PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 11084048-7 2001 Carbohydrate analysis shows that the endosialin core protein carries abundantly sialylated, O-linked oligosaccharides and is sensitive to O-sialoglycoprotein endopeptidase, placing it in the group of sialomucin-like molecules. Carbohydrates 0-12 CD248 molecule Homo sapiens 37-47 11084048-7 2001 Carbohydrate analysis shows that the endosialin core protein carries abundantly sialylated, O-linked oligosaccharides and is sensitive to O-sialoglycoprotein endopeptidase, placing it in the group of sialomucin-like molecules. o-linked oligosaccharides 92-117 CD248 molecule Homo sapiens 37-47 11114163-1 2001 In Gram-negative bacteria, TEM-1 beta-lactamase provides the major mechanism of plasmid-mediated beta-lactam resistance. beta-Lactams 33-44 CD248 molecule Homo sapiens 27-32 11114163-2 2001 Natural variants of TEM-1 with increased antibiotic resistance have appeared in response to the use of extended-spectrum beta-lactam antibiotics (e.g., ceftazidime) and beta-lactamase inhibitors (e.g., clavulanic acid). beta-Lactams 121-132 CD248 molecule Homo sapiens 20-25 11114163-2 2001 Natural variants of TEM-1 with increased antibiotic resistance have appeared in response to the use of extended-spectrum beta-lactam antibiotics (e.g., ceftazidime) and beta-lactamase inhibitors (e.g., clavulanic acid). Ceftazidime 152-163 CD248 molecule Homo sapiens 20-25 11114163-2 2001 Natural variants of TEM-1 with increased antibiotic resistance have appeared in response to the use of extended-spectrum beta-lactam antibiotics (e.g., ceftazidime) and beta-lactamase inhibitors (e.g., clavulanic acid). Clavulanic Acid 202-217 CD248 molecule Homo sapiens 20-25 11182316-10 2001 The acylglycineboronic acids have K(i) values as low as 20 nM against AmpC and as low as 390 nM against TEM-1. acylglycineboronic acids 4-28 CD248 molecule Homo sapiens 104-109 10949022-2 2000 Here, we show that Bfa1p and Bub2p bind the Ras-like GTPase Tem1p, a component of the mitotic exit network, to the cytoplasmic face of the SPB that enters the bud, whereas the GDP/GTP exchange factor Lte1p is associated with the cortex of the bud. Guanosine Diphosphate 176-179 CD248 molecule Homo sapiens 60-65 10837472-0 2000 Mechanism of inhibition of the class A beta -lactamases PC1 and TEM-1 by tazobactam. Tazobactam 73-83 CD248 molecule Homo sapiens 64-69 10837472-2 2000 The reactions of class A beta-lactamases PC1 and TEM-1 with tazobactam (TZB), a potent penicillanic sulfone inhibitor for class A beta-lactamases, were studied using electrospray ionization mass spectrometry (ESI/MS). Tazobactam 60-70 CD248 molecule Homo sapiens 49-54 10837472-2 2000 The reactions of class A beta-lactamases PC1 and TEM-1 with tazobactam (TZB), a potent penicillanic sulfone inhibitor for class A beta-lactamases, were studied using electrospray ionization mass spectrometry (ESI/MS). Tazobactam 72-75 CD248 molecule Homo sapiens 49-54 10837472-2 2000 The reactions of class A beta-lactamases PC1 and TEM-1 with tazobactam (TZB), a potent penicillanic sulfone inhibitor for class A beta-lactamases, were studied using electrospray ionization mass spectrometry (ESI/MS). penicillanic sulfone 87-107 CD248 molecule Homo sapiens 49-54 10929710-2 2000 We find that the GTP binding protein Tem1, a regulator of mitotic exit, is present on the spindle pole body that migrates into the bud during S phase and mitosis. Guanosine Triphosphate 17-20 CD248 molecule Homo sapiens 37-41 10949022-2 2000 Here, we show that Bfa1p and Bub2p bind the Ras-like GTPase Tem1p, a component of the mitotic exit network, to the cytoplasmic face of the SPB that enters the bud, whereas the GDP/GTP exchange factor Lte1p is associated with the cortex of the bud. Guanosine Triphosphate 53-56 CD248 molecule Homo sapiens 60-65 10623544-0 2000 Selection of beta-lactamases and penicillin binding mutants from a library of phage displayed TEM-1 beta-lactamase randomly mutated in the active site omega-loop. Penicillins 33-43 CD248 molecule Homo sapiens 94-99 10873536-0 2000 Overexpression and biosynthetic deuterium enrichment of TEM-1 beta-lactamase for structural characterization by magnetic resonance methods. Deuterium 32-41 CD248 molecule Homo sapiens 56-61 10873536-3 2000 With protein induction at 25 degrees C supported by LB medium supplemented with osmolytes (300 mM sucrose and 2.5 mM betaine), the extracellular, mature form of wild-type TEM-1 beta-lactamase was recovered at a level of 140 mg/L. lb medium 52-61 CD248 molecule Homo sapiens 171-176 10873536-3 2000 With protein induction at 25 degrees C supported by LB medium supplemented with osmolytes (300 mM sucrose and 2.5 mM betaine), the extracellular, mature form of wild-type TEM-1 beta-lactamase was recovered at a level of 140 mg/L. Sucrose 98-105 CD248 molecule Homo sapiens 171-176 10873536-3 2000 With protein induction at 25 degrees C supported by LB medium supplemented with osmolytes (300 mM sucrose and 2.5 mM betaine), the extracellular, mature form of wild-type TEM-1 beta-lactamase was recovered at a level of 140 mg/L. Betaine 117-124 CD248 molecule Homo sapiens 171-176 10440070-1 1999 Bacteria possessing TEM-1-like beta-lactamases are generally regarded as susceptible to ampicillin-sulbactam (SAM), while those harboring OXA-1 enzymes are considered resistant. sultamicillin 88-108 CD248 molecule Homo sapiens 20-25 10506286-6 1999 By determining the beta-lactam resistance levels of the 38 possible mutants at positions 66 and 76 in the TEM-1 enzyme, it was confirmed that position 76 is indeed more tolerant of non-conservative substitutions. beta-Lactams 19-30 CD248 molecule Homo sapiens 106-111 10440070-5 1999 At a fixed sulbactam concentration of 4 microg/ml, the activity of ampicillin-sulbactam appeared to be reduced, with large numbers of TEM-1 producers becoming frankly resistant. Sulbactam 11-20 CD248 molecule Homo sapiens 134-139 10231522-9 1999 A structural analysis of the highly different affinity of SHV-1 and TEM-1 for the beta-lactamase inhibitory protein BLIP focuses on interactions involving Asp/Glu104. Aspartic Acid 155-158 CD248 molecule Homo sapiens 68-73 10230626-3 1999 Of these substituents, only the 6beta-hydroxymethyl group of 15 improved the activity of sulbactam against both TEM-1 and AmpC beta-lactamases. Sulbactam 89-98 CD248 molecule Homo sapiens 112-117 10230627-3 1999 All four 6beta-(hydroxymethyl)penam sulfone derivatives demonstrated good IC50 against both TEM-1 and AmpC beta-lactamases. 6beta-(hydroxymethyl)penam sulfone 9-43 CD248 molecule Homo sapiens 92-97 10230627-4 1999 Of these, 6beta-hydroxymethyl penam sulfone derivative 25 was the most active inhibitor which was able to restore the activity of piperacillin in vitro and in vivo against both TEM-1 and AmpC beta-lactamases producing organisms. 6beta-hydroxymethyl penam sulfone 10-43 CD248 molecule Homo sapiens 177-182 10230627-4 1999 Of these, 6beta-hydroxymethyl penam sulfone derivative 25 was the most active inhibitor which was able to restore the activity of piperacillin in vitro and in vivo against both TEM-1 and AmpC beta-lactamases producing organisms. Piperacillin 130-142 CD248 molecule Homo sapiens 177-182 9878443-4 1999 Here we report the results of an experiment in which we have hypermutated the bacterial enzyme TEM-1 beta-lactamase and selected small pools (<1.5x10(5)) of clones for enzymatic activity against the beta-lactam antibiotic cefotaxime. beta-Lactams 101-112 CD248 molecule Homo sapiens 95-100 9878443-4 1999 Here we report the results of an experiment in which we have hypermutated the bacterial enzyme TEM-1 beta-lactamase and selected small pools (<1.5x10(5)) of clones for enzymatic activity against the beta-lactam antibiotic cefotaxime. Cefotaxime 225-235 CD248 molecule Homo sapiens 95-100 9878443-5 1999 The experiment resulted in the isolation of a number of TEM-1 mutants with greatly improved activity against cefotaxime. Cefotaxime 109-119 CD248 molecule Homo sapiens 56-61 9878443-6 1999 Among these, clone 3D.5 (E104K:M182T:G238S) exhibited a minimum inhibitory concentration for cefotaxime 20,000-fold higher than wild-type TEM-1 and a catalytic efficiency (kcat/Km) 2383 times higher than the wild-type enzyme. Cefotaxime 93-103 CD248 molecule Homo sapiens 138-143 9756899-8 1998 To assess the validity of each model, TEM-1 mutants with amino acids substitutions of Ala, Ser, Cys, Thr, Asn, and Val have been constructed. Alanine 86-89 CD248 molecule Homo sapiens 38-43 9114204-5 1997 Point mutations of specific amino acids of well-recognized PMBLs (e.g., TEM-1 and SHV-1) have also produced enzymes capable of attacking a wider spectrum of beta-lactam agents. beta-Lactams 157-168 CD248 molecule Homo sapiens 72-77 9756758-4 1998 It was found that the mechanism modulating ceftazidime hydrolysis in PSE-4 was different from that in TEM-1. Ceftazidime 43-54 CD248 molecule Homo sapiens 102-107 9533481-0 1998 Comparative in-vitro activities of GD-40 and other beta-lactamase inhibitors against TEM-1 and SHV-2 beta-lactamases. 