sapiens 31-36 1651591-6 1991 The glucose-regulated proteins GRP78 and GRP94, which are resident proteins of the ER, associated with partially glycosylated, faster-migrating forms of gB but not with the fully processed, more slowly migrating product. gb 153-155 heat shock protein 90 beta family member 1 Homo sapiens 41-46 1651591-7 1991 GRP78 and GRP94 formed complexes with the mutant gB-(Lk479), which was degraded in the ER. gb 49-51 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 1651591-7 1991 GRP78 and GRP94 formed complexes with the mutant gB-(Lk479), which was degraded in the ER. gb 49-51 heat shock protein 90 beta family member 1 Homo sapiens 10-15 1651591-8 1991 Our results indicate that GRP78, and perhaps also GRP94, acts as a chaperone in the assembly of native gB oligomers and also binds to aberrant forms of the molecule, arresting their transport from the ER and possibly serving as markers for protein degradation in this compartment of the exocytic pathway. gb 103-105 heat shock protein family A (Hsp70) member 5 Homo sapiens 26-31 1651591-8 1991 Our results indicate that GRP78, and perhaps also GRP94, acts as a chaperone in the assembly of native gB oligomers and also binds to aberrant forms of the molecule, arresting their transport from the ER and possibly serving as markers for protein degradation in this compartment of the exocytic pathway. gb 103-105 heat shock protein 90 beta family member 1 Homo sapiens 50-55 8396662-5 1993 Analysis of ANG and KOS DNA sequences in the relevant region of the gB gene revealed two nucleotide differences which result in amino acid differences in the gB protein. gb 68-70 angiogenin Homo sapiens 12-15 8396662-5 1993 Analysis of ANG and KOS DNA sequences in the relevant region of the gB gene revealed two nucleotide differences which result in amino acid differences in the gB protein. gb 158-160 angiogenin Homo sapiens 12-15 8396662-7 1993 The second, at codon 523 of the mature gB protein, encodes a valine in KOS and an alanine in ANG. gb 39-41 angiogenin Homo sapiens 93-96 8383236-3 1993 The results indicate that syn mutations occur within two essential and highly conserved hydrophilic, alpha-helical regions of the gB cytoplasmic domain. gb 130-132 synemin Homo sapiens 26-29 8383236-10 1993 Moreover, the observation that both roe and syn mutations occur in the cytoplasmic domain further suggests that gB functions in an analogous manner in both membrane fusion events. gb 112-114 synemin Homo sapiens 44-47 8390747-6 1993 Sequence analysis of the Kpnl-Pstl fragment of 17 hep syn revealed a single base pair change when compared to the 17 syn+ sequence, predicting an alanine (GCC codon) to valine (GTC codon) amino acid substitution at residue 825 of the mature gB protein, plus loss of an Ncol restriction endonuclease site. gb 241-243 synemin Homo sapiens 54-57 34768571-8 2021 A difference of 50% in CD14++CD16+ in the GB versus the PB was a significant risk factor (p = 0.002) for BL, increasing the risk seven times. gb 42-44 CD14 molecule Homo sapiens 23-27 34260096-4 2021 Among the Nedd4 family proteins, Nedd4, Nedd4L, and Itch induced the degradation of gB in transiently expressing cells. gb 84-86 NEDD4 E3 ubiquitin protein ligase Homo sapiens 10-15 34260096-4 2021 Among the Nedd4 family proteins, Nedd4, Nedd4L, and Itch induced the degradation of gB in transiently expressing cells. gb 84-86 NEDD4 E3 ubiquitin protein ligase Homo sapiens 33-38 34260096-4 2021 Among the Nedd4 family proteins, Nedd4, Nedd4L, and Itch induced the degradation of gB in transiently expressing cells. gb 84-86 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 40-46 34260096-4 2021 Among the Nedd4 family proteins, Nedd4, Nedd4L, and Itch induced the degradation of gB in transiently expressing cells. gb 84-86 itchy E3 ubiquitin protein ligase Homo sapiens 52-56 34260096-5 2021 The degradation of gB by Nedd4 was inhibited by proteasome inhibitor MG132, lysosome inhibitor chloroquine, and the co-expression of UL42 proteins. gb 19-21 NEDD4 E3 ubiquitin protein ligase Homo sapiens 25-30 34260096-5 2021 The degradation of gB by Nedd4 was inhibited by proteasome inhibitor MG132, lysosome inhibitor chloroquine, and the co-expression of UL42 proteins. gb 19-21 protein UL42 Human betaherpesvirus 5 133-137 34260096-6 2021 Among those Nedd4 family proteins, Itch was re-localized by the co-expression of gB to the perinuclear region of the cytoplasm. gb 81-83 NEDD4 E3 ubiquitin protein ligase Homo sapiens 12-17 34260096-6 2021 Among those Nedd4 family proteins, Itch was re-localized by the co-expression of gB to the perinuclear region of the cytoplasm. gb 81-83 itchy E3 ubiquitin protein ligase Homo sapiens 35-39 34260096-7 2021 A co-immunoprecipitation assay demonstrated an interaction between gB and Itch through its PPxY motif. gb 67-69 itchy E3 ubiquitin protein ligase Homo sapiens 74-78 34260096-8 2021 The 150 kDa gB precursor was aberrantly ubiquitinated, and the total amount of gB was quickly decreased in the absence of UL42. gb 12-14 protein UL42 Human betaherpesvirus 5 122-126 34260096-8 2021 The 150 kDa gB precursor was aberrantly ubiquitinated, and the total amount of gB was quickly decreased in the absence of UL42. gb 79-81 protein UL42 Human betaherpesvirus 5 122-126 34260096-9 2021 Our results indicate that UL42 prevent the degradation of gB by the inhibition of Nedd4 family proteins. gb 58-60 protein UL42 Human betaherpesvirus 5 26-30 34260096-9 2021 Our results indicate that UL42 prevent the degradation of gB by the inhibition of Nedd4 family proteins. gb 58-60 NEDD4 E3 ubiquitin protein ligase Homo sapiens 82-87 34768571-8 2021 A difference of 50% in CD14++CD16+ in the GB versus the PB was a significant risk factor (p = 0.002) for BL, increasing the risk seven times. gb 42-44 Fc gamma receptor IIIa Homo sapiens 29-33 34132577-11 2021 However, our data suggest important differences in the gH/gL of the two complexes and support a model in which gH/gL/gO can provide an activation signal for gB. gb 157-159 gamma-glutamyl hydrolase Homo sapiens 55-57 34623842-3 2021 GB migration and evolution of CTB network trigger formation of SC diamond. gb 0-2 chitobiase Homo sapiens 30-33 34667380-7 2021 Results: Levels of active MMP-9 (aMMP-9) and latent MMP-9 (lMMP-9) were significantly high in both Group A (GA) (aMMP-9: 2.05 arbitrary unit (AU)/lMMP-9: 2.54 AU) and Group B (GB) (aMMP-9: 1.32 AU/lMMP-9: 1.74 AU) when compared to that of Group C (GC) (aMMP-9: 0.93/lMMP-9: 1.08 AU). gb 176-178 matrix metallopeptidase 9 Homo sapiens 26-31 34667380-7 2021 Results: Levels of active MMP-9 (aMMP-9) and latent MMP-9 (lMMP-9) were significantly high in both Group A (GA) (aMMP-9: 2.05 arbitrary unit (AU)/lMMP-9: 2.54 AU) and Group B (GB) (aMMP-9: 1.32 AU/lMMP-9: 1.74 AU) when compared to that of Group C (GC) (aMMP-9: 0.93/lMMP-9: 1.08 AU). gb 176-178 matrix metallopeptidase 9 Homo sapiens 52-57 34377305-13 2021 After the therapy, the patients" serum IFN-gamma and IL-4 levels in GB were significantly better than they were in GA. After the therapy, the quality of life of the patients in GB was significantly higher than it was in in GA (P<0.05). gb 68-70 interferon gamma Homo sapiens 39-48 34377305-13 2021 After the therapy, the patients" serum IFN-gamma and IL-4 levels in GB were significantly better than they were in GA. After the therapy, the quality of life of the patients in GB was significantly higher than it was in in GA (P<0.05). gb 68-70 interleukin 4 Homo sapiens 53-57 34377305-13 2021 After the therapy, the patients" serum IFN-gamma and IL-4 levels in GB were significantly better than they were in GA. After the therapy, the quality of life of the patients in GB was significantly higher than it was in in GA (P<0.05). gb 177-179 interferon gamma Homo sapiens 39-48 34377305-13 2021 After the therapy, the patients" serum IFN-gamma and IL-4 levels in GB were significantly better than they were in GA. After the therapy, the quality of life of the patients in GB was significantly higher than it was in in GA (P<0.05). gb 177-179 interleukin 4 Homo sapiens 53-57 34220511-2 2021 To explore that GB can reduce neuroinflammation through regulating nuclear factor-kappaB (NF-kappaB) signaling pathway and overcome cognitive dysfunction in rats with vascular dementia (VD), we aim at investigating the potential effect of GB on enhancing cognitive function in rats with VD. gb 16-18 nuclear factor kappa B subunit 1 Homo sapiens 90-99 34220511-3 2021 It was found that GB improved survival of oxygen-glucose deprivation (OGD) treated SH-SY5Y cells by attenuating inflammatory response via Toll-like Receptor 4 (TLR4)/NF-kappaB pathway. gb 18-20 toll like receptor 4 Homo sapiens 138-158 34220511-3 2021 It was found that GB improved survival of oxygen-glucose deprivation (OGD) treated SH-SY5Y cells by attenuating inflammatory response via Toll-like Receptor 4 (TLR4)/NF-kappaB pathway. gb 18-20 toll like receptor 4 Homo sapiens 160-164 34220511-3 2021 It was found that GB improved survival of oxygen-glucose deprivation (OGD) treated SH-SY5Y cells by attenuating inflammatory response via Toll-like Receptor 4 (TLR4)/NF-kappaB pathway. gb 18-20 nuclear factor kappa B subunit 1 Homo sapiens 166-175 34220511-8 2021 The results found that GB can significantly improve the learning and memory ability of VD rats by reducing TLR4/NF-kappaB mediated neuroinflammation. gb 23-25 toll-like receptor 4 Rattus norvegicus 107-111 34220511-8 2021 The results found that GB can significantly improve the learning and memory ability of VD rats by reducing TLR4/NF-kappaB mediated neuroinflammation. gb 23-25 nuclear factor kappa B subunit 1 Homo sapiens 112-121 35390439-8 2022 Subjects with GB and SG had greater plasma glucagon levels after eating (AUCGlucagon) compared to CN (p < 0.05). gb 14-16 glucagon Homo sapiens 43-51 35526487-4 2022 As Siglec-7, but not Siglec-4, is expressed on hematopoietic cells such as monocytes, the regulatory mechanism by which Siglec-7 associates with gB is important to our understanding of VZV infection of blood cells. gb 145-147 sialic acid binding Ig like lectin 7 Homo sapiens 3-11 35526487-4 2022 As Siglec-7, but not Siglec-4, is expressed on hematopoietic cells such