6-chloro-2-chloromethyl-2-methylpenam-3-carboxylic acid 1,1-dioxide 35-40 CD248 molecule Homo sapiens 85-90 8089110-0 1994 Characterization of TEM-1 beta-lactamase mutants from positions 238 to 241 with increased catalytic efficiency for ceftazidime. Ceftazidime 115-126 CD248 molecule Homo sapiens 20-25 18611801-2 1997 Tazobactam and clavulanate were potent inhibitors of TEM-1, SHV-1, SHV-2 and SHV-5 while sulbactam was less effective. Tazobactam 0-10 CD248 molecule Homo sapiens 53-58 18611801-2 1997 Tazobactam and clavulanate were potent inhibitors of TEM-1, SHV-1, SHV-2 and SHV-5 while sulbactam was less effective. Clavulanic Acid 15-26 CD248 molecule Homo sapiens 53-58 8964456-2 1996 They belong to molecular class A, and differ by one amino acid at position 39:TEM-1 have a glutamine and TEM-2 a lysine. Glutamine 91-100 CD248 molecule Homo sapiens 78-83 8964456-4 1996 For all antibiotics except methicillin and cefazolin, the catalytic efficiency values of TEM-2 are clearly greater than that of TEM-1. Methicillin 27-38 CD248 molecule Homo sapiens 128-133 8964456-4 1996 For all antibiotics except methicillin and cefazolin, the catalytic efficiency values of TEM-2 are clearly greater than that of TEM-1. Cefazolin 43-52 CD248 molecule Homo sapiens 128-133 8964456-5 1996 Molecular modelling of TEM-2, when compared to that of TEM-1, showed an additional ionic bond between Lys-39 and Glu-281. Lysine 102-105 CD248 molecule Homo sapiens 55-60 8964456-5 1996 Molecular modelling of TEM-2, when compared to that of TEM-1, showed an additional ionic bond between Lys-39 and Glu-281. Glutamic Acid 113-116 CD248 molecule Homo sapiens 55-60 8605624-3 1996 Other than the fact that BLIP is an effective inhibitor of a number of beta-lactamase enzymes (KI for TEM-1 approximately 100 pM) no other biochemical or structural data were available to assist the practitioners in their molecular docking. blip 25-29 CD248 molecule Homo sapiens 102-107 8605632-5 1996 The carboxylate of Asp 49 forms hydrogen bonds to four conserved, catalytic residues in the beta-lactamase, thereby mimicking the position of the penicillin G carboxylate observed in the acyl-enzyme complex of TEM-1 with substrate. carboxylate 4-15 CD248 molecule Homo sapiens 210-215 8605632-5 1996 The carboxylate of Asp 49 forms hydrogen bonds to four conserved, catalytic residues in the beta-lactamase, thereby mimicking the position of the penicillin G carboxylate observed in the acyl-enzyme complex of TEM-1 with substrate. Aspartic Acid 19-22 CD248 molecule Homo sapiens 210-215 8605632-5 1996 The carboxylate of Asp 49 forms hydrogen bonds to four conserved, catalytic residues in the beta-lactamase, thereby mimicking the position of the penicillin G carboxylate observed in the acyl-enzyme complex of TEM-1 with substrate. Hydrogen 32-40 CD248 molecule Homo sapiens 210-215 8605632-5 1996 The carboxylate of Asp 49 forms hydrogen bonds to four conserved, catalytic residues in the beta-lactamase, thereby mimicking the position of the penicillin G carboxylate observed in the acyl-enzyme complex of TEM-1 with substrate. penicillin g carboxylate 146-170 CD248 molecule Homo sapiens 210-215 9093433-5 1997 Resistance to amoxycillin was due to production of TEM-1 (89%) and TEM-2 (11%). Amoxicillin 14-25 CD248 molecule Homo sapiens 51-56 8891161-2 1996 A novel hydrogen bond between the hydroxyl of Thr-182 and the carbonyl of Glu-64 was expected to be responsible for the increase in the catalytic activity of the IST-T182 and IRT-3 enzymes compared with those of TEM-1 and IRT-169, respectively. Hydrogen 8-16 CD248 molecule Homo sapiens 212-217 8891161-2 1996 A novel hydrogen bond between the hydroxyl of Thr-182 and the carbonyl of Glu-64 was expected to be responsible for the increase in the catalytic activity of the IST-T182 and IRT-3 enzymes compared with those of TEM-1 and IRT-169, respectively. Threonine 46-49 CD248 molecule Homo sapiens 212-217 8891161-2 1996 A novel hydrogen bond between the hydroxyl of Thr-182 and the carbonyl of Glu-64 was expected to be responsible for the increase in the catalytic activity of the IST-T182 and IRT-3 enzymes compared with those of TEM-1 and IRT-169, respectively. Glutamic Acid 74-77 CD248 molecule Homo sapiens 212-217 8756327-1 1996 The structure of the plasmid-mediated beta-lactamase TEM-1 has been solved in complex with a designed boronic acid inhibitor (1R)-1-acetamido-2-(3-carboxyphenyl)ethane boronic acid at 1.7 A resolution. Boronic Acids 102-114 CD248 molecule Homo sapiens 53-58 8756327-1 1996 The structure of the plasmid-mediated beta-lactamase TEM-1 has been solved in complex with a designed boronic acid inhibitor (1R)-1-acetamido-2-(3-carboxyphenyl)ethane boronic acid at 1.7 A resolution. 1r)-1-acetamido-2-(3-carboxyphenyl)ethane boronic acid 126-180 CD248 molecule Homo sapiens 53-58 8756327-2 1996 The boronate inhibitor was designed based on the crystallographic coordinates of the acyl-enzyme intermediate of TEM-1 bound to the substrate penicillin G. glutamyl-gamma-boronate 4-12 CD248 molecule Homo sapiens 113-118 8756327-2 1996 The boronate inhibitor was designed based on the crystallographic coordinates of the acyl-enzyme intermediate of TEM-1 bound to the substrate penicillin G. Penicillin G 142-154 CD248 molecule Homo sapiens 113-118 8756327-3 1996 The boronate-TEM-1 complex is highly ordered and defines a novel transition state analogue of the deacylation step in the beta-lactamase reaction pathway. glutamyl-gamma-boronate 4-12 CD248 molecule Homo sapiens 13-18 8700829-0 1996 The catalytic mechanism of beta-lactamases: NMR titration of an active-site lysine residue of the TEM-1 enzyme. Lysine 76-82 CD248 molecule Homo sapiens 98-103 7589264-3 1995 Iso-electric focusing of the beta-lactamases, extracted from the transconjugants, demonstrated that ampicillin resistance resulted from the presence of the TEM-1, TEM-2 and SHV-1 beta-lactamases in 94.3%, 2.5% and 3.2% of isolates respectively. Ampicillin 100-110 CD248 molecule Homo sapiens 156-161 7547898-0 1995 Mass spectral kinetic study of acylation and deacylation during the hydrolysis of penicillins and cefotaxime by beta-lactamase TEM-1 and the G238S mutant. Penicillins 82-93 CD248 molecule Homo sapiens 127-132 7547898-0 1995 Mass spectral kinetic study of acylation and deacylation during the hydrolysis of penicillins and cefotaxime by beta-lactamase TEM-1 and the G238S mutant. Cefotaxime 98-108 CD248 molecule Homo sapiens 127-132 7547898-1 1995 The G238S substitution found in extended-spectrum natural mutants of TEM-1 beta-lactamase induces a new capacity to hydrolyze cefotaxime and a large loss of activity against the good substrates of TEM-1. Cefotaxime 126-136 CD248 molecule Homo sapiens 69-74 7547898-1 1995 The G238S substitution found in extended-spectrum natural mutants of TEM-1 beta-lactamase induces a new capacity to hydrolyze cefotaxime and a large loss of activity against the good substrates of TEM-1. Cefotaxime 126-136 CD248 molecule Homo sapiens 197-202 7547898-3 1995 The hydrolysis of penicillins and cefotaxime by TEM-1 and the G238S mutant shows that the behavior of penicillins and cefotaxime is very different. Penicillins 18-29 CD248 molecule Homo sapiens 48-53 7547898-3 1995 The hydrolysis of penicillins and cefotaxime by TEM-1 and the G238S mutant shows that the behavior of penicillins and cefotaxime is very different. Cefotaxime 34-44 CD248 molecule Homo sapiens 48-53 7547898-3 1995 The hydrolysis of penicillins and cefotaxime by TEM-1 and the G238S mutant shows that the behavior of penicillins and cefotaxime is very different. Penicillins 102-113 CD248 molecule Homo sapiens 48-53 7547898-3 1995 The hydrolysis of penicillins and cefotaxime by TEM-1 and the G238S mutant shows that the behavior of penicillins and cefotaxime is very different. Cefotaxime 118-128 CD248 molecule Homo sapiens 48-53 7486932-4 1995 All of the beta-lactamase inhibitors tested had poorer inhibitory activities at pH 5.8 than at pH 7.5 except clavulanic acid for TEM-1. Clavulanic Acid 109-124 CD248 molecule Homo sapiens 129-134 7785992-5 1995 These three strains produced two beta-lactamases with pIs of 5.4 (TEM-1) and 7.6. beta-Lactamase assays revealed that the pI 7.6 enzyme hydrolyzed cefotaxime faster (at a relative hydrolysis rate of 30% compared with that of benzylpenicillin) than either ceftazidime or aztreonam (relative hydrolysis rates of 13 and 3.3%, respectively). Cefotaxime 147-157 CD248 molecule Homo sapiens 66-71 8031044-8 1994 In particular, clavulanic acid was 60 and 580 times more potent than sulbactam against TEM-1 and SHV-1, respectively, currently the two most clinically prevalent gram-negative plasmid-mediated beta-lactamases. Clavulanic Acid 15-30 CD248 molecule Homo sapiens 87-92 8067776-5 1994 The cephacetrile-related compounds Ro 25-4095 and Ro 25-4835 were hydrolyzed by all three beta-lactamases with catalytic efficiencies (relative to penicillin G) ranging from approximately 5 (TEM-1, AmpC) to approximately 25 (TEM-3). Cephacetrile 4-16 CD248 molecule Homo sapiens 191-196 8031044-8 1994 In particular, clavulanic acid was 60 and 580 times more potent than sulbactam against TEM-1 and SHV-1, respectively, currently the two most clinically prevalent gram-negative plasmid-mediated beta-lactamases. Sulbactam 69-78 CD248 molecule Homo sapiens 87-92 1292600-5 1992 RESULTS: By analytical isoelectrofocusing we found that 26 out of the 27 ampicillin-resistant strains produced beta-lactamases with pl 5.4 and/or 5.6 corresponding to TEM-1 and/or TEM-2 type. Ampicillin 73-83 CD248 molecule Homo sapiens 167-172 8089110-2 1994 To identify other amino acid substitutions that alter the activity of TEM-1 toward extended-spectrum cephalosporins, a random library was constructed that contained all possible amino acid substitutions over the 3-residue window of 238-241 (ABL numbering). Cephalosporins 101-115 CD248 molecule Homo sapiens 70-75 8089110-2 1994 To identify other amino acid substitutions that alter the activity of TEM-1 toward extended-spectrum cephalosporins, a random library was constructed that contained all possible amino acid substitutions over the 3-residue window of 238-241 (ABL numbering). lauric acid 241-244 CD248 molecule Homo sapiens 70-75 8324021-0 1993 [Oligonucleotide probes for the characterization of TEM-1 and TEM-2 beta lactamases in Salmonella strains]. Oligonucleotides 1-16 CD248 molecule Homo sapiens 52-57 8324021-1 1993 BACKGROUND: The aim of this study was to develop molecular biology techniques as hybridization with oligonucleotide probes to characterize TEM-1 and TEM-2 beta-lactamases in strains of Salmonella spp. Oligonucleotides 100-115 CD248 molecule Homo sapiens 139-144 8324021-14 1993 CONCLUSIONS: PCR technique plus oligonucleotide probes are a good alternative for the specific characterization of TEM-1 and TEM-2 beta-lactamases in Salmonella spp. Oligonucleotides 32-47 CD248 molecule Homo sapiens 115-120 2095262-1 1990 We have tested two non-isotopic labels: digoxigenin--11-dUTP and biotin-7-dATP for the detection of TEM-1 beta-lactamase gene with a TEM-1 probe by DNA:DNA hybridisation (using spot technique). digoxigenin-11-deoxyuridine triphosphate 40-60 CD248 molecule Homo sapiens 100-105 1644749-3 1992 To identify other amino acid substitutions that alter the activity of TEM-1 towards extended-spectrum cephalosporins, we probed regions around the active-site pocket by random-replacement mutagenesis. Cephalosporins 102-116 CD248 molecule Homo sapiens 70-75 1644749-6 1992 Substitutions at positions 104, 168, and 238 in the TEM-1 beta-lactamase that resulted in increased enzyme activity towards extended-spectrum cephalosporins were found. Cephalosporins 142-156 CD248 molecule Homo sapiens 52-57 1606226-3 1992 The amplification product was a 516 bp fragment internal to bla-TEM-1 from pBR 322. pentabromophenol 75-78 CD248 molecule Homo sapiens 64-69 1516458-2 1992 The most common enzymes responsible for resistance to aminopenicillins and older (1st generation) cephalosporins are the TEM-1, TEM-2, OXA-1 and SHV-1 enzymes, all of which are plasmid-mediated. aminopenicillins 54-70 CD248 molecule Homo sapiens 121-126 1516458-2 1992 The most common enzymes responsible for resistance to aminopenicillins and older (1st generation) cephalosporins are the TEM-1, TEM-2, OXA-1 and SHV-1 enzymes, all of which are plasmid-mediated. Cephalosporins 98-112 CD248 molecule Homo sapiens 121-126 2095262-1 1990 We have tested two non-isotopic labels: digoxigenin--11-dUTP and biotin-7-dATP for the detection of TEM-1 beta-lactamase gene with a TEM-1 probe by DNA:DNA hybridisation (using spot technique). digoxigenin-11-deoxyuridine triphosphate 40-60 CD248 molecule Homo sapiens 133-138 2095262-1 1990 We have tested two non-isotopic labels: digoxigenin--11-dUTP and biotin-7-dATP for the detection of TEM-1 beta-lactamase gene with a TEM-1 probe by DNA:DNA hybridisation (using spot technique). biotin-7-datp 65-78 CD248 molecule Homo sapiens 100-105 34568667-0 2021 Inhibition of Class A beta-Lactamase (TEM-1) by Narrow Fractions of Humic Substances. Humic Substances 68-84 CD248 molecule Homo sapiens 38-43 2380766-1 1990 The in vitro sensitivity of amoxicillin alone and combined with clavulanic acid (ratio 4:1) as been studied by a spectrophotometric method utilizing crude extract of the following enzymes: TEM1, TEM2, SHV1, SHV2, TLE1, HMS1, LXA, P99, ENT208. Amoxicillin 28-39 CD248 molecule Homo sapiens 189-193 2380766-1 1990 The in vitro sensitivity of amoxicillin alone and combined with clavulanic acid (ratio 4:1) as been studied by a spectrophotometric method utilizing crude extract of the following enzymes: TEM1, TEM2, SHV1, SHV2, TLE1, HMS1, LXA, P99, ENT208. Clavulanic Acid 64-79 CD248 molecule Homo sapiens 189-193 34929294-5 2022 Dissemination of strains producing TEM-1 variants generated from these two evolution routes underlies the markedly increased prevalence of bacterial resistance to beta-lactams in the past few decades. beta-Lactams 163-175 CD248 molecule Homo sapiens 35-40 34885044-0 2021 Copper-64-Labeled 1C1m-Fc, a New Tool for TEM-1 PET Imaging and Prediction of Lutetium-177-Labeled 1C1m-Fc Therapy Efficacy and Safety. Copper 0-6 CD248 molecule Homo sapiens 42-47 34568667-4 2021 To test these hypotheses, we used humic substances (HS) from different sources (coal, peat, and soil) and of different fractional compositions (humic acids, hymatomelanic acids, and narrow fractions from solid-phase extraction) for inhibiting serine beta-lactamase TEM-1. Humic Substances 34-50 CD248 molecule Homo sapiens 265-270 34568667-4 2021 To test these hypotheses, we used humic substances (HS) from different sources (coal, peat, and soil) and of different fractional compositions (humic acids, hymatomelanic acids, and narrow fractions from solid-phase extraction) for inhibiting serine beta-lactamase TEM-1. Serine 243-249 CD248 molecule Homo sapiens 265-270 34302811-4 2021 Hydrogen deuterium exchange mass spectrometry revealed that the flexibility of the interdomain region was significantly suppressed upon strong binding to TEM1, but was not significantly changed upon weak binding to SHV1 or PC1. Hydrogen 0-8 CD248 molecule Homo sapiens 154-158 34270157-4 2021 Using a b -lactamase binding protein (BLIP2) as the capture protein attached to carbon nanotube field effect transistors in different defined orientations, device conductance was influenced on binding TEM-1, an important b -lactamase involved in antimicrobial resistance (AMR). Carbon 80-86 CD248 molecule Homo sapiens 201-206 34302811-4 2021 Hydrogen deuterium exchange mass spectrometry revealed that the flexibility of the interdomain region was significantly suppressed upon strong binding to TEM1, but was not significantly changed upon weak binding to SHV1 or PC1. Deuterium 9-18 CD248 molecule Homo sapiens 154-158 35491852-3 2022 In the present study, tebipenem was tested for stability to hydrolysis by a set of clinically relevant beta-lactamases, including TEM-1, AmpC, CTX-M, OXA-48, KPC, and NDM-1 enzymes. tebipenem 22-31 CD248 molecule Homo sapiens 130-135 35491852-5 2022 It was found that, similar to other carbapenems, tebipenem was resistant to hydrolysis by TEM-1, CTX-M, and AmpC beta-lactamases but was susceptible to hydrolysis by KPC, OXA-48, and NDM-1 enzymes with catalytic efficiency values (kcat/Km) ranging from 0.1 to 2 x 106 M-1s-1. tebipenem 49-58 CD248 molecule Homo sapiens 90-95 2550326-2 1989 The TEM-4 enzyme, which confers high-level resistance to cefotaxime (Ctx) and ceftazidime (Caz), differed from the TEM-1 penicillinase by four amino acid substitutions. Cefotaxime 57-67 CD248 molecule Homo sapiens 115-120 35134504-8 2022 RESULTS: Using TAZ concentrations <=64 mg/L, one isolate hyperproducing TEM-1 had a PIP MIC of 8 at TAZ 16 mg/L and two additional isolates at TAZ 64 mg/L. Tazobactam 15-18 CD248 molecule Homo sapiens 72-77 35134504-8 2022 RESULTS: Using TAZ concentrations <=64 mg/L, one isolate hyperproducing TEM-1 had a PIP MIC of 8 at TAZ 16 mg/L and two additional isolates at TAZ 64 mg/L. Piperacillin 84-87 CD248 molecule Homo sapiens 72-77 35134504-8 2022 RESULTS: Using TAZ concentrations <=64 mg/L, one isolate hyperproducing TEM-1 had a PIP MIC of 8 at TAZ 16 mg/L and two additional isolates at TAZ 64 mg/L. Tazobactam 100-103 CD248 molecule Homo sapiens 72-77 35134504-8 2022 RESULTS: Using TAZ concentrations <=64 mg/L, one isolate hyperproducing TEM-1 had a PIP MIC of 8 at TAZ 16 mg/L and two additional isolates at TAZ 64 mg/L. Tazobactam 143-146 CD248 molecule Homo sapiens 72-77 2550326-5 1989 Analysis of the location of the mutations in the primary and tertiary structures of class A beta-lactamases suggests that interactions between the substituted residues and beta-lactam antibiotics non-hydrolysable by TEM-1 and TEM-2 allow TEM-4 and TEM-5 to hydrolyse efficiently novel broad-spectrum cephalosporins such as Ctx and Caz. Cephalosporins 300-314 CD248 molecule Homo sapiens 216-221 2550326-2 1989 The TEM-4 enzyme, which confers high-level resistance to cefotaxime (Ctx) and ceftazidime (Caz), differed from the TEM-1 penicillinase by four amino acid substitutions. Ceftazidime 78-89 CD248 molecule Homo sapiens 115-120 2550326-2 1989 The TEM-4 enzyme, which confers high-level resistance to cefotaxime (Ctx) and ceftazidime (Caz), differed from the TEM-1 penicillinase by four amino acid substitutions. Ceftazidime 91-94 CD248 molecule Homo sapiens 115-120 2550326-5 1989 Analysis of the location of the mutations in the primary and tertiary structures of class A beta-lactamases suggests that interactions between the substituted