as monocytes, the regulatory mechanism by which Siglec-7 associates with gB is important to our understanding of VZV infection of blood cells. gb 145-147 sialic acid binding Ig like lectin 7 Homo sapiens 120-128 35526487-8 2022 These results demonstrate that the Siglec-7 cis-ligands present on primary monocytes play an important role in VZV infection through regulation of the interaction between gB and Siglec-7. gb 171-173 sialic acid binding Ig like lectin 7 Homo sapiens 35-43 35526487-8 2022 These results demonstrate that the Siglec-7 cis-ligands present on primary monocytes play an important role in VZV infection through regulation of the interaction between gB and Siglec-7. gb 171-173 sialic acid binding Ig like lectin 7 Homo sapiens 178-186 35395673-2 2022 DNA sequences of four antigenic domains (AD1, AD2, AD4/5 and AD5) of gB were amplified from six reference and 12 clinical CMV strains, and the most divergent genotypes were determined by phylogenetic analysis. gb 69-71 amyloid beta precursor protein Homo sapiens 41-44 35395673-2 2022 DNA sequences of four antigenic domains (AD1, AD2, AD4/5 and AD5) of gB were amplified from six reference and 12 clinical CMV strains, and the most divergent genotypes were determined by phylogenetic analysis. gb 69-71 apolipoprotein E Homo sapiens 46-49 35395673-2 2022 DNA sequences of four antigenic domains (AD1, AD2, AD4/5 and AD5) of gB were amplified from six reference and 12 clinical CMV strains, and the most divergent genotypes were determined by phylogenetic analysis. gb 69-71 presenilin 2 Homo sapiens 51-56 35395673-2 2022 DNA sequences of four antigenic domains (AD1, AD2, AD4/5 and AD5) of gB were amplified from six reference and 12 clinical CMV strains, and the most divergent genotypes were determined by phylogenetic analysis. gb 69-71 Alzheimer disease, familial, type 5 Homo sapiens 61-64 35578268-8 2022 In the latter, loss of methylation in the GB is linked to decreases in transcription: this group included the PRKAR1B/HEATR2 genes and the dopamine receptor regulator PDE4C. gb 42-44 protein kinase cAMP-dependent type I regulatory subunit beta Homo sapiens 110-117 35594678-4 2022 The average GB values of Cu, Zn, Cd, Pb, Cr, total carbon (TC), total nitrogen (TN) and total phosphorus (TP) are 45.14 mg/kg, 86.99 mg/kg, 0.29 mg/kg, 33.71 mg/kg, 110.90 mg/kg, 17.20 mg/g, 1.60 mg/g, and 665.78 mg/kg, respectively. gb 12-14 C-type lectin domain family 3 member B Homo sapiens 80-82 35578268-8 2022 In the latter, loss of methylation in the GB is linked to decreases in transcription: this group included the PRKAR1B/HEATR2 genes and the dopamine receptor regulator PDE4C. gb 42-44 dynein axonemal assembly factor 5 Homo sapiens 118-124 3140904-7 1988 Weak inhibitions were found when soybean trypsin inhibitor (SBTI) was included with the GT assay and when GB hydrolysis was assayed in the presence of alpha-lactalbumin or asialo-agalacto-(alpha 1-acid glycoprotein). gb 106-108 lactalbumin, alpha Mus musculus 151-168 2834864-4 1988 The gB gene was coupled to the SV40 early promoter and inserted into the E3 region of two adenovirus vectors, one in which the E1 region was deleted (AdgB-1) and another which contained E1 sequences (AdgB-2). gb 4-6 androglobin Homo sapiens 150-154 2452895-11 1988 Antibodies to sites I (B1 and B3) and IV (B6) slowed the rate at which viruses penetrated cell surfaces, supporting the conclusion that antibody binding to gB can inhibit penetration by a virus. gb 156-158 immunoglobulin kappa variable 7-3 (pseudogene) Homo sapiens 23-32 2834864-4 1988 The gB gene was coupled to the SV40 early promoter and inserted into the E3 region of two adenovirus vectors, one in which the E1 region was deleted (AdgB-1) and another which contained E1 sequences (AdgB-2). gb 4-6 androglobin Homo sapiens 200-204 2824843-3 1988 The expression of the gB gene was dependent on the presence of functional alpha 4 protein. gb 22-24 immunoglobulin binding protein 1 Homo sapiens 74-81 7073364-3 1982 CCK release was correlated with changes in GB volume determined simultaneously by ultrasonography. gb 43-45 cholecystokinin Homo sapiens 0-3 3740283-2 1986 After either MB or GB, the dose-MAP response curve for AVP and PE was shifted to the left of the I response curve; a greater shift was observed with AVP than with PE. gb 19-21 arginine vasopressin Canis lupus familiaris 55-58 3740283-2 1986 After either MB or GB, the dose-MAP response curve for AVP and PE was shifted to the left of the I response curve; a greater shift was observed with AVP than with PE. gb 19-21 arginine vasopressin Canis lupus familiaris 149-152 3740283-3 1986 The MAP threshold after GB for AVP and PE occurred at 10 and 50% of the threshold dose observed during the I response, respectively. gb 24-26 arginine vasopressin Canis lupus familiaris 31-34 3740283-8 1986 Our results show that MB and GB equally potentiate the pressor effects of AVP and PE, and the augmentation was much greater for AVP than for PE. gb 29-31 arginine vasopressin Canis lupus familiaris 74-77 7073364-9 1982 Plasma concentrations of CCK and GB volume were highly correlated in the 12 normal volunteers (r = -0.89, p < 0.01) and in the 14 contractors (r= -0.99, p < 0.01)), but the GB was significantly (p < 0.01) more sensitive to changes in plasma CCK in the gallstone contractors than in the normal volunteers. gb 179-181 cholecystokinin Homo sapiens 25-28 7073364-11 1982 Stasis may be important in the pathogenesis of gallstones in the noncontractors, whereas in contractors, the authors speculate that an abnormality in the CCK-gallbladder relationship (characterized by diminished CCK release and increased GB sensitivity to CCK) may be involved in the evolution of the disease. gb 238-240 cholecystokinin Homo sapiens 154-157 165869-3 1975 Only GB patients with acute illness produced MIF in response to neuritogenic P2 protein and crude human nerve. gb 5-7 macrophage migration inhibitory factor Homo sapiens 45-48 33524710-3 2021 Structure-electrochemical sensing performance studies reveal that GB hydrogel nanofibers with relatively strong biomolecular affinity such as -SH modified GB hydrogel (GB-SH) show a high sensitivity of response and low limit of detection for tumour marker alpha-fetoprotein sensing (AFP; 0.076 pg mL-1). gb 66-68 alpha fetoprotein Homo sapiens 256-273 33524710-3 2021 Structure-electrochemical sensing performance studies reveal that GB hydrogel nanofibers with relatively strong biomolecular affinity such as -SH modified GB hydrogel (GB-SH) show a high sensitivity of response and low limit of detection for tumour marker alpha-fetoprotein sensing (AFP; 0.076 pg mL-1). gb 66-68 alpha fetoprotein Homo sapiens 283-286 33524710-3 2021 Structure-electrochemical sensing performance studies reveal that GB hydrogel nanofibers with relatively strong biomolecular affinity such as -SH modified GB hydrogel (GB-SH) show a high sensitivity of response and low limit of detection for tumour marker alpha-fetoprotein sensing (AFP; 0.076 pg mL-1). gb 66-68 L1 cell adhesion molecule Mus musculus 297-301 33524710-3 2021 Structure-electrochemical sensing performance studies reveal that GB hydrogel nanofibers with relatively strong biomolecular affinity such as -SH modified GB hydrogel (GB-SH) show a high sensitivity of response and low limit of detection for tumour marker alpha-fetoprotein sensing (AFP; 0.076 pg mL-1). gb 155-157 alpha fetoprotein Homo sapiens 256-273 33524710-3 2021 Structure-electrochemical sensing performance studies reveal that GB hydrogel nanofibers with relatively strong biomolecular affinity such as -SH modified GB hydrogel (GB-SH) show a high sensitivity of response and low limit of detection for tumour marker alpha-fetoprotein sensing (AFP; 0.076 pg mL-1). gb 155-157 alpha fetoprotein Homo sapiens 283-286 33524710-3 2021 Structure-electrochemical sensing performance studies reveal that GB hydrogel nanofibers with relatively strong biomolecular affinity such as -SH modified GB hydrogel (GB-SH) show a high sensitivity of response and low limit of detection for tumour marker alpha-fetoprotein sensing (AFP; 0.076 pg mL-1). gb 155-157 L1 cell adhesion molecule Mus musculus 297-301 33595875-7 2021 Co-expression network analysis demonstrated that miR530b-ethylene responsive factor 96 (ERF96) and miRn211-thaumatin-like protein (TLP) play crucial roles in GB response. gb 158-160 TATA-box binding protein like 1 Homo sapiens 99-129 33595875-7 2021 Co-expression network analysis demonstrated that miR530b-ethylene responsive factor 96 (ERF96) and miRn211-thaumatin-like protein (TLP) play crucial roles in GB response. gb 158-160 TATA-box binding protein like 1 Homo sapiens 131-134 33595875-10 2021 Our results collectively demonstrate that ERF96 was a negative regulator, while TLP was a positive regulator in the tea plant"s response to GB. gb 140-142 TATA-box binding protein like 1 Homo sapiens 80-83 33155438-0 2020 gB co-immunization with GP96 enhances pulmonary-resident CD8 T cells and exerts a long-term defence against MCMV pneumonitis. gb 0-2 heat shock protein 90 beta family member 1 Homo sapiens 24-28 33283275-3 2021 AD-2 epitope is a highly conserved linear neutralising epitope of gB and a critical target for antibodies, however, only 50% of seropositive individuals make IgG antibodies to this site and IgA responses have not been fully investigated. gb 66-68 apolipoprotein E Homo sapiens 0-4 33283275-9 2021 V-region matched AD-2 specific recombinant IgG and IgA bound both to gB and AD-2 and neutralized HCMV infection in vitro. gb 69-71 apolipoprotein E Homo sapiens 17-21 33155438-0 2020 gB co-immunization with GP96 enhances pulmonary-resident CD8 T cells and exerts a long-term defence against MCMV pneumonitis. gb 0-2 CD8a molecule Homo sapiens 57-60 32723814-0 2020 HCMV-induced signaling through gB-EGFR engagement is required for viral trafficking and nuclear translocation in primary human monocytes. gb 31-33 epidermal growth factor receptor Homo sapiens 34-38 32999035-10 2020 Finally, we demonstrated that MDV gB colocalizes with cholesterol and LAMP-1, suggesting that viral protein trafficking is mediated by LAMP-1-positive vesicles in association with cholesterol. gb 34-36 lysosomal associated membrane protein 1 Homo sapiens 70-76 32999035-10 2020 Finally, we demonstrated that MDV gB colocalizes with cholesterol and LAMP-1, suggesting that viral protein trafficking is mediated by LAMP-1-positive vesicles in association with cholesterol. gb 34-36 lysosomal associated membrane protein 1 Homo sapiens 135-141 33105643-3 2020 This paper describes technology computer aided design (TCAD) device simulations performed to investigate the sensing margin and retention time of poly-Si 1T-DRAM as a function of its lateral GB location. gb 191-193 DNA damage regulated autophagy modulator 1 Homo sapiens 157-161 33105643-6 2020 We also performed simulations to analyze the effect of a lateral GB on the operation of a poly-Si 1T-DRAM that has a vertical GB. gb 65-67 DNA damage regulated autophagy modulator 1 Homo sapiens 101-105 33105643-6 2020 We also performed simulations to analyze the effect of a lateral GB on the operation of a poly-Si 1T-DRAM that has a vertical GB. gb 126-128 DNA damage regulated autophagy modulator 1 Homo sapiens 101-105 33105643-8 2020 This means that poly-Si 1T-DRAM devices with a lateral GB can operate reliably without any memory performance degradation from randomly determined vertical GB locations. gb 55-57 DNA damage regulated autophagy modulator 1 Homo sapiens 27-31 33105643-8 2020 This means that poly-Si 1T-DRAM devices with a lateral GB can operate reliably without any memory performance degradation from randomly determined vertical GB locations. gb 156-158 DNA damage regulated autophagy modulator 1 Homo sapiens 27-31 32723814-8 2020 HCMV appears to manipulate the EGFR kinase postentry, via gB-EGFR interaction, to be active at the critical points throughout the trafficking process that leads to nuclear translocation and productive infection of peripheral blood monocytes. gb 58-60 epidermal growth factor receptor Homo sapiens 31-35 32723814-8 2020 HCMV appears to manipulate the EGFR kinase postentry, via gB-EGFR interaction, to be active at the critical points throughout the trafficking process that leads to nuclear translocation and productive infection of peripheral blood monocytes. gb 58-60 epidermal growth factor receptor Homo sapiens 61-65 30298459-12 2019 Significantly more GB patients developed high ALT at 6 and high AST at 6 and 12 months. gb 19-21 solute carrier family 17 member 5 Homo sapiens 64-67 32745149-6 2020 A 1.8 A crystal structure of 3-25 Fab in complex with the peptide epitope revealed the molecular determinants of 3-25 binding to gB at atomic resolution. gb 129-131 FA complementation group B Homo sapiens 34-37 32745149-7 2020 Negative-staining electron microscopy (EM) 3D reconstruction of 3-25 Fab in complex with de-glycosylated postfusion gB showed that 3-25 Fab fully occupied the gB trimer at the N-terminus with flexible binding angles. gb 116-118 FA complementation group B Homo sapiens 136-139 32745149-7 2020 Negative-staining electron microscopy (EM) 3D reconstruction of 3-25 Fab in complex with de-glycosylated postfusion gB showed that 3-25 Fab fully occupied the gB trimer at the N-terminus with flexible binding angles. gb 159-161 FA complementation group B Homo sapiens 69-72 32745149-7 2020 Negative-staining electron microscopy (EM) 3D reconstruction of 3-25 Fab in complex with de-glycosylated postfusion gB showed that 3-25 Fab fully occupied the gB trimer at the N-terminus with flexible binding angles. gb 159-161 FA complementation group B Homo sapiens 136-139 31427511-10 2019 Moreover, gB(275Y) caused the formation of syncytia with numerous centrosomes, suggesting that cell fusion triggered caspase-2 activation. gb 10-12 caspase 2 Homo sapiens 117-126 32102235-6 2020 This means that a poly-Si 1T-DRAM can perform memory operations by using GB as a storage region in thin body devices with a small FB area. gb 73-75 DNA damage regulated autophagy modulator 1 Homo sapiens 29-33 31538224-6 2020 The mRNA and protein expressions of p53, Bax, caspase-3 were increased, while anti-apoptotic protein Bcl-2 was decreased and this effect could be reversed by GB pretreatment in a dose-dependent manner. gb 158-160 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 36-39 31538224-6 2020 The mRNA and protein expressions of p53, Bax, caspase-3 were increased, while anti-apoptotic protein Bcl-2 was decreased and this effect could be reversed by GB pretreatment in a dose-dependent manner. gb 158-160 BCL2 associated X, apoptosis regulator Rattus norvegicus 41-44 31538224-6 2020 The mRNA and protein expressions of p53, Bax, caspase-3 were increased, while anti-apoptotic protein Bcl-2 was decreased and this effect could be reversed by GB pretreatment in a dose-dependent manner. gb 158-160 caspase 3 Rattus norvegicus 46-55 31538224-6 2020 The mRNA and protein expressions of p53, Bax, caspase-3 were increased, while anti-apoptotic protein Bcl-2 was decreased and this effect could be reversed by GB pretreatment in a dose-dependent manner. gb 158-160 BCL2, apoptosis regulator Rattus norvegicus 101-106 31538224-7 2020 In vivo, the application of GB could alleviate the skin damage of SD rats and improve the superficial inflammation of the dermis as well as inhibit the expressions of P53 and Caspase-3 induced by UVB irradiation. gb 28-30 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 167-170 31538224-7 2020 In vivo, the application of GB could alleviate the skin damage of SD rats and improve the superficial inflammation of the dermis as well as inhibit the expressions of P53 and Caspase-3 induced by UVB irradiation. gb 28-30 caspase 3 Rattus norvegicus 175-184 30541132-9 2019 RESULTS: FSH and GB treatment increased CYP19A1 promoter activity, mRNA, and protein levels as well as estradiol when compared with cells treated with FSH only. gb 17-19 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 40-47 30541132-10 2019 GB treatment potentiated cAMP stimulation of aromatase and IGF2 stimulation by FSH. gb 0-2 insulin like growth factor 2 Homo sapiens 59-63 30541132-11 2019 GB effects were inhibited by SMAD3 inhibitors and IGF1 receptor inhibitors. gb 0-2 SMAD family member 3 Homo sapiens 29-34 30541132-12 2019 GB, but not FSH, stimulates SMAD3 phosphorylation. gb 0-2 SMAD family member 3 Homo sapiens 28-33 31068966-7 2019 Interestingly, a biphasic characteristic of P-TEFb-dependent transcription of serum responsive ncRNA genes was observed: Pol II carboxyl-terminal domain phosphorylated at serine 2 (S2) was largely increased in the transcription start site (TSS, -300 to +300) whereas overall, it was decreased in the gene body (GB, > +350) upon chemical inhibition of P-TEFb. gb 311-313 RNANC Homo sapiens 95-100 30298459-13 2019 Undergoing GB was associated with smaller 0-12-month changes in ALT, AST, and ALP. gb 11-13 solute carrier family 17 member 5 Homo sapiens 69-72 30298459-13 2019 Undergoing GB was associated with smaller 0-12-month changes in ALT, AST, and ALP. gb 11-13 alkaline phosphatase, placental Homo sapiens 78-81 30052682-4 2018 Here, we report the identification of F-box only protein 2 (FBXO2), an SCF ubiquitin ligase substrate adaptor that preferentially binds high-mannose glycans and attenuates EBV infectivity by targeting N-glycosylated gB for degradation. gb 216-218 F-box protein 2 Homo sapiens 60-65 30052682-7 2018 Depletion of FBXO2 not only stabilizes gB but also promotes its transport from the ER to the PM, resulting in enhanced membrane fusion and viral entry. gb 39-41 F-box protein 2 Homo sapiens 13-18 30487534-5 2018 Comparison of redirecting T cells with the bispecific antibody versus a chimeric antigen receptor (CAR) based on the same scFv showed a similar sensitivity for gB expression. gb 160-162 nuclear receptor subfamily 1 group I member 3 Homo sapiens 99-102 29849800-7 2018 In addition, alterations in HCMV gB-modulated protein levels of transforming growth factor-beta (TGF-beta) and Mothers against decapentaplegic homologs 2/3 (Smad2/3) were detected using western blot analysis. gb 33-35 transforming growth factor beta 1 Homo sapiens 97-105 29314441-3 2018 Here, the roles of the GB in POI in relation to TLR4-dependent signaling pathways were explored. gb 23-25 toll-like receptor 4 Mus musculus 48-52 29849800-7 2018 In addition, alterations in HCMV gB-modulated protein levels of transforming growth factor-beta (TGF-beta) and Mothers against decapentaplegic homologs 2/3 (Smad2/3) were detected using western blot analysis. gb 33-35 SMAD family member 3 Homo sapiens 157-164 29321326-0 2018 The Amino Terminus of Herpes Simplex Virus 1 Glycoprotein K (gK) Is Required for gB Binding to Akt, Release of Intracellular Calcium, and Fusion of the Viral Envelope with Plasma Membranes. gb 81-83 AKT serine/threonine kinase 1 Homo sapiens 95-98 29728654-6 2018 However, hyperfusogenic mutations, which destabilize the prefusion state of gB, target key interfaces and structural motifs that reinforce the observed CTD structure. gb 76-78 CTD Homo sapiens 152-155 29728654-7 2018 Thus, a similar CTD structure must stabilize gB in its prefusion state. gb 45-47 CTD Homo sapiens 16-19 29321326-3 2018 Proximity ligation and two-way immunoprecipitation assays using monoclonal antibodies against gB and Akt-1 phosphorylated at S473 [Akt-1(S473)] confirmed that HSV-1(McKrae) gB interacted with Akt-1(S473) during virus entry into human neuroblastoma (SK-N-SH) cells and induced the release of intracellular calcium. gb 173-175 AKT serine/threonine kinase 1 Homo sapiens 131-134 29321326-3 2018 Proximity ligation and two-way immunoprecipitation assays using monoclonal antibodies against gB and Akt-1 phosphorylated at S473 [Akt-1(S473)] confirmed that HSV-1(McKrae) gB interacted with Akt-1(S473) during virus entry into human neuroblastoma (SK-N-SH) cells and induced the release of intracellular calcium. gb 173-175 AKT serine/threonine kinase 1 Homo sapiens 131-134 29321326-2 2018 Recently, it has been shown that gB binds to Akt during virus entry and induces Akt phosphorylation and intracellular calcium release. gb 33-35 AKT serine/threonine kinase 1 Homo sapiens 45-48 29321326-8 2018 Herein, we show that a deletion in the amino terminus of glycoprotein K (gK) inhibits gB binding to Akt-1(S473), the release of intracellular