residues and beta-lactam antibiotics non-hydrolysable by TEM-1 and TEM-2 allow TEM-4 and TEM-5 to hydrolyse efficiently novel broad-spectrum cephalosporins such as Ctx and Caz. beta-Lactams 92-103 CD248 molecule Homo sapiens 216-221 3259123-0 1988 Oligonucleotide probes (TEM-1, OXA-1) versus isoelectric focusing in beta-lactamase characterization of 114 resistant strains. Oligonucleotides 0-15 CD248 molecule Homo sapiens 24-29 2660637-4 1989 New characters of resistance to beta-lactam antibiotics in enterobacteria result from the apparition of mutant of the TEM-1 and TEM-2 penicillinases. beta-Lactams 32-43 CD248 molecule Homo sapiens 118-123 2667097-4 1989 TEM-1 beta-lactamase occurred simultaneously in 82% of strains showing the AAC(3)-V type of aminoglycoside resistance mechanism. Aminoglycosides 92-106 CD248 molecule Homo sapiens 0-5 3145862-2 1988 From the results it seemed that gene dosage is a more efficient mechanism than inoculum size for increasing TEM-1 mediated resistance to beta-lactam antibiotics. beta-Lactams 137-148 CD248 molecule Homo sapiens 108-113 3141170-2 1988 OXA-2, TEM-1, TEM-2, PSE-1, CEP-1, CARB-3 and SHV-1 beta-lactamases showed similar activity against LY163892 and cefaclor, whereas OXA-1 hydrolyzed the latter more rapidly. loracarbef 100-108 CD248 molecule Homo sapiens 7-12 3141170-2 1988 OXA-2, TEM-1, TEM-2, PSE-1, CEP-1, CARB-3 and SHV-1 beta-lactamases showed similar activity against LY163892 and cefaclor, whereas OXA-1 hydrolyzed the latter more rapidly. Cefaclor 113-121 CD248 molecule Homo sapiens 7-12 3259123-1 1988 Oligonucleotide probes specific for detection of the TEM-1 and OXA-1 beta-lactamase genes were compared with isoelectric focusing in 114 gram-negative beta-lactamase-producing strains representing at least 16 species. Oligonucleotides 0-15 CD248 molecule Homo sapiens 53-58 2834979-4 1988 Using TEM-1 as the model beta-lactamase, a Km of 46 microM was observed with benzylpenicillin serving as the substrate. Penicillin G 77-93 CD248 molecule Homo sapiens 6-11 3116487-2 1987 Titration curves of TEM-1 (pI 5.4) and TEM-2 (pI 5.6) together were consistent with the known substitution of a glutamic acid in the former by a lysin in the latter. Glutamic Acid 112-125 CD248 molecule Homo sapiens 20-25 3311735-1 1987 A 998 bp fragment of plasmid pBR322, comprising part of the TEM-1 beta-lactamase gene, was labelled with biotin-11-dUTP for use as a DNA probe in a rapid non-isotopic spot hybridisation test. biotin-11-dUTP 105-119 CD248 molecule Homo sapiens 60-65 3032386-0 1987 Oligonucleotide probes for the detection of TEM-1 and TEM-2 beta-lactamase genes and their transposons. Oligonucleotides 0-15 CD248 molecule Homo sapiens 44-49 3032386-6 1987 The use of these oligonucleotides enables us to discriminate between TEM-1 and TEM-2 genes. Oligonucleotides 17-33 CD248 molecule Homo sapiens 69-74 3040368-3 1987 Clavulanic acid and sulbactam had high affinities for the purified plasmid-mediated beta-lactamases such as SHV-1, TEM-1 and PSE-4, and were potent inhibitors as shown by their low Ki values. Clavulanic Acid 0-15 CD248 molecule Homo sapiens 115-120 3040368-3 1987 Clavulanic acid and sulbactam had high affinities for the purified plasmid-mediated beta-lactamases such as SHV-1, TEM-1 and PSE-4, and were potent inhibitors as shown by their low Ki values. Sulbactam 20-29 CD248 molecule Homo sapiens 115-120 6097119-5 1984 In the case of the penicillinase (TEM-1), only cefoperazone was subject to some hydrolysis. Cefoperazone 47-59 CD248 molecule Homo sapiens 34-39 3939122-3 1985 Microacidimetry showed poor interactions of cefmenoxime with penicillinase TEM-1 (low Vm, poor affinity) whereas it showed a high affinity for the cephalosporinases, as is also the case for cefotaxime or lamoxactam. Cefmenoxime 44-55 CD248 molecule Homo sapiens 75-80 3875602-12 1985 The plasmid-determined beta-lactamases, TEM-1 and OHIO-1, contributed little to resistance to most of the newer beta-lactams but were strongly associated with aminoglycoside resistance in these selected isolates. beta-Lactams 112-124 CD248 molecule Homo sapiens 40-45 3875602-12 1985 The plasmid-determined beta-lactamases, TEM-1 and OHIO-1, contributed little to resistance to most of the newer beta-lactams but were strongly associated with aminoglycoside resistance in these selected isolates. Aminoglycosides 159-173 CD248 molecule Homo sapiens 40-45 30501088-9 2018 A more exhaustive dynamic analysis, using a selection pressure for ampicillin and cefotaxime resistance on all possible types of substitutions in the amino acid sequence of TEM-1, further demonstrated the observed mechanism. Ampicillin 67-77 CD248 molecule Homo sapiens 173-178 6243991-1 1980 A new beta-lactam sulfone, CP 45899, has been proved to be a time-dependent irreversible inhibitor of three R-factor-mediated beta-lactamases (penicillin amido-beta-lactamhydrolase, EC 3.5.2.6): TEM-1 (pI = 5.4), TEM-2 (pI = 5.6) and Pitton"s type 2 (pI = 7.7). beta-lactam sulfone 6-25 CD248 molecule Homo sapiens 195-200 363163-1 1978 The mechanisms of action of 3 R-factors on beta-lactamases (penicillin amido-beta-lactamhydrolase, EC 3.5.2.6) (TEM-1 pI = 5.4, TEM-2 pI = 5.6 and Pitton"s type 2 pI = 7.7) have been kinetically analyzed for clavulanic acid inactivation. Penicillins 60-70 CD248 molecule Homo sapiens 112-117 32814938-2 2020 A protein complementation assay (PCA), split TEM-1 beta-lactamase, interacts with xenon at the interface of the TEM-1 fragments. Xenon 82-87 CD248 molecule Homo sapiens 45-50 32814938-3 2020 Reconstitution of TEM-1-promoted here by cFos/cJun leucine zipper interaction-gives rise to sensitive 129Xe NMR signal in bacterial cells. Leucine 51-58 CD248 molecule Homo sapiens 18-23 31993928-0 2020 Preclinical Evaluation and Dosimetry of [111In]CHX-DTPA-scFv78-Fc Targeting Endosialin/Tumor Endothelial Marker 1 (TEM1). cyclohexyldiethylenetriamine pentaacetic acid 47-55 CD248 molecule Homo sapiens 76-86 31993928-0 2020 Preclinical Evaluation and Dosimetry of [111In]CHX-DTPA-scFv78-Fc Targeting Endosialin/Tumor Endothelial Marker 1 (TEM1). cyclohexyldiethylenetriamine pentaacetic acid 47-55 CD248 molecule Homo sapiens 87-113 31993928-0 2020 Preclinical Evaluation and Dosimetry of [111In]CHX-DTPA-scFv78-Fc Targeting Endosialin/Tumor Endothelial Marker 1 (TEM1). cyclohexyldiethylenetriamine pentaacetic acid 47-55 CD248 molecule Homo sapiens 115-119 31993928-6 2020 The radiopharmaceutical biodistribution was assessed in immunodeficient mice grafted with Ewing"s sarcoma RD-ES and neuroblastoma SK-N-AS human TEM1-positive tumors. sk-n 130-134 CD248 molecule Homo sapiens 144-148 31993928-15 2020 CONCLUSIONS: [111In]CHX-DTPA-scFv78-Fc binds specifically to endosialin/TEM1 in vitro and in vivo. cyclohexyldiethylenetriamine pentaacetic acid 20-28 CD248 molecule Homo sapiens 61-71 31993928-15 2020 CONCLUSIONS: [111In]CHX-DTPA-scFv78-Fc binds specifically to endosialin/TEM1 in vitro and in vivo. cyclohexyldiethylenetriamine pentaacetic acid 20-28 CD248 molecule Homo sapiens 72-76 32951040-1 2020 STUDY QUESTION: Is endosialin a specific marker of human stem Leydig cells (SLCs) with the ability to differentiate into testosterone-producing Leydig cells (LCs) in vitro and in vivo? Testosterone 121-133 CD248 molecule Homo sapiens 19-29 32951040-2 2020 SUMMARY ANSWER: Endosialin is a specific marker of human SLCs which differentiate into testosterone-producing LCs in vitro and in vivo. Testosterone 87-99 CD248 molecule Homo sapiens 16-26 32951040-18 2020 Furthermore, transplanted human endosialin+ cells appear to colonize the murine host testes, localize to peritubular and perivascular regions, proliferate measurably and differentiate partially into testosterone-producing LCs in vivo. Testosterone 199-211 CD248 molecule Homo sapiens 32-42 32198704-0 2020 Correction to: Preclinical Evaluation and Dosimetry of [111In] CHX-DTPA-scFv78-Fc Targeting Endosialin/Tumor Endothelial Marker 1 (TEM1). cyclohexyldiethylenetriamine pentaacetic acid 63-71 CD248 molecule Homo sapiens 92-102 32198704-0 2020 Correction to: Preclinical Evaluation and Dosimetry of [111In] CHX-DTPA-scFv78-Fc Targeting Endosialin/Tumor Endothelial Marker 1 (TEM1). cyclohexyldiethylenetriamine pentaacetic acid 63-71 CD248 molecule Homo sapiens 103-129 32198704-0 2020 Correction to: Preclinical Evaluation and Dosimetry of [111In] CHX-DTPA-scFv78-Fc Targeting Endosialin/Tumor Endothelial Marker 1 (TEM1). cyclohexyldiethylenetriamine pentaacetic acid 63-71 CD248 molecule Homo sapiens 131-135 31355207-4 2019 In this work, a newly developed machine learning analysis approach to the recognition of protein dynamics states was applied to compare the binding modes of TEM-1 beta-lactamase with regard to penicillin in different catalytic states. Penicillins 193-203 CD248 molecule Homo sapiens 157-162 30501088-9 2018 A more exhaustive dynamic analysis, using a selection pressure for ampicillin and cefotaxime resistance on all possible types of substitutions in the amino acid sequence of TEM-1, further demonstrated the observed mechanism. Cefotaxime 82-92 CD248 molecule Homo sapiens 173-178 28947977-4 2017 It consists of a humanized endosialin monoclonal antibody, named hMP-E-8.3, conjugated