calcium, and virus entry via fusion of the viral envelope with cellular plasma membranes. gb 86-88 AKT serine/threonine kinase 1 Homo sapiens 100-110 29321326-2 2018 Recently, it has been shown that gB binds to Akt during virus entry and induces Akt phosphorylation and intracellular calcium release. gb 33-35 AKT serine/threonine kinase 1 Homo sapiens 80-83 29160076-2 2017 Here we use density functional theory (DFT) in conjunction with a thermodynamic approach to determine the stability and electronic properties of all native point defects and their interplays with Sigma5-(210) GB in MAPbI3. gb 209-211 adaptor related protein complex 5 subunit sigma 1 Homo sapiens 196-202 30863520-11 2018 Conclusion: The most common CMV gB genotype in CMV-infected kidney transplant recipients in Iran was gB1. gb 32-34 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 101-104 28565773-7 2017 It was revealed that GB significantly reduced serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyl transpeptidase and total bilirubin levels in the serum induced by CCl4. gb 21-23 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 52-78 28490594-6 2017 Remarkably, gB-specific CD8+ T cells almost completely disappeared in the spleens of DKO mice during latency, and the reduction of CD8+ effector memory T (Tem) cells was more severe than that of CD8+ central memory T (Tcm) cells. gb 12-14 CD8a molecule Homo sapiens 24-27 28490594-6 2017 Remarkably, gB-specific CD8+ T cells almost completely disappeared in the spleens of DKO mice during latency, and the reduction of CD8+ effector memory T (Tem) cells was more severe than that of CD8+ central memory T (Tcm) cells. gb 12-14 CD8a molecule Homo sapiens 131-134 28490594-6 2017 Remarkably, gB-specific CD8+ T cells almost completely disappeared in the spleens of DKO mice during latency, and the reduction of CD8+ effector memory T (Tem) cells was more severe than that of CD8+ central memory T (Tcm) cells. gb 12-14 CD8a molecule Homo sapiens 131-134 28490594-7 2017 The percentage of gB-specific CD8+ T cells in TG during latency was also dramatically reduced in DKO mice; however, they were phenotypically similar to those from WT mice. gb 18-20 CD8a molecule Homo sapiens 30-33 28490594-9 2017 Thus, Dok-1 and Dok-2 promote survival of gB-specific CD8+ T cells in TG latently infected with HSV-1.IMPORTANCE HSV-1 establishes lifelong latency in sensory neurons of trigeminal ganglia (TG). gb 42-44 docking protein 1 Mus musculus 6-11 28490594-9 2017 Thus, Dok-1 and Dok-2 promote survival of gB-specific CD8+ T cells in TG latently infected with HSV-1.IMPORTANCE HSV-1 establishes lifelong latency in sensory neurons of trigeminal ganglia (TG). gb 42-44 docking protein 2 Mus musculus 16-21 28490594-9 2017 Thus, Dok-1 and Dok-2 promote survival of gB-specific CD8+ T cells in TG latently infected with HSV-1.IMPORTANCE HSV-1 establishes lifelong latency in sensory neurons of trigeminal ganglia (TG). gb 42-44 CD8a molecule Homo sapiens 54-57 28565773-7 2017 It was revealed that GB significantly reduced serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyl transpeptidase and total bilirubin levels in the serum induced by CCl4. gb 21-23 gamma-glutamyltransferase 1 Rattus norvegicus 128-157 28565773-7 2017 It was revealed that GB significantly reduced serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyl transpeptidase and total bilirubin levels in the serum induced by CCl4. gb 21-23 C-C motif chemokine ligand 4 Rattus norvegicus 209-213 28565773-9 2017 CCl4-induced reductions in endogenous liver antioxidant enzyme activities of superoxide dismutase, glutathione and glutathione peroxidase as well as increases in malondialdehyde and thiobarbituric acid reactive substances were inhibited by GB treatment. gb 240-242 C-C motif chemokine ligand 4 Rattus norvegicus 0-4 28565773-10 2017 Activated NF-kappaB in liver tissues was also significantly increased by CCl4, which was attenuated by GB as indicated by immunohistochemical and PCR analysis. gb 103-105 C-C motif chemokine ligand 4 Rattus norvegicus 73-77 28565773-11 2017 Furthermore, CCl4-mediated increases in the inflammatory factors tumor necrosis factor-alpha and interleukin-1beta secretion into the serum and their expression in liver tissues were reversed following GB treatment, as revealed by ELISA and PCR, respectively. gb 202-204 C-C motif chemokine ligand 4 Rattus norvegicus 13-17 28565773-11 2017 Furthermore, CCl4-mediated increases in the inflammatory factors tumor necrosis factor-alpha and interleukin-1beta secretion into the serum and their expression in liver tissues were reversed following GB treatment, as revealed by ELISA and PCR, respectively. gb 202-204 tumor necrosis factor Rattus norvegicus 65-92 28565773-11 2017 Furthermore, CCl4-mediated increases in the inflammatory factors tumor necrosis factor-alpha and interleukin-1beta secretion into the serum and their expression in liver tissues were reversed following GB treatment, as revealed by ELISA and PCR, respectively. gb 202-204 interleukin 1 beta Rattus norvegicus 97-114 28565773-12 2017 These findings suggested that GB protects against CCl4-induced hepatic injury, inflammation and oxidative damage in rats and may be useful in future clinical application of liver injury and disease. gb 30-32 C-C motif chemokine ligand 4 Rattus norvegicus 50-54 26843465-2 2016 To investigate the contribution of furin-mediated gB cleavage to EHV-1 growth, canonical furin cleavage sites were mutated. gb 50-52 furin, paired basic amino acid cleaving enzyme Homo sapiens 35-40 28423057-0 2017 Insertion of a ligand to HER2 in gB retargets HSV tropism and obviates the need for activation of the other entry glycoproteins. gb 33-35 erb-b2 receptor tyrosine kinase 2 Homo sapiens 25-29 28423057-9 2017 Furthermore, a soluble form of HER2 could replace the membrane-bound HER2 in mediating virus entry, hinting that HER2 acted by inducing conformational changes to the chimeric gB. gb 175-177 erb-b2 receptor tyrosine kinase 2 Homo sapiens 31-35 28423057-9 2017 Furthermore, a soluble form of HER2 could replace the membrane-bound HER2 in mediating virus entry, hinting that HER2 acted by inducing conformational changes to the chimeric gB. gb 175-177 erb-b2 receptor tyrosine kinase 2 Homo sapiens 69-73 28119397-3 2017 By using an overexpression approach, we demonstrated that transient expression of gB induces giant vesicles of early endosomal origin, which contained Rab5, early endosomal antigen 1 (EEA1), and large amounts of MHC-II molecules [human leukocyte antigen (HLA)-DR, and HLA-DM], but no CD63. gb 82-84 RAB5A, member RAS oncogene family Homo sapiens 151-155 28119397-3 2017 By using an overexpression approach, we demonstrated that transient expression of gB induces giant vesicles of early endosomal origin, which contained Rab5, early endosomal antigen 1 (EEA1), and large amounts of MHC-II molecules [human leukocyte antigen (HLA)-DR, and HLA-DM], but no CD63. gb 82-84 early endosome antigen 1 Homo sapiens 157-182 28119397-3 2017 By using an overexpression approach, we demonstrated that transient expression of gB induces giant vesicles of early endosomal origin, which contained Rab5, early endosomal antigen 1 (EEA1), and large amounts of MHC-II molecules [human leukocyte antigen (HLA)-DR, and HLA-DM], but no CD63. gb 82-84 early endosome antigen 1 Homo sapiens 184-188 28119397-3 2017 By using an overexpression approach, we demonstrated that transient expression of gB induces giant vesicles of early endosomal origin, which contained Rab5, early endosomal antigen 1 (EEA1), and large amounts of MHC-II molecules [human leukocyte antigen (HLA)-DR, and HLA-DM], but no CD63. gb 82-84 CD63 molecule Homo sapiens 284-288 27888111-3 2017 Our present study focused on the selection of neutralizing single-chain Fv (scFv) antibodies of a phage-displayed nonimmune human scFv antibody library against gB of HSV-1. gb 160-162 immunglobulin heavy chain variable region Homo sapiens 76-80 27888111-3 2017 Our present study focused on the selection of neutralizing single-chain Fv (scFv) antibodies of a phage-displayed nonimmune human scFv antibody library against gB of HSV-1. gb 160-162 immunglobulin heavy chain variable region Homo sapiens 130-134 27795301-3 2017 Immunization with the gB(dCt) vector alone elicited a comparable gB-binding antibody response and a superior neutralizing response to that elicited by adjuvanted subunit gB. gb 65-67 dopachrome tautomerase Homo sapiens 22-29 27661376-3 2016 A simulation link for the 40 Gbit/s 16-QAM SSB-OOFDM signal with a reduced GB is built to demonstrate the feasibility of our proposed scheme. gb 76-78 small RNA binding exonuclease protection factor La Homo sapiens 44-47 28423057-9 2017 Furthermore, a soluble form of HER2 could replace the membrane-bound HER2 in mediating virus entry, hinting that HER2 acted by inducing conformational changes to the chimeric gB. gb 175-177 erb-b2 receptor tyrosine kinase 2 Homo sapiens 69-73 27475038-7 2016 Our results suggest that dedifferentiation is associated with Tag1 activation and that CMT3 rather than DDM1 plays a central role in restraining Tag1 activation via inducing GB CHG methylation. gb 174-176 chromomethylase 3 Arabidopsis thaliana 87-91 27475038-7 2016 Our results suggest that dedifferentiation is associated with Tag1 activation and that CMT3 rather than DDM1 plays a central role in restraining Tag1 activation via inducing GB CHG methylation. gb 174-176 membrane bound O-acyl transferase (MBOAT) family protein Arabidopsis thaliana 145-149 26843465-4 2016 Treating infected cells with either convertase or furin inhibitors reduced gB cleavage efficiency. gb 75-77 furin, paired basic amino acid cleaving enzyme Homo sapiens 50-55 27058552-6 2016 In addition, GB treatment promoted the migration of CD103+CD11c+ cDCs and expansion of Foxp3+ regulatory T cells in the colons of DSS-treated mice. gb 13-15 integrin alpha E, epithelial-associated Mus musculus 52-57 27058552-6 2016 In addition, GB treatment promoted the migration of CD103+CD11c+ cDCs and expansion of Foxp3+ regulatory T cells in the colons of DSS-treated mice. gb 13-15 integrin alpha X Mus musculus 58-63 27058552-5 2016 The administration of GB to DSS-treated mice also reduced the numbers and inhibited the activation of colon-infiltrating T cells, neutrophils, intestinal CD103(-)CD11c+ dendritic cells (cDCs), and macrophages. gb 22-24 integrin alpha X Mus musculus 154-167 27058552-6 2016 In addition, GB treatment promoted the migration of CD103+CD11c+ cDCs and expansion of Foxp3+ regulatory T cells in the colons of DSS-treated mice. gb 13-15 forkhead box P3 Mus musculus 87-92 26885773-5 2016 The region, in which the gB precursor protein is cleaved into two fragments by a cellular endoprotease, is characterized by genetic variability, and based on that HCMV is classified into four major genotypes: gB1, gB2, gB3 and gB4. gb 25-27 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 219-222 26365435-4 2015 The gB/1G2 interaction is dominated by aromatic residues in the 1G2 heavy chain CDR3 protruding into a hydrophobic cleft in the gB antigenic domain 5 (AD-5). gb 4-6 CDR3 Homo sapiens 80-84 26316298-6 2015 RESULTS: The GB subjects had less suppression of fasting beta-cell secretion during the insulin clamp compared to controls. gb 13-15 insulin Homo sapiens 88-95 26316298-9 2015 CONCLUSIONS: Among subjects with GB, the response of insulin and glucagon secretion to decreasing blood glucose is blunted, but meal-induced insulin secretion is stimulated even at fixed systemic sub-basal glycemia. gb 33-35 insulin Homo sapiens 53-60 26363059-7 2015 Additionally, gB-specific CD4(+) T cells exhibited a more cytotoxic phenotype, with high levels of granzyme B expression. gb 14-16 granzyme B Homo sapiens 99-109 26105052-6 2015 In this study, we found that SAs on gB are essential for the association with MAG as well as for membrane fusion during VZV infection. gb 36-38 myelin associated glycoprotein Homo sapiens 78-81 26105052-12 2015 Therefore, these results suggest that SAs on gB play important roles in MAG-mediated VZV infection. gb 45-47 myelin associated glycoprotein Homo sapiens 72-75 26090808-6 2015 Moreover, in vivo administration of GB promoted up-regulation of CD86, MHC class I and MHC class II and production of IL-6, IL-12 and TNF-alpha in spleen DCs. gb 36-38 CD86 antigen Mus musculus 65-69 25994965-8 2015 Measurement of gB-specific cytokines demonstrated that gB-CCL19 fusion constructs induced balanced Th1 and Th2 cellular immune responses. gb 15-17 C-C motif chemokine ligand 19 Homo sapiens 58-63 26079615-5 2015 Strikingly, ELISA and neutralization titers were significantly lower in the gB/GP83 combined vaccine group than in the gB group. gb 76-78 ADAM metallopeptidase domain 7 Homo sapiens 79-83 26079615-8 2015 We conclude that, using the MVA platform, the addition of GP83 to a gB subunit vaccine interferes with antibody responses and diminishes protection against congenital GPCMV infection, but does not decrease protection against pup mortality. gb 68-70 ADAM metallopeptidase domain 7 Homo sapiens 58-62 26090808-6 2015 Moreover, in vivo administration of GB promoted up-regulation of CD86, MHC class I and MHC class II and production of IL-6, IL-12 and TNF-alpha in spleen DCs. gb 36-38 interleukin 6 Mus musculus 118-122 26090808-6 2015 Moreover, in vivo administration of GB promoted up-regulation of CD86, MHC class I and MHC class II and production of IL-6, IL-12 and TNF-alpha in spleen DCs. gb 36-38 tumor necrosis factor Mus musculus 134-143 26090808-7 2015 GB also promoted the generation of Th1 and Tc1 cells. gb 0-2 negative elongation factor complex member C/D, Th1l Mus musculus 35-38 26090808-8 2015 Furthermore, Toll like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MyD88) signaling pathway were essential for DC activation induced by GB. gb 159-161 toll-like receptor 4 Mus musculus 13-33 26090808-8 2015 Furthermore, Toll like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MyD88) signaling pathway were essential for DC activation induced by GB. gb 159-161 toll-like receptor 4 Mus musculus 35-39 26090808-8 2015 Furthermore, Toll like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MyD88) signaling pathway were essential for DC activation induced by GB. gb 159-161 myeloid differentiation primary response gene 88 Mus musculus 90-95 25448630-8 2014 In Hans, 4 CMV gB genotypes were identified: gB1, gB2, gB1+gB2, and gB2+gB3. gb 15-17 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 45-48 25736129-7 2015 CONCLUSION: GB combined with MP produces better therapeutic effects for treating SCI than GB or MP used alone, and such effects are probably related with enhanced BDNF expression in the spinal cord. gb 12-14 brain-derived neurotrophic factor Rattus norvegicus 163-167 25654240-8 2015 In conclusion, our results show that the exchange of gB between EHV-1 and EHV-4 is possible, but results in a significant attenuation of virus growth in the case of EHV-4_gB1. gb 53-55 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 171-174 25428876-7 2015 IMPORTANCE: Herpes simplex virus 1 (HSV-1) was reported to utilize nonmuscle myosin heavy chain IIA (NMHC-IIA) as an entry coreceptor associating with gB. gb 151-153 myosin heavy chain 9 Homo sapiens 101-109 25448630-8 2014 In Hans, 4 CMV gB genotypes were identified: gB1, gB2, gB1+gB2, and gB2+gB3. gb 15-17 gamma-aminobutyric acid type B receptor subunit 2 Homo sapiens 50-53 25448630-8 2014 In Hans, 4 CMV gB genotypes were identified: gB1, gB2, gB1+gB2, and gB2+gB3. gb 15-17 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 55-58 25448630-8 2014 In Hans, 4 CMV gB genotypes were identified: gB1, gB2, gB1+gB2, and gB2+gB3. gb 15-17 gamma-aminobutyric acid type B receptor subunit 2 Homo sapiens 59-62 25448630-8 2014 In Hans, 4 CMV gB genotypes were identified: gB1, gB2, gB1+gB2, and gB2+gB3. gb 15-17 gamma-aminobutyric acid type B receptor subunit 2 Homo sapiens 59-62 25448630-8 2014 In Hans, 4 CMV gB genotypes were identified: gB1, gB2, gB1+gB2, and gB2+gB3. gb 15-17 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 72-75 25606896-4 2014 Based on the simulation system, the 40 Gb/s 16QAM SSB-OOFDM signal with 5 GHz GB is converted to the OFDM signal by the ICRBD with the suppressed SSBI. gb 78-80 small RNA binding exonuclease protection factor La Homo sapiens 50-53 24704672-2 2014 However, the gB-specific human CD8(+) T cell responses remain poorly understood. gb 13-15 CD8a molecule Homo sapiens 31-34 24668543-5 2014 CONCLUSION: GB rapidly decreased BMI, HbA1c, and insulin requirements in severely obese women with type 1 diabetes. gb 12-14 insulin Homo sapiens 49-56 24704672-3 2014 gB antigen-specific CD8(+) T cells were stained with seven major histocompatibility complex (MHC)-peptide pentamers in 16 human leukocyte antigen (HLA)-A 1101-positive, HCMV-seropositive patients following hematopoietic stem cell transplantation (HSCT). gb 0-2 CD8a molecule Homo sapiens 20-23 24704672-3 2014 gB antigen-specific CD8(+) T cells were stained with seven major histocompatibility complex (MHC)-peptide pentamers in 16 human leukocyte antigen (HLA)-A 1101-positive, HCMV-seropositive patients following hematopoietic stem cell transplantation (HSCT). gb 0-2 major histocompatibility complex, class I, A Homo sapiens 128-153 24843130-8 2014 Mutation of L108 to tryptophan in PILRbeta restored the gB-binding capacity. gb 56-58 paired immunoglobin like type 2 receptor beta Homo sapiens 34-42 24101547-3 2013 In this study, we used multiple prediction algorithms to identify 10 potential HLA-A*02:01-restricted CD8(+) T cell epitopes from the HSV-1 gB amino acid sequence. gb 140-142 major histocompatibility complex, class I, A Homo sapiens 79-84 24855352-6 2014 In particular, interleukin (IL)-23-, IL-6-, IL-8- or macrophage inflammatory protein (MIP)-2-, and tumor necrosis factor (TNF)-alpha-release increased considerably when cells were treated with the gB-micelles or gD-micelles compared with the production of the same cytokines when the stimulus was the single gB or gD peptide. gb 197-199 C-X-C motif chemokine ligand 2 Homo sapiens 53-92 24855352-6 2014 In particular, interleukin (IL)-23-, IL-6-, IL-8- or macrophage inflammatory protein (MIP)-2-, and tumor necrosis factor (TNF)-alpha-release increased considerably when cells were treated with the gB-micelles or gD-micelles compared with the production of the same cytokines when the stimulus was the single gB or gD peptide. gb 197-199 tumor necrosis factor Homo sapiens 99-132 24658280-4 2014 We demonstrate that gB is endogenously expressed in primary GBM samples and show that ectopic gB expression in glioma cells induced sustained phosphorylation of PDGFRalpha, Akt, and Src. gb 94-96 platelet derived growth factor receptor alpha Homo sapiens 161-171 24658280-4 2014 We demonstrate that gB is endogenously expressed in primary GBM samples and show that ectopic gB expression in glioma cells induced sustained phosphorylation of PDGFRalpha, Akt, and Src. gb 94-96 AKT serine/threonine kinase 1 Homo sapiens 173-176 24658280-4 2014 We demonstrate that gB is endogenously expressed in primary GBM samples and show that ectopic gB expression in glioma cells induced sustained phosphorylation of PDGFRalpha, Akt, and Src. gb 94-96 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 182-185 24658280-7 2014 gB overexpression promoted in vivo glioma growth and enhanced phosphor-Akt levels and tumor cell dispersal relative to controls. gb 0-2 AKT serine/threonine kinase 1 Homo sapiens 71-74 24463331-3 2014 The polyepitope protein includes contiguous multiple MHC class I-restricted epitopes with an aim to induce CD8(+) T cell immunity, while gB is an important target for CD4(+) T cell immunity and neutralizing antibodies. gb 137-139 CD4 molecule Homo sapiens 167-170 24177087-2 2013 Simulation demonstration of the ICRBD for a 40 Gbit/s 16-QAM SSB-OOFDM signal with a reduced GB was achieved successfully. gb 93-95 small RNA binding exonuclease protection factor La Homo sapiens 61-64 24044679-9 2013 However, only IL-6 production was significantly increased with GB. gb 63-65 interleukin 6 Homo sapiens 14-18 24039967-5 2013 Indeed, GB elicited an increase of TNF-alpha production, caspase-8 and caspase-3 activation, and PARP-1 cleavage within pre-B acute lymphoblastic leukemia Nalm-6 cells. gb 8-10 tumor necrosis factor Homo sapiens 