to a potent duocarmycin derivative. duocarmycin 99-110 CD248 molecule Homo sapiens 27-37 29477271-5 2018 Further inhibition assays with RA related compounds revealed that salvianolic acid A, a derivative of RA, manifests potent inhibition to VIM-2, more interestingly, which shows inhibitory activity against the NDM-1, another clinically relevant MBL subtype, and the serine-beta-lactamase TEM-1 that is structurally and mechanistically distinct from the VIM-2 and NDM-1. salvianolic acid A 66-84 CD248 molecule Homo sapiens 286-291 29964048-3 2018 In this work, we use a unique approach based on millisecond hydrogen-deuterium exchange mass spectrometry to identify dynamic modes linked to individual catalytic processes in the antibiotic resistance enzyme TEM-1 beta-lactamase. Hydrogen 60-68 CD248 molecule Homo sapiens 209-214 29964048-3 2018 In this work, we use a unique approach based on millisecond hydrogen-deuterium exchange mass spectrometry to identify dynamic modes linked to individual catalytic processes in the antibiotic resistance enzyme TEM-1 beta-lactamase. Deuterium 69-78 CD248 molecule Homo sapiens 209-214 29812917-2 2018 Here, we perform combined quantum mechanics/molecular mechanics simulations of several covalent complexes of clavulanate with class A beta-lactamases KPC-2 and TEM-1. Clavulanic Acid 109-120 CD248 molecule Homo sapiens 160-165 29527530-4 2018 Oxyimino-cephalosporins, such as cefotaxime and ceftazidime, however, are poor substrates for TEM-1 and were introduced, in part, to circumvent beta-lactamase-mediated resistance. oxyimino-cephalosporins 0-23 CD248 molecule Homo sapiens 94-99 29527530-4 2018 Oxyimino-cephalosporins, such as cefotaxime and ceftazidime, however, are poor substrates for TEM-1 and were introduced, in part, to circumvent beta-lactamase-mediated resistance. Cefotaxime 33-43 CD248 molecule Homo sapiens 94-99 29527530-4 2018 Oxyimino-cephalosporins, such as cefotaxime and ceftazidime, however, are poor substrates for TEM-1 and were introduced, in part, to circumvent beta-lactamase-mediated resistance. Ceftazidime 48-59 CD248 molecule Homo sapiens 94-99 27403811-8 2016 Representative results using this protocol are provided by assessing the fitness effects of all single amino acid mutations in TEM-1 at a clinically relevant dosage of ampicillin. Ampicillin 168-178 CD248 molecule Homo sapiens 127-132 28281425-7 2017 RESULTS: Our results revealed high resistance rates to co-trimoxazole (54.0%), penicillin (47.1%) and tetracycline (44.8%) in our isolates, and indicated that the beta-lactamase TEM-1 is a prevalent source of beta-lactam resistance. beta-Lactams 163-174 CD248 molecule Homo sapiens 178-183 26774799-7 2016 Compared to standard tissue culture plastic, AMSCs grown in the porous titanium microenvironment showed differences in temporal expression for genes involved in cell cycle progression (CCNB2, HIST2H4), extracellular matrix production (COL1A1, COL3A1), mesenchymal lineage identity (ACTA2, CD248, CD44), osteoblastic transcription factors (DLX3, DLX5, ID3), and epigenetic regulators (EZH1, EZH2). Titanium 71-79 CD248 molecule Homo sapiens 289-294 26055690-7 2017 Among 44 cephalosporin-resistant isolates, TEM-1, CMY-2, CMY-14, CTX-M-3-like and CTX-M-15-like determinants were present in 31 (70.5%), 32 (72.7%), 1 (2.3%), 1 (2.3%), and 1 (2.3%) of isolates, respectively. Cephalosporins 9-22 CD248 molecule Homo sapiens 43-48 27173379-4 2016 We measured the effect on ampicillin resistance of ~12,500 unique single amino acid mutants of the TEM-1, TEM-17, TEM-19, and TEM-15 beta-lactamase alleles, which constitute an adaptive path in the evolution of cefotaxime resistance. Ampicillin 26-36 CD248 molecule Homo sapiens 99-104 27173379-4 2016 We measured the effect on ampicillin resistance of ~12,500 unique single amino acid mutants of the TEM-1, TEM-17, TEM-19, and TEM-15 beta-lactamase alleles, which constitute an adaptive path in the evolution of cefotaxime resistance. Cefotaxime 211-221 CD248 molecule Homo sapiens 99-104 27267601-16 2016 Among 12 cephalosporin-resistant Salmonella isolates, TEM-1 and CTX-M-14 determinants were present in two (16.7 %) isolates. Cephalosporins 9-22 CD248 molecule Homo sapiens 54-59 27267601-23 2016 TEM-1 and CTX-M-14 genetic determinants, and gyrA mutations, were the major mechanisms associated with high levels of cephalosporin and quinolone resistance, respectively, in Salmonella isolates. Cephalosporins 118-131 CD248 molecule Homo sapiens 0-5 27267601-23 2016 TEM-1 and CTX-M-14 genetic determinants, and gyrA mutations, were the major mechanisms associated with high levels of cephalosporin and quinolone resistance, respectively, in Salmonella isolates. Quinolones 136-145 CD248 molecule Homo sapiens 0-5 27073009-6 2016 In contrast, alanine substitutions of the catalytic serine in TEM-1, OXA-48, and OXA-163 did not alter stability, suggesting removal of the Cbeta atom is key to the stability increase associated with the glycine mutants. Serine 52-58 CD248 molecule Homo sapiens 62-67 26336878-6 2015 Significant correlations between CAF-TEM1-positivity or CAF-TEM1-intensity and RFS, OS, or COS were observed (P < 0.001, Kaplan-Meier curves); however, no significant correlation between vessel-TEM1-intensity and RFS, OS, or COS was observed. carbonyl sulfide 91-94 CD248 molecule Homo sapiens 37-41 26446903-4 2016 Compared with recent large-scale mutagenesis data of the beta-lactamase TEM-1, a protein providing resistance against beta-lactam antibiotics, our method leads to an increase of about 40% in explicative power as compared with approaches neglecting epistasis. beta-Lactams 57-68 CD248 molecule Homo sapiens 72-77 26386961-0 2016 15N, 13C and 1H backbone resonance assignments of an artificially engineered TEM-1/PSE-4 class A beta-lactamase chimera and its deconvoluted mutant. 15n 0-3 CD248 molecule Homo sapiens 77-82 26386961-0 2016 15N, 13C and 1H backbone resonance assignments of an artificially engineered TEM-1/PSE-4 class A beta-lactamase chimera and its deconvoluted mutant. Hydrogen 13-15 CD248 molecule Homo sapiens 77-82 26541303-1 2015 In order to enhance the therapeutic efficacy and intracellular concentration of bevacizumab (BVC), we have designed a novel tumor endothelial marker 1 (TEM1)/endosialin (Ab-/scFv)-conjugated mesoporous silica nanoparticles (MSN) to target ovarian cancer cell. Silicon Dioxide 202-208 CD248 molecule Homo sapiens 124-150 26541303-1 2015 In order to enhance the therapeutic efficacy and intracellular concentration of bevacizumab (BVC), we have designed a novel tumor endothelial marker 1 (TEM1)/endosialin (Ab-/scFv)-conjugated mesoporous silica nanoparticles (MSN) to target ovarian cancer cell. Silicon Dioxide 202-208 CD248 molecule Homo sapiens 152-156 26541303-1 2015 In order to enhance the therapeutic efficacy and intracellular concentration of bevacizumab (BVC), we have designed a novel tumor endothelial marker 1 (TEM1)/endosialin (Ab-/scFv)-conjugated mesoporous silica nanoparticles (MSN) to target ovarian cancer cell. Silicon Dioxide 202-208 CD248 molecule Homo sapiens 158-168 26336878-6 2015 Significant correlations between CAF-TEM1-positivity or CAF-TEM1-intensity and RFS, OS, or COS were observed (P < 0.001, Kaplan-Meier curves); however, no significant correlation between vessel-TEM1-intensity and RFS, OS, or COS was observed. carbonyl sulfide 91-94 CD248 molecule Homo sapiens 60-64 26336878-6 2015 Significant correlations between CAF-TEM1-positivity or CAF-TEM1-intensity and RFS, OS, or COS were observed (P < 0.001, Kaplan-Meier curves); however, no significant correlation between vessel-TEM1-intensity and RFS, OS, or COS was observed. carbonyl sulfide 91-94 CD248 molecule Homo sapiens 60-64 26300407-4 2015 In addition, it was shown that endosialin-overexpressing SP cells were able to regenerate the tumor population and had a high invasive potential. sp 57-59 CD248 molecule Homo sapiens 31-41 24790428-6 2014 The surface of NPs was further decorated with solubilizing agent polyethylene glycol (PEG) and tumor endothelial marker 1 (TEM1)/endosialin-targeting antibody (Ab) through carbodiimide/N-hydroxysuccinimide chemistry. Carbodiimides 172-184 CD248 molecule Homo sapiens 95-121 25216042-2 2015 TEM1-beta-lactamase and its inhibitor protein BLIP were conjugated to different oligonucleotides, resulting in enzyme inhibition in the presence of template strand. Oligonucleotides 80-96 CD248 molecule Homo sapiens 0-4 25713062-2 2015 TEM-1 is a prevalent plasmid-encoded beta-lactamase in Gram-negative bacteria that efficiently catalyzes the hydrolysis of penicillins and early cephalosporins but not oxyimino-cephalosporins. Penicillins 123-134 CD248 molecule Homo sapiens 0-5 25713062-2 2015 TEM-1 is a prevalent plasmid-encoded beta-lactamase in Gram-negative bacteria that efficiently catalyzes the hydrolysis of penicillins and early cephalosporins but not oxyimino-cephalosporins. Cephalosporins 145-159 CD248 molecule Homo sapiens 0-5 25713062-2 2015 TEM-1 is a prevalent plasmid-encoded beta-lactamase in Gram-negative bacteria that efficiently catalyzes the hydrolysis of penicillins and early cephalosporins but not oxyimino-cephalosporins. oxyimino-cephalosporins 168-191 CD248 