35-44 24039967-5 2013 Indeed, GB elicited an increase of TNF-alpha production, caspase-8 and caspase-3 activation, and PARP-1 cleavage within pre-B acute lymphoblastic leukemia Nalm-6 cells. gb 8-10 caspase 8 Homo sapiens 57-66 24039967-5 2013 Indeed, GB elicited an increase of TNF-alpha production, caspase-8 and caspase-3 activation, and PARP-1 cleavage within pre-B acute lymphoblastic leukemia Nalm-6 cells. gb 8-10 caspase 3 Homo sapiens 71-80 24039967-5 2013 Indeed, GB elicited an increase of TNF-alpha production, caspase-8 and caspase-3 activation, and PARP-1 cleavage within pre-B acute lymphoblastic leukemia Nalm-6 cells. gb 8-10 poly(ADP-ribose) polymerase 1 Homo sapiens 97-103 24039967-7 2013 Furthermore, intracellular signaling analyses determined that GB treatment enhanced constitutive activation of Lck and Src tyrosine kinases in Nalm-6 cells. gb 62-64 LCK proto-oncogene, Src family tyrosine kinase Homo sapiens 111-114 24039967-8 2013 Taken together, these findings indicate that GB induced preferential anti-proliferative and pro-apoptotic signals within B-lineage leukemia/lymphoma cells, as determined by the following biochemical hallmarks of apoptosis: PS externalization, enhanced release of TNF-alpha, caspase-8 and caspase-3 activation, PARP-1 cleavage and DNA fragmentation Our observations reveal that GB has potential as an anti-leukemia/lymphoma agent alone or in combination with standard cancer therapies and thus warrants further evaluation in vivo to support these findings. gb 45-47 tumor necrosis factor Homo sapiens 263-272 24039967-8 2013 Taken together, these findings indicate that GB induced preferential anti-proliferative and pro-apoptotic signals within B-lineage leukemia/lymphoma cells, as determined by the following biochemical hallmarks of apoptosis: PS externalization, enhanced release of TNF-alpha, caspase-8 and caspase-3 activation, PARP-1 cleavage and DNA fragmentation Our observations reveal that GB has potential as an anti-leukemia/lymphoma agent alone or in combination with standard cancer therapies and thus warrants further evaluation in vivo to support these findings. gb 45-47 caspase 8 Homo sapiens 274-283 24039967-8 2013 Taken together, these findings indicate that GB induced preferential anti-proliferative and pro-apoptotic signals within B-lineage leukemia/lymphoma cells, as determined by the following biochemical hallmarks of apoptosis: PS externalization, enhanced release of TNF-alpha, caspase-8 and caspase-3 activation, PARP-1 cleavage and DNA fragmentation Our observations reveal that GB has potential as an anti-leukemia/lymphoma agent alone or in combination with standard cancer therapies and thus warrants further evaluation in vivo to support these findings. gb 45-47 caspase 3 Homo sapiens 288-297 24039967-8 2013 Taken together, these findings indicate that GB induced preferential anti-proliferative and pro-apoptotic signals within B-lineage leukemia/lymphoma cells, as determined by the following biochemical hallmarks of apoptosis: PS externalization, enhanced release of TNF-alpha, caspase-8 and caspase-3 activation, PARP-1 cleavage and DNA fragmentation Our observations reveal that GB has potential as an anti-leukemia/lymphoma agent alone or in combination with standard cancer therapies and thus warrants further evaluation in vivo to support these findings. gb 45-47 poly(ADP-ribose) polymerase 1 Homo sapiens 310-316 22797815-6 2012 RESULTS: We isolated several gB-specific CD4(+) T-cell clones directed against peptides gB(190-204), gB(396-410), gB(22-36) and gB(598-617) presented by HLA-DR7, HLA-DP10 and HLA-DP2. gb 29-31 CD4 molecule Homo sapiens 41-44 23740990-3 2013 Using human monoclonal antibodies (MAbs), we have recently identified antigenic region 4 (AD-4) on gB as an important target for neutralizing antibodies. gb 99-101 presenilin 2 Homo sapiens 90-94 23811559-1 2013 This study aimed to show if two different sulphur containing drugs sulbutiamine and acetylcysteine (NAC) could attenuate the effects of two different insults being serum deprivation and glutamate/buthionine sulfoximine (GB)-induced death to transformed retinal ganglion cell line (RGC-5) in culture. gb 220-222 NLR family, pyrin domain containing 1A Mus musculus 100-103 23811559-6 2013 However NAC but not sulbutiamine attenuated GB-induced cell death. gb 44-46 NLR family, pyrin domain containing 1A Mus musculus 8-11 23811559-10 2013 The neuroprotective actions of NAC and sulbutiamine in GB or serum-deprivation insult are therefore different. gb 55-57 NLR family, pyrin domain containing 1A Mus musculus 31-34 22797815-6 2012 RESULTS: We isolated several gB-specific CD4(+) T-cell clones directed against peptides gB(190-204), gB(396-410), gB(22-36) and gB(598-617) presented by HLA-DR7, HLA-DP10 and HLA-DP2. gb 88-90 CD4 molecule Homo sapiens 41-44 23829744-7 2013 In this Letter we report on atomistic simulations of Ag diffusion and segregation in two different structural phases of the Cu Sigma5(310) GB which transform to each other with temperature. gb 139-141 adaptor related protein complex 5 subunit sigma 1 Homo sapiens 127-133 22797815-6 2012 RESULTS: We isolated several gB-specific CD4(+) T-cell clones directed against peptides gB(190-204), gB(396-410), gB(22-36) and gB(598-617) presented by HLA-DR7, HLA-DP10 and HLA-DP2. gb 88-90 CD4 molecule Homo sapiens 41-44 22797815-6 2012 RESULTS: We isolated several gB-specific CD4(+) T-cell clones directed against peptides gB(190-204), gB(396-410), gB(22-36) and gB(598-617) presented by HLA-DR7, HLA-DP10 and HLA-DP2. gb 88-90 CD4 molecule Homo sapiens 41-44 22797815-6 2012 RESULTS: We isolated several gB-specific CD4(+) T-cell clones directed against peptides gB(190-204), gB(396-410), gB(22-36) and gB(598-617) presented by HLA-DR7, HLA-DP10 and HLA-DP2. gb 88-90 CD4 molecule Homo sapiens 41-44 22797815-8 2012 CONCLUSIONS: The characterization of such gB-epitopes presented by HLA-class II should help to understand the contribution of CD4(+) T-cell responses to CMV and may be of importance both in designing a vaccine against CMV infection and in immunomonitoring of subjects immunized with recombinant gB or with vectors encoding gB. gb 42-44 CD4 molecule Homo sapiens 126-129 22414065-6 2012 Specific SNPs in TLR7 and IKBKE (inhibitor of nuclear factor kappa-B kinase subunit epsilon) were associated with antibody responses to gB vaccine. gb 136-138 toll like receptor 7 Homo sapiens 17-21 22623783-3 2012 The gB cytodomain appears to restrict fusion, because point or truncation mutations within it increase the extent of fusion (syn mutations). gb 4-6 synemin Homo sapiens 125-128 22623783-4 2012 Previously, we showed that the hyperfusion phenotype correlated with reduced membrane binding in gB syn truncation mutants and proposed that membrane binding was important in regulating fusion. gb 97-99 synemin Homo sapiens 100-103 22644833-4 2012 We have previously shown that, under hypoxia GB primary cells increased the expression of stemness markers as well as the expression of the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha) and also the crucial role played by PPARs in mouse neural stem cells maintenance and differentiation. gb 45-47 peroxisome proliferator activated receptor alpha Mus musculus 207-216 22695228-3 2012 Here we show that the human ocular and highly neurovirulent HSV-1 strain McKrae enters substantially more efficiently into cells via the gB-specific human paired immunoglobulin-like type-2 receptor-alpha (hPILR-alpha). gb 137-139 paired immunoglobin like type 2 receptor alpha Homo sapiens 205-216 22414065-6 2012 Specific SNPs in TLR7 and IKBKE (inhibitor of nuclear factor kappa-B kinase subunit epsilon) were associated with antibody responses to gB vaccine. gb 136-138 inhibitor of nuclear factor kappa B kinase subunit epsilon Homo sapiens 26-31 22414065-6 2012 Specific SNPs in TLR7 and IKBKE (inhibitor of nuclear factor kappa-B kinase subunit epsilon) were associated with antibody responses to gB vaccine. gb 136-138 inhibitor of nuclear factor kappa B kinase subunit epsilon Homo sapiens 33-91 22414065-7 2012 Homozygous carriers of the minor allele at four SNPs in TLR7 showed higher vaccination-induced antibody responses to gB compared to heterozygotes or homozygotes for the common allele. gb 117-119 toll like receptor 7 Homo sapiens 56-60 22057089-4 2012 RESULTS: The distribution of gB genotypes was as follows: gB1, 54/102 (52.9%); gB3, 21/102 (20.6%); and mixtures, 27/102 (26.5%). gb 29-31 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 58-61 22650040-6 2012 RESULTS: After spinal cord contusion, GB resulted in a significant increase on the number of BDNF positive neurons compared with traumatic group, and increased BBB score and decreased NMDA receptor were also found in GB group. gb 38-40 brain-derived neurotrophic factor Rattus norvegicus 93-97 20805692-5 2011 Pro-BNP levels were lower in GB patients as the body mass index increased; the opposite occurred in GA. gb 29-31 natriuretic peptide B Homo sapiens 4-7 22470437-8 2012 Further local application of force resulted in redistribution of non muscle myosin-II in the GB layer. gb 93-95 zipper Drosophila melanogaster 65-85 21653669-6 2011 gB initiates the interaction with CD1d in the endoplasmic reticulum and stably associates with it throughout CD1d trafficking. gb 0-2 CD1d molecule Homo sapiens 34-38 21653669-6 2011 gB initiates the interaction with CD1d in the endoplasmic reticulum and stably associates with it throughout CD1d trafficking. gb 0-2 CD1d molecule Homo sapiens 109-113 21653669-8 2011 US3 expression in infected cells leads to gB enrichment in the trans-Golgi network (TGN) and enhances the relocalization of both gB and CD1d to this compartment, suggesting that following internalization CD1d is translocated from the endocytic pathway to the TGN by its association with gB. gb 42-44 serine/threonine protein kinase US3 Human alphaherpesvirus 1 0-3 21653669-8 2011 US3 expression in infected cells leads to gB enrichment in the trans-Golgi network (TGN) and enhances the relocalization of both gB and CD1d to this compartment, suggesting that following internalization CD1d is translocated from the endocytic pathway to the TGN by its association with gB. gb 129-131 serine/threonine protein kinase US3 Human alphaherpesvirus 1 0-3 21653669-8 2011 US3 expression in infected cells leads to gB enrichment in the trans-Golgi network (TGN) and enhances the relocalization of both gB and CD1d to this compartment, suggesting that following internalization CD1d is translocated from the endocytic pathway to the TGN by its association with gB. gb 129-131 serine/threonine protein kinase US3 Human alphaherpesvirus 1 0-3 21653669-9 2011 Importantly, both US3 and gB are required for efficient inhibition of CD1d antigen presentation and NKT cell activation. gb 26-28 CD1b molecule Homo sapiens 70-73 21386720-6 2011 Recovery HR (RecHR) (15 minutes postexercise) was significantly higher for GB (91 +- 14 b min(-1)) than for DDR (80 +- 11 b min(-1)) and neared significance vs. CE (84 +- 14 b min(-1), p = 0.059). gb 75-77 CD59 molecule (CD59 blood group) Homo sapiens 92-98 21491978-3 2011 The distribution of gB genotypes was as follows: 12 (27.3%) gB1, 11 (25%) gB2, 9 (20.4%) gB3, 4 (9.1%) gB4, 0 gB5, and 8 (18.2%) mixed genotypes. gb 20-22 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 60-63 21491978-3 2011 The distribution of gB genotypes was as follows: 12 (27.3%) gB1, 11 (25%) gB2, 9 (20.4%) gB3, 4 (9.1%) gB4, 0 gB5, and 8 (18.2%) mixed genotypes. gb 20-22 gamma-aminobutyric acid type B receptor subunit 2 Homo sapiens 74-77 21491978-3 2011 The distribution of gB genotypes was as follows: 12 (27.3%) gB1, 11 (25%) gB2, 9 (20.4%) gB3, 4 (9.1%) gB4, 0 gB5, and 8 (18.2%) mixed genotypes. gb 20-22 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 89-92 21389132-3 2011 In the present study, we demonstrated that Us3 phosphorylation of gB Thr-887 upregulated the accumulation of endocytosed gB from the surfaces of infected cells. gb 66-68 serine/threonine protein kinase US3 Human alphaherpesvirus 1 43-46 21304064-3 2011 Fasting FFAa were not significantly different between the three study groups but during both doses of insulin were significantly higher in O than in either GB or L. The effective insulin concentration resulting in half-maximal suppression of FFA was similar in L and GB and significantly less in both groups compared with O. gb 156-158 insulin Homo sapiens 179-186 21304064-5 2011 During high-dose insulin, glucose infusion rates were significantly greater in GB than in O but less than in L. Endogenous glucose production in GB was significantly lower than O only during low dose of insulin. gb 145-147 insulin Homo sapiens 203-210 21357536-3 2011 Of 376 predicted HSV-1 CD8(+) T cell epitopes in C57BL/6 mice, 19 (gB(498-505) and 18 subdominant epitopes) stimulated CD8(+) T cells in the spleens and TG of HSV-1 acutely infected mice. gb 67-69 CD8a molecule Homo sapiens 119-122 20719985-4 2010 On the basis of our previous findings that dendritic cells (DC) reveal major histocompatibility complex (MHC) class I epitopes in gB, we used a DC-based system to identify 2 novel epitopes in gB, 2 in K8.1, 5 in LANA-1, and 1 in K12. gb 192-194 keratin 81 Homo sapiens 201-205 20943984-3 2010 We determined the crystal structures of the ectodomains of two FL1 mutants of herpes simplex virus type 1 (HSV-1) gB to clarify whether their fusion-null phenotypes were due to global or local effects of the mutations on the structure of the gB ectodomain. gb 114-116 FL1 Homo sapiens 63-66 20864524-5 2010 Also, we demonstrate that such a profound inhibitory effect of gB on the lytic cycle of virus replication is by repressing the ability of Egr-1 (early growth response-1) to bind and activate the ORF50 promoter. gb 63-65 early growth response 1 Homo sapiens 138-143 20944748-5 2010 Here we show that non-muscle myosin heavy chain IIA (NMHC-IIA), a subunit of non-muscle myosin IIA (NM-IIA), functions as an HSV-1 entry receptor by interacting with gB. gb 166-168 myosin heavy chain 9 Homo sapiens 53-61 20944748-8 2010 Furthermore, knockdown of NMHC-IIA in the permissive cells inhibited HSV-1 infection as well as cell-cell fusion when gB, gD, gH and gL were coexpressed. gb 118-120 myosin heavy chain 9 Homo sapiens 26-34 20686018-2 2010 Two threonine residues (Thr-53 and Thr-480) in gB, which are required for the addition of the principal gB O-glycans, are essential for binding to soluble PILRalpha. gb 47-49 paired immunoglobin like type 2 receptor alpha Homo sapiens 155-164 20573821-3 2010 We hypothesized that the low-level expression of gB from its native promoter before viral DNA synthesis is critical for the retention and activation of gB-CD8 cells in the TG during HSV-1 latency and for their ability to block HSV-1 reactivation from latency. gb 49-51 CD8a molecule Homo sapiens 155-158 20686018-6 2010 These results support the hypothesis that gB Thr-53 and Thr-480 as well as gB O-glycosylation, probably at these sites, are critical for PILRalpha-dependent viral entry. gb 42-44 paired immunoglobin like type 2 receptor alpha Homo sapiens 137-146 20573821-4 2010 To test this, we created a recombinant HSV-1 in which gB is expressed only after viral DNA synthesis from the true late gC promoter (gCp-gB). gb 54-56 folate hydrolase 1 Mus musculus 120-122 20573821-4 2010 To test this, we created a recombinant HSV-1 in which gB is expressed only after viral DNA synthesis from the true late gC promoter (gCp-gB). gb 54-56 folate hydrolase 1 Mus musculus 133-136 20573821-6 2010 The gCp-gB- and rescuant-infected mice mounted similar gB-CD8 effector responses, but the size and activation phenotypes of the memory gB-CD8 cells were diminished in gCp-gB latently infected TG, suggesting that the stimulation of gB-CD8 cells requires gB expression before viral DNA synthesis. gb 8-10 folate hydrolase 1 Mus musculus 4-7 20573821-6 2010 The gCp-gB- and rescuant-infected mice mounted similar gB-CD8 effector responses, but the size and activation phenotypes of the memory gB-CD8 cells were diminished in gCp-gB latently infected TG, suggesting that the stimulation of gB-CD8 cells requires gB expression before viral DNA synthesis. gb 8-10 folate hydrolase 1 Mus musculus 167-170 20573830-6 2010 Domain swaps between PILRalpha and PILRbeta reveal that the Ig-like V-type domain of PILRalpha, but not PILRbeta, plays a critical role in cell membrane fusion activity and the binding of PILRalpha to gB. gb 201-203 paired immunoglobin like type 2 receptor alpha Homo sapiens 21-30 20573830-6 2010 Domain swaps between PILRalpha and PILRbeta reveal that the Ig-like V-type domain of PILRalpha, but not PILRbeta, plays a critical role in cell membrane fusion activity and the binding of PILRalpha to gB. gb 201-203 paired immunoglobin like type 2 receptor beta Homo sapiens 35-43 20573830-6 2010 Domain swaps between PILRalpha and PILRbeta reveal that the Ig-like V-type domain of PILRalpha, but not PILRbeta, plays a critical role in cell membrane fusion activity and the binding of PILRalpha to gB. gb 201-203 paired immunoglobin like type 2 receptor alpha Homo sapiens 85-94 20573830-6 2010 Domain swaps between PILRalpha and PILRbeta reveal that the Ig-like V-type domain of PILRalpha, but not PILRbeta, plays a critical role in cell membrane fusion activity and the binding of PILRalpha to gB. gb 201-203 paired immunoglobin like type 2 receptor alpha Homo sapiens 85-94 20538950-4 2010 Initiation of the gB-specific CD8+ T cell response during HSV-1 infection, or cross-priming, is highly GILT-dependent, as is initiation of the response to the envelope glycoproteins of influenza A virus. gb 18-20 IFI30 lysosomal thiol reductase Homo sapiens 103-107 19846518-7 2010 In addition, we generated a monoclonal antibody that specifically reacted with phosphorylated gB Thr-887 and used this antibody to show that Us3 phosphorylation of gB Thr-887 regulated subcellular localization of gB, particularly on the cell surface of infected cells. gb 94-96 serine/threonine protein kinase US3 Human alphaherpesvirus 1 141-144 19955303-4 2010 In this study, the short interfering RNA (siRNA)-mediated inhibition of either gB or K8.1 transcription by anti-gB or -K8.1 siRNAs caused a substantial reduction in virion egress and a decrease in both vIL-6 and VEGF production. gb 79-81 keratin 81 Homo sapiens 119-123 19955303-4 2010 In this study, the short interfering RNA (siRNA)-mediated inhibition of either gB or K8.1 transcription by anti-gB or -K8.1 siRNAs caused a substantial reduction in virion egress and a decrease in both vIL-6 and VEGF production. gb 79-81 K2 Human gammaherpesvirus 8 202-207 19955303-4 2010 In this study, the short interfering RNA (siRNA)-mediated inhibition of either gB or K8.1 transcription by anti-gB or -K8.1 siRNAs caused a substantial reduction in virion egress and a decrease in both vIL-6 and VEGF production. gb 79-81 vascular endothelial growth factor A Homo sapiens 212-216 19955303-5 2010 Similarly, the treatment of BCBL-1 cells with anti-gB or anti-K8.1 antibodies caused a substantial reduction in vIL-6 and VEGF production. gb 51-53 K2 Human gammaherpesvirus 8 112-117 19955303-5 2010 Similarly, the treatment of BCBL-1 cells with anti-gB or anti-K8.1 antibodies caused a substantial reduction in vIL-6 and VEGF production. gb 51-53 vascular endothelial growth factor A Homo sapiens 122-126 19955303-6 2010 Codon-optimized versions of either wild-type gB, mutant gB having the RGD amino acid motif changed to RAA, or K8.1 efficiently rescued virion egress and VEGF and vIL-6 production. gb 56-58 vascular endothelial growth factor A Homo sapiens 153-157 19955303-6 2010 Codon-optimized versions of either wild-type gB, mutant gB having the RGD amino acid motif changed to RAA, or K8.1 efficiently rescued virion egress and VEGF and vIL-6 production. gb 56-58 K2 Human gammaherpesvirus 8 162-167 19955303-9 2010 Furthermore, medium obtained from BCBL-1 cells expressing smaller amounts of gB and K8.1 produced a substantial reduction in endothelial cell migration in a vertical migration assay compared to that of control medium containing wild-type levels of gB and K8.1. gb 77-79 keratin 81 Homo sapiens 255-259 19955303-9 2010 Furthermore, medium obtained from BCBL-1 cells expressing smaller amounts of gB and K8.1 produced a substantial reduction in endothelial cell migration in a vertical