molecule Homo sapiens 0-5 25713062-5 2015 Ceftazidime contains a large, bulky side chain that does not fit optimally in the wild-type TEM-1 active site. Ceftazidime 0-11 CD248 molecule Homo sapiens 92-97 25489790-3 2015 Many of the active site residues are conserved between the CTX-M family and non-ESBL beta-lactamases such as TEM-1, but the residues Ser237 and Arg276 are specific to the CTX-M family, suggesting that they may help to define the increased specificity for cefotaxime hydrolysis. Cefotaxime 255-265 CD248 molecule Homo sapiens 109-114 25489790-5 2015 Substitutions of Ser237 and Arg276 with their TEM-1 counterparts, Ala237 and Asn276, had a modest effect on cefotaxime hydrolysis, as did removal of the Arg276 side chain in an R276A mutant. Cefotaxime 108-118 CD248 molecule Homo sapiens 46-51 25312912-7 2015 The modern TEM-1 lactamase shows a comparatively rigid active-site region, likely reflecting adaptation for efficient degradation of a specific substrate (penicillin), whereas enhanced deformability at the active-site neighborhood in the ancestral resurrected proteins likely accounts for the binding and subsequent degradation of antibiotic molecules of different size and shape. Penicillins 155-165 CD248 molecule Homo sapiens 11-16 26085332-3 2015 Endosialin expression in paraffin-embedded archival tissue block (PEAT) melanoma tissues was assessed using immunohistochemistry (IHC) with the anti-endosialin, MAb 9G5, in the vessels of American Joint Commission on Cancer (AJCC) Stage III (n = 18) and Stage IV (n = 48) specimens. Paraffin 25-33 CD248 molecule Homo sapiens 0-10 26085332-8 2015 Endosialin expression was detected in 86 % (n = 117) of stage IV TMA specimens, while no expression was detected in 29 normal tissue controls. 4,4-dimethylcholesta-8,14-dien-3-ol 65-68 CD248 molecule Homo sapiens 0-10 25074398-2 2014 The Val216 residue in TEM-1 is replaced with a cysteine residue, and the environment-sensitive fluorophore fluorescein-5-maleimide is specifically attached to the Cys216 residue in the V216C mutant for sensing drug binding at the active site. fluorescein 5-maleimide 107-130 CD248 molecule Homo sapiens 22-27 24790428-6 2014 The surface of NPs was further decorated with solubilizing agent polyethylene glycol (PEG) and tumor endothelial marker 1 (TEM1)/endosialin-targeting antibody (Ab) through carbodiimide/N-hydroxysuccinimide chemistry. Carbodiimides 172-184 CD248 molecule Homo sapiens 123-127 24790428-6 2014 The surface of NPs was further decorated with solubilizing agent polyethylene glycol (PEG) and tumor endothelial marker 1 (TEM1)/endosialin-targeting antibody (Ab) through carbodiimide/N-hydroxysuccinimide chemistry. Carbodiimides 172-184 CD248 molecule Homo sapiens 129-139 24790428-6 2014 The surface of NPs was further decorated with solubilizing agent polyethylene glycol (PEG) and tumor endothelial marker 1 (TEM1)/endosialin-targeting antibody (Ab) through carbodiimide/N-hydroxysuccinimide chemistry. N-hydroxysuccinimide 185-205 CD248 molecule Homo sapiens 95-121 21867672-0 2011 Fluorogenic cephalosporin substrates for beta-lactamase TEM-1. Cephalosporins 12-25 CD248 molecule Homo sapiens 56-61 23314151-8 2013 Molecular dynamics simulations on the Trp229Ala mutants of TEM-1 and SHV-1 resulted in decreased stability in the apo form, possibly due to loss of the stacking interaction as a result of the mutation. trp229ala 38-47 CD248 molecule Homo sapiens 59-64 23284969-2 2012 In one such effort, chimeras of two class-A beta-lactamases - TEM-1 and PSE-4 - were created according to structure-guided protein recombination and selected for their capacity to promote bacterial proliferation in the presence of ampicillin (Voigt et al., Nat. Ampicillin 231-241 CD248 molecule Homo sapiens 62-67 23991837-4 2013 In this work, molecular docking, molecular dynamic simulations, and relative free energy calculations were applied in order to get a comprehensive and thorough analysis of TEM-1/ampicillin and TEM-1/amoxicillin complexes. Ampicillin 178-188 CD248 molecule Homo sapiens 172-177 23991837-4 2013 In this work, molecular docking, molecular dynamic simulations, and relative free energy calculations were applied in order to get a comprehensive and thorough analysis of TEM-1/ampicillin and TEM-1/amoxicillin complexes. Amoxicillin 199-210 CD248 molecule Homo sapiens 193-198 22720063-10 2012 Mutagenesis and molecular modeling of an intact TEM-1 domain near MBP within the RG13 framework indicated a close surface proximity of the two domains with maltose switching being critically dependent on MBP linker anchoring residues and linker length. Maltose 156-163 CD248 molecule Homo sapiens 48-53 22720063-12 2012 Maltose activation and zinc inhibition of RG13 are hypothesized to have opposite effects on productive relaxation of the TEM-1 beta3 linker region via steric and/or linker juxtapositioning mechanisms. Maltose 0-7 CD248 molecule Homo sapiens 121-126 21867672-1 2011 Cephalosporin was used to synthesize soluble and precipitating fluorogenic beta-lactam substrates that demonstrated differential catalytic hydrolysis by three different subtypes of beta-lactamase: TEM-1 (class A), p99 (class C), and a Bacillus cereus enzyme sold by Genzyme (class B). Cephalosporins 0-13 CD248 molecule Homo sapiens 197-202 21867672-1 2011 Cephalosporin was used to synthesize soluble and precipitating fluorogenic beta-lactam substrates that demonstrated differential catalytic hydrolysis by three different subtypes of beta-lactamase: TEM-1 (class A), p99 (class C), and a Bacillus cereus enzyme sold by Genzyme (class B). beta-Lactams 75-86 CD248 molecule Homo sapiens 197-202 21362178-7 2011 In the RT group, endosialin expression in the stroma was positively associated with expression of cyclooxygenase-2 (Cox-2) (p = 0.03), p73 (p = 0.01) and phosphates of regenerating liver (PRL) (p = 0.002). Phosphates 154-164 CD248 molecule Homo sapiens 17-27 21425229-0 2011 Engineering an allosteric binding site for aminoglycosides into TEM1-beta-Lactamase. Aminoglycosides 43-58 CD248 molecule Homo sapiens 64-68 20921316-0 2010 Mechanistic studies of the inactivation of TEM-1 and P99 by NXL104, a novel non-beta-lactam beta-lactamase inhibitor. avibactam 60-66 CD248 molecule Homo sapiens 43-48 20927785-3 2010 In the presence of the clinically significant TEM-1 beta-lactamase, the DTA-antibiotic complex on the solid beads is hydrolyzed, thus releasing the DTA dye into solution. deoxythymidylyl-3'-5'-deoxyadenylate 72-75 CD248 molecule Homo sapiens 46-51 20927785-3 2010 In the presence of the clinically significant TEM-1 beta-lactamase, the DTA-antibiotic complex on the solid beads is hydrolyzed, thus releasing the DTA dye into solution. deoxythymidylyl-3'-5'-deoxyadenylate 148-151 CD248 molecule Homo sapiens 46-51 20921316-3 2010 The principal inhibitory characteristics of NXL104 against TEM-1 and P99 beta-lactamases were determined, including partition ratios, dissociation constants (K), rate constants for deactivation (k(2)), and reactivation rates. avibactam 44-50 CD248 molecule Homo sapiens 59-64 20921316-4 2010 NXL104 is a potent inhibitor of TEM-1 and P99, characterized by high carbamylation efficiencies (k(2)/K of 3.7 x 10(5) M(-1) s(-1) for TEM-1 and 1 x 10(4) M(-1) s(-1) for P99) and slow decarbamylation. avibactam 0-6 CD248 molecule Homo sapiens 32-37 20921316-4 2010 NXL104 is a potent inhibitor of TEM-1 and P99, characterized by high carbamylation efficiencies (k(2)/K of 3.7 x 10(5) M(-1) s(-1) for TEM-1 and 1 x 10(4) M(-1) s(-1) for P99) and slow decarbamylation. avibactam 0-6 CD248 molecule Homo sapiens 135-146 20921316-8 2010 In-depth studies on TEM-1 and P99 demonstrated that NXL104 had a comparable or better affinity and inactivation rate than clavulanate and tazobactam and in all cases an improved stability of the covalent enzyme/inhibitor complex. avibactam 52-58 CD248 molecule Homo sapiens 20-25 19736945-1 2009 Extended-spectrum beta-lactamases (ESBLs) are derivatives of enzymes such as SHV-1 and TEM-1 that have undergone site-specific mutations that enable them to hydrolyze, and thus inactivate, oxyimino-cephalosporins, such as cefotaxime and ceftazidime. oxyimino-cephalosporins 189-212 CD248 molecule Homo sapiens 87-92 19919101-6 2009 The carboxylate attached to the beta-lactam ring of doripenem is stabilized by a salt bridge to K212 and a hydrogen bond with T213, in lieu of the interaction with an arginine side chain found in most other beta-lactamase-beta-lactam complexes (e.g., R244 in the class A member TEM-1). carboxylate 4-15 CD248 molecule Homo sapiens 278-283 19919101-6 2009 The carboxylate attached to the beta-lactam ring of doripenem is stabilized by a salt bridge to K212 and a hydrogen bond with T213, in lieu of the interaction with an arginine side chain found in most other beta-lactamase-beta-lactam complexes (e.g., R244 in the class A member TEM-1). beta-Lactams 32-43 CD248 molecule Homo sapiens 278-283 19919101-6 2009 The carboxylate attached to the beta-lactam ring of doripenem is stabilized by a salt bridge to K212 and a hydrogen bond with T213, in lieu of the interaction with an arginine side chain found in most other beta-lactamase-beta-lactam complexes (e.g., R244 in the class A member TEM-1). Doripenem 52-61 CD248 molecule Homo sapiens 278-283 19504148-8 2009 The ampicillin resistance mechanism of 71% of the isolates was due to the gene bla ( TEM1 ). Ampicillin 4-14 CD248 molecule Homo sapiens 85-89 19791786-3 2009 We have investigated the first step in acylation (the formation of the tetrahedral intermediate) for the reaction of benzylpenicillin in the TEM-1 enzyme using high level combined quantum mechanics/molecular mechanics (QM/MM) methods. Penicillin G 117-133 CD248 molecule Homo sapiens 141-146 19736945-1 2009 Extended-spectrum beta-lactamases (ESBLs) are derivatives of enzymes such as SHV-1 and TEM-1 that have undergone site-specific mutations that enable them to hydrolyze, and thus inactivate, oxyimino-cephalosporins, such as cefotaxime and ceftazidime. Cefotaxime 222-232 CD248 molecule Homo sapiens 87-92 19736945-1 2009 Extended-spectrum beta-lactamases (ESBLs) are derivatives of enzymes such as SHV-1 and TEM-1 that have undergone site-specific mutations that enable them to hydrolyze, and thus inactivate, oxyimino-cephalosporins, such as cefotaxime and ceftazidime. Ceftazidime 237-248 CD248 molecule Homo sapiens 87-92 18822298-1 2008 TEM-1 beta-lactamase confers bacterial resistance to penicillin antibiotics and has acquired mutations that permit the enzyme to hydrolyze extended-spectrum cephalosporins or to avoid inactivation by beta-lactamase inhibitors. Penicillins 53-63 CD248 molecule Homo sapiens 0-5 19538149-3 2009 Thus, penicillin G was undermined by swift accumulation of staphylococcal penicillinase, ampicillin by TEM-1 enzyme and modern oxymino cephalosporins by "extended-spectrum" beta-lactamases. Penicillin G 6-18 CD248 molecule Homo sapiens 103-108 18840610-1 2009 In a previous study, we examined thermodynamic parameters for 20 alanine mutants in beta-lactamase inhibitory protein (BLIP) for binding to TEM-1 beta-lactamase. Alanine 65-72 CD248 molecule Homo sapiens 140-145 18840610-4 2009 We previously determined that BLIP Tyr51 is a canonical and Trp150 an anti-canonical TEM-1-contact residue, where canonical refers to the alanine substitution resulting in a matched change in the hydrophobicity of binding free energy. Alanine 138-145 CD248 molecule Homo sapiens 85-90 18822298-1 2008 TEM-1 beta-lactamase confers bacterial resistance to penicillin antibiotics and has acquired mutations that permit the enzyme to hydrolyze extended-spectrum cephalosporins or to avoid inactivation by beta-lactamase inhibitors. Cephalosporins 157-171 CD248 molecule Homo sapiens 0-5 18822298-3 2008 In order to gain more information concerning the tradeoffs associated with active site substitutions, a genetic selection was used to find second site mutations that partially restore ampicillin resistance levels conferred by an R244A active site TEM-1 beta-lactamase mutant. Ampicillin 184-194 CD248 molecule Homo sapiens 247-252 18822298-4 2008 An L201P substitution distant from the active site that enhanced ampicillin resistance levels and increased protein expression levels of the R244A TEM-1 mutant was identified. Ampicillin 65-75 CD248 molecule Homo sapiens 147-152 18687656-4 2008 The frequency of genes conferring a new function (degradation of a cephalosporin antibiotic) was measured at various stages of the drift, and a model that accounts for the differences in the observed adaptation dynamics of the drifting TEM-1 populations was derived. Cephalosporins 67-80 CD248 molecule Homo sapiens 236-241 18625770-1 2008 We passaged cells expressing TEM-1 and TEM-12 from a single plasmid through either ampicillin or ceftazidime. Ampicillin 83-93 CD248 molecule Homo sapiens 29-34 18559360-3 2008 The bla gene encoding TEM-1 beta-lactamase was used as a model to demonstrate the effectiveness of TriNEx. Trichlorfon 99-105 CD248 molecule Homo sapiens 22-27 18559360-5 2008 Many of the resulting amino acid substitutions had significant effects on the in vivo activity of TEM-1, including up to a 64-fold increased activity toward ceftazidime and up to an 8-fold increased resistance to the inhibitor clavulanate. Ceftazidime 157-168 CD248 molecule Homo sapiens 98-103 18559360-5 2008 Many of the resulting amino acid substitutions had significant effects on the in vivo activity of TEM-1, including up to a 64-fold increased activity toward ceftazidime and up to an 8-fold increased resistance to the inhibitor clavulanate. Clavulanic Acid 227-238 CD248 molecule Homo sapiens 98-103 17600829-0 2007 Simulated annealing exploration of an active-site tyrosine in TEM-1 beta-lactamase suggests the existence of alternate conformations. Tyrosine 50-58 CD248 molecule Homo sapiens 62-67 18625770-1 2008 We passaged cells expressing TEM-1 and TEM-12 from a single plasmid through either ampicillin or ceftazidime. Ceftazidime 97-108 CD248 molecule Homo sapiens 29-34 18625770-2 2008 We found that the combined effects of recombination and selection removed the bla(TEM-1) allele from the bacterial population when it was passaged through ceftazidime or the bla(TEM-12) allele when cultures were passaged through ampicillin. Ceftazidime 155-166 CD248 molecule Homo sapiens 82-87 18625770-2 2008 We found that the combined effects of recombination and selection removed the bla(TEM-1) allele from the bacterial population when it was passaged through ceftazidime or the bla(TEM-12) allele when cultures were passaged through ampicillin. Ampicillin 229-239 CD248 molecule Homo sapiens 82-87 18192970-5 2008 However, by taking advantage of a technique which allows for multiple fluorescent labeling of formalin-fixed paraffin-embedded archival sections, we demonstrate unambiguously that endosialin is not expressed by the glioma endothelial cells but on closely associated perivascular cells. Formaldehyde 94-102 CD248 molecule Homo sapiens 180-190 18192970-5 2008 However, by taking advantage of a technique which allows for multiple fluorescent labeling of formalin-fixed paraffin-embedded archival sections, we demonstrate unambiguously that endosialin is not expressed by the glioma endothelial cells but on closely associated perivascular cells. Paraffin 109-117 CD248 molecule Homo sapiens 180-190 17600829-1 2007 TEM-1 is a class A beta-lactamase that contributes to the primary defensive measure used by bacteria to hydrolyze the clinically-relevant beta-lactam antibiotics. beta-Lactams 19-30 CD248 molecule Homo sapiens 0-5 17600829-10 2007 Our results add to the body of evidence suggesting that Tyr105 displays a dynamical behavior resulting in alternate ligand binding modes and are consistent with the lower affinity of TEM-1 for cephalosporins relative to penicillins. Cephalosporins 193-207 CD248 molecule Homo sapiens 183-188 17070843-3 2007 Here we extend this study to cover the entire interface of TEM1 beta-lactamase and its protein inhibitor BLIP using an improved method for deriving interaction maps based on REDUCE to add hydrogen atoms and then by evaluating the interactions using modifications of the programs PROBE, NCI and PARE. Hydrogen 188-196 CD248 molecule Homo sapiens 59-63 17662719-4 2007 Several deletion variants had enhanced activity towards ceftazidime compared to the wild-type TEM-1 demonstrating that removal of an amino acid can have a beneficial outcome. Ceftazidime 56-67 CD248 molecule Homo sapiens 94-99 17070843-10 2007 Here, a double mutation replacing the wild-type Glu,Tyr to Tyr,Asn on TEM1 (res id 104,105) caused a major backbone structural rearrangement of BLIP, changing the composition of two modules but not of other modules within the interface. Glutamic Acid 48-51 CD248 molecule Homo sapiens 70-74 17070843-10 2007 Here, a double mutation replacing the wild-type Glu,Tyr to Tyr,Asn on TEM1 (res id 104,105) caused a major backbone structural rearrangement of BLIP, changing the composition of two modules but not of other modules within the interface. Tyrosine 52-55 CD248 molecule Homo sapiens 70-74 17070843-10 2007 Here, a double mutation replacing the wild-type Glu,Tyr to Tyr,Asn on TEM1 (res id 104,105) caused a major backbone structural rearrangement of BLIP, changing the composition of two modules but not of other modules within the interface. Tyrosine 59-62 CD248 molecule Homo sapiens 70-74 17070843-10 2007 Here, a double mutation replacing the wild-type Glu,Tyr to Tyr,Asn on TEM1 (res id 104,105) caused a major backbone structural rearrangement of BLIP, changing the composition of two modules but not of other modules within the interface. Asparagine 63-66 CD248 molecule Homo sapiens 70-74 16809340-6 2006 Comparison of the SHV-1.BLIP structure with the published TEM-1.BLIP structure suggests that the increased volume of Glu-104 stabilizes a key binding loop in the interface. Glutamic Acid 117-120 CD248 molecule Homo sapiens 58-63 16940114-1 2006 The antimicrobial activity of amoxicillin against TEM-1-expressing strains could be fully recovered when bacteria were preincubated with sublethal doses of an antibacterial peptide derivative. Amoxicillin 30-41 CD248 molecule Homo sapiens 50-55 15987690-2 2005 Clavulanic acid is a potent mechanism-based inhibitor of TEM-1 and SHV-1beta-lactamases, enzymes that confer resistance to beta-lactams in many gram-negative pathogens. beta-Lactams 