migration assay compared to that of control medium containing wild-type levels of gB and K8.1. gb 248-250 keratin 81 Homo sapiens 84-88 19949097-9 2010 Interestingly, increasing expression of gB strongly elevated the amount of DR and CD63 released into the exosome pathway. gb 40-42 CD63 molecule Homo sapiens 82-86 20362496-5 2010 RESULTS: In all cases only one gB-gH-UL10 genotype was detected. gb 31-33 membrane protein UL10 Human betaherpesvirus 5 37-41 19193805-7 2009 We generated fibroblasts expressing HCMV gB that complement pAD/CreDeltaUL55 and produce infectious virions lacking the UL55 gene but containing wild-type gB on the virion surface (DeltaUL55-gB HCMV). gb 41-43 envelope glycoprotein B Human betaherpesvirus 5 72-76 19824673-5 2009 However, the main biradical intermediate GB2 of the GB reaction is 6.2 kcal/mol lower in energy than the biradical MS2, which is the main intermediate of MS reaction, so GB cyclization is thermodynamically favored over MS cyclization. gb 41-43 MS2 Homo sapiens 115-118 19824673-5 2009 However, the main biradical intermediate GB2 of the GB reaction is 6.2 kcal/mol lower in energy than the biradical MS2, which is the main intermediate of MS reaction, so GB cyclization is thermodynamically favored over MS cyclization. gb 52-54 gamma-aminobutyric acid type B receptor subunit 2 Homo sapiens 41-44 19824673-5 2009 However, the main biradical intermediate GB2 of the GB reaction is 6.2 kcal/mol lower in energy than the biradical MS2, which is the main intermediate of MS reaction, so GB cyclization is thermodynamically favored over MS cyclization. gb 52-54 MS2 Homo sapiens 115-118 19751151-6 2009 RESULTS: Among 239 patients with CMV disease, the prevalence of gB strain types was 26% for gB1, 10% for gB2, 10% for gB3, and 5% for gB4, whereas mixed infections were present in 49%. gb 64-66 gamma-aminobutyric acid type B receptor subunit 1 Homo sapiens 92-95 19751151-6 2009 RESULTS: Among 239 patients with CMV disease, the prevalence of gB strain types was 26% for gB1, 10% for gB2, 10% for gB3, and 5% for gB4, whereas mixed infections were present in 49%. gb 64-66 gamma-aminobutyric acid type B receptor subunit 2 Homo sapiens 105-108 19751151-6 2009 RESULTS: Among 239 patients with CMV disease, the prevalence of gB strain types was 26% for gB1, 10% for gB2, 10% for gB3, and 5% for gB4, whereas mixed infections were present in 49%. gb 64-66 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 118-121 19457990-4 2009 The purpose of this study was to determine whether insertional mutations in gB had differential effects on its function with PILRalpha and the gD receptor, nectin-1. gb 76-78 paired immunoglobin like type 2 receptor alpha Homo sapiens 125-134 19457990-4 2009 The purpose of this study was to determine whether insertional mutations in gB had differential effects on its function with PILRalpha and the gD receptor, nectin-1. gb 76-78 nectin cell adhesion molecule 1 Homo sapiens 156-164 19457990-6 2009 We found that insertional mutations near the N terminus and C terminus of gB and especially in the central region of the ectodomain reduced cell fusion activity when PILRalpha was overexpressed much more than when nectin-1 was overexpressed. gb 74-76 paired immunoglobin like type 2 receptor alpha Homo sapiens 166-175 19457990-6 2009 We found that insertional mutations near the N terminus and C terminus of gB and especially in the central region of the ectodomain reduced cell fusion activity when PILRalpha was overexpressed much more than when nectin-1 was overexpressed. gb 74-76 nectin cell adhesion molecule 1 Homo sapiens 214-222 19457990-7 2009 Most of the insertions reduced the binding of gB to PILRalpha, for at least some forms of gB, but this reduction did not necessarily correlate with the selective reduction in cell fusion activity with PILRalpha. gb 46-48 paired immunoglobin like type 2 receptor alpha Homo sapiens 52-61 19457990-7 2009 Most of the insertions reduced the binding of gB to PILRalpha, for at least some forms of gB, but this reduction did not necessarily correlate with the selective reduction in cell fusion activity with PILRalpha. gb 90-92 paired immunoglobin like type 2 receptor alpha Homo sapiens 52-61 19646921-4 2009 Immunisation with Ad-gBCMVpoly consistently generated strong gB-specific neutralizing antibody and a broad range of HCMV-specific pluripotent CD8(+) and CD4(+) T-cells. gb 21-23 CD8a molecule Homo sapiens 142-145 19646921-4 2009 Immunisation with Ad-gBCMVpoly consistently generated strong gB-specific neutralizing antibody and a broad range of HCMV-specific pluripotent CD8(+) and CD4(+) T-cells. gb 21-23 CD4 molecule Homo sapiens 153-156 19812165-0 2009 Binding of herpes simplex virus glycoprotein B (gB) to paired immunoglobulin-like type 2 receptor alpha depends on specific sialylated O-linked glycans on gB. gb 48-50 paired immunoglobin like type 2 receptor alpha Homo sapiens 55-103 19812165-4 2009 Here, we found that the presence of sialylated O-glycans on gB is required for gB to associate with PILRalpha. gb 60-62 paired immunoglobin like type 2 receptor alpha Homo sapiens 100-109 19812165-4 2009 Here, we found that the presence of sialylated O-glycans on gB is required for gB to associate with PILRalpha. gb 79-81 paired immunoglobin like type 2 receptor alpha Homo sapiens 100-109 19812165-5 2009 Furthermore, we identified two threonine residues on gB that are essential for the addition of the principal O-glycans acquired by gB and that are also essential for the binding of PILRalpha to gB. gb 53-55 paired immunoglobin like type 2 receptor alpha Homo sapiens 181-190 19812165-5 2009 Furthermore, we identified two threonine residues on gB that are essential for the addition of the principal O-glycans acquired by gB and that are also essential for the binding of PILRalpha to gB. gb 131-133 paired immunoglobin like type 2 receptor alpha Homo sapiens 181-190 19812165-5 2009 Furthermore, we identified two threonine residues on gB that are essential for the addition of the principal O-glycans acquired by gB and that are also essential for the binding of PILRalpha to gB. gb 131-133 paired immunoglobin like type 2 receptor alpha Homo sapiens 181-190 18799581-5 2008 Peptides gB(161-175) and gB(166-180) within G4 and gB(661-675) within G14 recalled the strongest HLA-DR-dependent CD4(+) T-cell proliferation and gamma interferon production. gb 9-11 CD4 molecule Homo sapiens 114-117 18799581-5 2008 Peptides gB(161-175) and gB(166-180) within G4 and gB(661-675) within G14 recalled the strongest HLA-DR-dependent CD4(+) T-cell proliferation and gamma interferon production. gb 25-27 CD4 molecule Homo sapiens 114-117 18799581-5 2008 Peptides gB(161-175) and gB(166-180) within G4 and gB(661-675) within G14 recalled the strongest HLA-DR-dependent CD4(+) T-cell proliferation and gamma interferon production. gb 25-27 CD4 molecule Homo sapiens 114-117 18799581-6 2008 gB(166-180), gB(661-675), and gB(666-680) elicited ex vivo CD4(+) cytotoxic T cells (CTLs) that lysed autologous HSV-1- and vaccinia virus (expressing gB)-infected lymphoblastoid cell lines. gb 0-2 CD4 molecule Homo sapiens 59-62 18799581-6 2008 gB(166-180), gB(661-675), and gB(666-680) elicited ex vivo CD4(+) cytotoxic T cells (CTLs) that lysed autologous HSV-1- and vaccinia virus (expressing gB)-infected lymphoblastoid cell lines. gb 13-15 CD4 molecule Homo sapiens 59-62 18799581-6 2008 gB(166-180), gB(661-675), and gB(666-680) elicited ex vivo CD4(+) cytotoxic T cells (CTLs) that lysed autologous HSV-1- and vaccinia virus (expressing gB)-infected lymphoblastoid cell lines. gb 13-15 CD4 molecule Homo sapiens 59-62 18799581-6 2008 gB(166-180), gB(661-675), and gB(666-680) elicited ex vivo CD4(+) cytotoxic T cells (CTLs) that lysed autologous HSV-1- and vaccinia virus (expressing gB)-infected lymphoblastoid cell lines. gb 13-15 CD4 molecule Homo sapiens 59-62 18799581-7 2008 Interestingly, gB(166-180) and gB(666-680) peptide epitopes were strongly recognized by CD4(+) T cells from 10 of 10 asymptomatic patients but not by CD4(+) T cells from 10 of 10 symptomatic patients (P < 0.0001; analysis of variance posttest). gb 15-17 CD4 molecule Homo sapiens 88-91 18799581-7 2008 Interestingly, gB(166-180) and gB(666-680) peptide epitopes were strongly recognized by CD4(+) T cells from 10 of 10 asymptomatic patients but not by CD4(+) T cells from 10 of 10 symptomatic patients (P < 0.0001; analysis of variance posttest). gb 31-33 CD4 molecule Homo sapiens 88-91 18799581-8 2008 Inversely, CD4(+) T cells from symptomatic patients preferentially recognized gB(661-675) (P < 0.0001). gb 78-80 CD4 molecule Homo sapiens 11-14 19045132-3 2008 In this paper, we analyze a boundary-integral equation interpretation for the Coulomb-field approximation (CFA), which plays a central role in most GB models. gb 148-150 tubulin folding cofactor A Homo sapiens 107-110 21817214-2 2009 The Sigma5(310)/[001] tilt GB of NiAl has been chosen because (i) the Sigma = 5 GB has been observed to be a higher fraction in NiAl experimentally, and (ii) the Sigma5(310)/[001] is energetically favorable in comparison with the Sigma5(210)/[001]. gb 27-29 adaptor related protein complex 5 subunit sigma 1 Homo sapiens 4-10 18945776-5 2009 (ii) In in vitro kinase assays, the threonine residue at position 887 (Thr-887) in the gB domain was specifically phosphorylated by Us3, while the serine residue at position 560 was not. gb 87-89 serine/threonine protein kinase US3 Human alphaherpesvirus 1 132-135 18945776-9 2009 The upregulation of gB expression on the cell surface also was observed in cells infected with a recombinant HSV-1 encoding catalytically inactive Us3. gb 20-22 serine/threonine protein kinase US3 Human alphaherpesvirus 1 147-150 18945776-10 2009 These results supported the hypothesis that Us3 phosphorylates gB and downregulates the cell surface expression of gB in HSV-1-infected cells. gb 63-65 serine/threonine protein kinase US3 Human alphaherpesvirus 1 44-47 18945776-10 2009 These results supported the hypothesis that Us3 phosphorylates gB and downregulates the cell surface expression of gB in HSV-1-infected cells. gb 115-117 serine/threonine protein kinase US3 Human alphaherpesvirus 1 44-47