123-135 CD248 molecule Homo sapiens 57-62 16632911-3 2006 Among 79 Hib isolates, 45 (57%) were beta-lactamase-producing and ampicillin-resistant (44 and 1 isolates produced TEM-1- and ROB-1-type beta-lactamases, respectively), and 34 isolates (43%) were beta-lactamase-nonproducing and ampicillin-sensitive. Ampicillin 66-76 CD248 molecule Homo sapiens 115-120 15953677-6 2006 Such immunoliposomes loaded with the cytotoxic drug N4-octadecyl-1-beta-D-arabinofuranosylcytosine-(5"-5")-3"-C-ethinylcytidine showed increased binding affinity and up to 80% higher cytotoxic activity towards TEM1-expressing IMR-32 tumor cells compared with control liposomes. n4-octadecyl-1-beta-d-arabinofuranosylcytosine-(5"-5")-3"-c-ethinylcytidine 52-127 CD248 molecule Homo sapiens 210-214 15987690-4 2005 Unfortunately, the emergence of clavulanic acid-resistant variants of TEM-1 and SHV-1 beta-lactamase significantly compromise the efficacy of this combination. Clavulanic Acid 32-47 CD248 molecule Homo sapiens 70-75 15880093-5 2005 TEM-1 was the most prevalent beta-lactamase and conferred resistance to ampicillin, piperacillin, and cephalothin. Piperacillin 84-96 CD248 molecule Homo sapiens 0-5 16048956-3 2005 Traditional class A beta-lactamases, such as TEM-1 and SHV-1, are unable to hydrolyze carbapenem antibiotics and exhibit some differences in sequence from those that are able to hydrolyze carbapenem antibiotics. Carbapenems 86-108 CD248 molecule Homo sapiens 45-50 16048956-3 2005 Traditional class A beta-lactamases, such as TEM-1 and SHV-1, are unable to hydrolyze carbapenem antibiotics and exhibit some differences in sequence from those that are able to hydrolyze carbapenem antibiotics. Carbapenems 188-210 CD248 molecule Homo sapiens 45-50 15880093-5 2005 TEM-1 was the most prevalent beta-lactamase and conferred resistance to ampicillin, piperacillin, and cephalothin. Ampicillin 72-82 CD248 molecule Homo sapiens 0-5 15880093-5 2005 TEM-1 was the most prevalent beta-lactamase and conferred resistance to ampicillin, piperacillin, and cephalothin. Cephalothin 102-113 CD248 molecule Homo sapiens 0-5 14711619-8 2004 Resistance to ampicillin was most often associated with a TEM-1 family beta-lactamase gene. Ampicillin 14-24 CD248 molecule Homo sapiens 58-63 15214794-1 2004 The reactions of 6-methylidene penems 4-7 with beta-lactamases (TEM-1, SHV-1, Amp-C) were characterized by electrospray ionization mass spectrometry (ESI-MS). 6-methylidene penems 17-37 CD248 molecule Homo sapiens 64-69 15214794-5 2004 ESI-MS/MS analysis of the T-6 trypsin-digested fragments of TEM-1 and SHV-1 demonstrated that the penems were only attached to Ser-70 of these class A beta-lactamases and that the penem ring structures were rearranged to seven-membered dihydro[1,4]thiazepines. Serine 127-130 CD248 molecule Homo sapiens 60-65 15214794-5 2004 ESI-MS/MS analysis of the T-6 trypsin-digested fragments of TEM-1 and SHV-1 demonstrated that the penems were only attached to Ser-70 of these class A beta-lactamases and that the penem ring structures were rearranged to seven-membered dihydro[1,4]thiazepines. dihydro[1,4]thiazepines 236-259 CD248 molecule Homo sapiens 60-65 12526667-0 2003 Insights into the acylation mechanism of class A beta-lactamases from molecular dynamics simulations of the TEM-1 enzyme complexed with benzylpenicillin. Penicillin G 136-152 CD248 molecule Homo sapiens 108-113 15294072-2 2004 Two 10-23 mono-DNAzymes (Dz1, Dz2) and a di-DNAzyme (Dz1-2) targeted to beta-lactamase mRNA were designed to determine to what degree the growth of ampicillin-resistant bacteria (TEM-1, TEM-3) was inhibited. Ampicillin 148-158 CD248 molecule Homo sapiens 179-184 12435704-3 2002 This conformation resembles that of imipenem bound to the class A enzyme TEM-1 but is different from that of moxalactam bound to AmpC. Imipenem 36-44 CD248 molecule Homo sapiens 73-78 12354765-2 2002 Mutations at Met-69, an amino acid proximal to the active site Ser-70 in the TEM-1 and SHV-1 beta-lactamases, have emerged as a puzzling cause of bacterial resistance to inhibitors of beta-lactamases. Methionine 13-16 CD248 molecule Homo sapiens 77-82 12354765-2 2002 Mutations at Met-69, an amino acid proximal to the active site Ser-70 in the TEM-1 and SHV-1 beta-lactamases, have emerged as a puzzling cause of bacterial resistance to inhibitors of beta-lactamases. Serine 63-66 CD248 molecule Homo sapiens 77-82 12435704-3 2002 This conformation resembles that of imipenem bound to the class A enzyme TEM-1 but is different from that of moxalactam bound to AmpC. Moxalactam 109-119 CD248 molecule Homo sapiens 73-78 12435704-3 2002 This conformation resembles that of imipenem bound to the class A enzyme TEM-1 but is different from that of moxalactam bound to AmpC. ampc 129-133 CD248 molecule Homo sapiens 73-78 11870868-1 2002 The class A beta-lactamase TEM-1 is a key bacterial resistance enzyme against beta-lactam antibiotics, but little is known about the energetic bases for complementarity between TEM-1 and its inhibitors. beta-Lactams 12-23 CD248 molecule Homo sapiens 27-32 12183265-1 2002 In an early example of DNA shuffling, Stemmer (W. P. C. Stemmer, Nature 370:389-390, 1994) demonstrated a dramatic improvement in the activity of the TEM-1 beta-lactamase toward cefotaxime as the consequence of six amino acid substitutions. Cefotaxime 178-188 CD248 molecule Homo sapiens 150-155 11996574-9 2002 Apart from its mechanistic implications, this atomic resolution structure affords an unusually detailed view of the structure, dynamics, and hydrogen-bonding networks of TEM-1, which may be useful for the design of inhibitors against this key antibiotic resistance target. Hydrogen 141-149 CD248 molecule Homo sapiens 170-175 11870868-1 2002 The class A beta-lactamase TEM-1 is a key bacterial resistance enzyme against beta-lactam antibiotics, but little is known about the energetic bases for complementarity between TEM-1 and its inhibitors. beta-Lactams 12-23 CD248 molecule Homo sapiens 177-182 11870868-7 2002 Surprisingly, all beta-lactam covalent acyl--enzyme complexes tested destabilize TEM-1 significantly relative to the apo-enzyme. beta-Lactams 18-29 CD248 molecule Homo sapiens 81-86 11870868-8 2002 For instance, the clinically used inhibitor clavulanic acid and the beta-lactamase-resistant beta-lactams moxalactam and imipenem destabilize TEM-1 by over 2.6C (1.2 kcal/mol) in their covalent adducts. Clavulanic Acid 44-59 CD248 molecule Homo sapiens 142-147 11870868-8 2002 For instance, the clinically used inhibitor clavulanic acid and the beta-lactamase-resistant beta-lactams moxalactam and imipenem destabilize TEM-1 by over 2.6C (1.2 kcal/mol) in their covalent adducts. beta-Lactams 93-105 CD248 molecule Homo sapiens 142-147 11870868-8 2002 For instance, the clinically used inhibitor clavulanic acid and the beta-lactamase-resistant beta-lactams moxalactam and imipenem destabilize TEM-1 by over 2.6C (1.2 kcal/mol) in their covalent adducts. Moxalactam 106-116 CD248 molecule Homo sapiens 142-147 11870868-8 2002 For instance, the clinically used inhibitor clavulanic acid and the beta-lactamase-resistant beta-lactams moxalactam and imipenem destabilize TEM-1 by over 2.6C (1.2 kcal/mol) in their covalent adducts. Imipenem 121-129 CD248 molecule Homo sapiens 142-147 11870868-9 2002 Based on the structure of the TEM-1/imipenem complex (Maveyraud et al., J Am Chem Soc 1998;120:9748--52), destabilization by moxalactam and imipenem is thought to be caused by a steric clash between the side-chain of Asn132 and the 6(7)-alpha group of these beta-lactams. Imipenem 36-44 CD248 molecule Homo sapiens 30-35 11870868-9 2002 Based on the structure of the TEM-1/imipenem complex (Maveyraud et al., J Am Chem Soc 1998;120:9748--52), destabilization by moxalactam and imipenem is thought to be caused by a steric clash between the side-chain of Asn132 and the 6(7)-alpha group of these beta-lactams. Moxalactam 125-135 CD248 molecule Homo sapiens 30-35 11870868-9 2002 Based on the structure of the TEM-1/imipenem complex (Maveyraud et al., J Am Chem Soc 1998;120:9748--52), destabilization by moxalactam and imipenem is thought to be caused by a steric clash between the side-chain of Asn132 and the 6(7)-alpha group of these beta-lactams. Imipenem 140-148 CD248 molecule Homo sapiens 30-35 11870868-9 2002 Based on the structure of the TEM-1/imipenem complex (Maveyraud et al., J Am Chem Soc 1998;120:9748--52), destabilization by moxalactam and imipenem is thought to be caused by a steric clash between the side-chain of Asn132 and the 6(7)-alpha group of these beta-lactams. beta-Lactams 258-270 CD248 molecule Homo sapiens 30-35 11733064-1 2001 During mitosis, a ras-related GTPase (Tem1) binds GTP and activates a signal transduction pathway to allow mitotic exit. Guanosine Triphosphate 30-33 CD248 molecule Homo sapiens 38-42 11885594-1 2001 Completion of mitosis is triggered by the activation of the Ras-like GTP-binding protein Tem1p. Guanosine Triphosphate 69-72 CD248 molecule Homo sapiens 89-94 11885594-3 2001 suggest that Tem1p activation is achieved by inhibition of its two-component GAP Bub2p/Bfa1p via phosphorylation of Bfa1p by the Polo kinase Cdc5p. bfa1p 87-92 CD248 molecule Homo sapiens 13-18