HUGO ID Detailed Result 9604


HUGO ID 9604
Symbol PTGS1
Name prostaglandin-endoperoxide synthase 1 (prostaglandin G/H synthase and cyclooxygenase)
#Occurrence 160
#Paper 7

 


PMID Match String Actual String Score Flanking text Edited by Edit
14511332COX-1COX-15.4two different isoforms of the cyclooxygenase (COX) COX enzyme namely COX-1 and COX-2 
14511332COX-1COX-15.4Therefore we investigated the expression of COX-1 and COX-2 in the spinal cord of seven human sporadic 
14511332COX-1COX-15.4In contrast COX-1 expression was predominantly confined to microglia and no apparent difference 
14511332COX-1COX-15.4Currently two COX isoforms are known namely COX-1 and COX-2 ( Vane et al . 1998 
14511332COX-1COX-15.4Whereas COX-1 mainly subserves _amp_#8216 house-keeping_amp_#8217 functions COX-2 is the product of 
14511332COX-1COX-15.4Therefore we compared the spinal expression of COX-1 and COX-2 in sALS and control patients by means of 
14511332COX-1COX-15.4COX-1 expression did not differ between sALS and control tissues 
14511332COX-1COX-15.4Briefly goat polyclonal antisera raised against human COX-1 and COX-2 protein (Santa Santa Cruz Biotechnology Santa Cruz CA 
14511332COX-1COX-15.4To further differentiate the cellular distributions of COX-1 and COX-2 proteins a double staining procedure using a mouse 
14511332COX-1COX-15.4Specimens were coded and assessed observer-blinded for presence of COX-1 and COX-2 immunoreactivity (IR) IR 
14511332COX-1COX-15.4Membranes were probed with polyclonal goat antihuman COX-1 or COX-2 serum (diluted diluted 1 1000 followed by a 
14511332COX-1COX-15.4immunohistochemistry we performed Western blotting experiments for the detection of COX-1 and COX-2 protein with spinal protein extracts from human donors 
14511332COX-1COX-15.4cords (segments segments L1-L5 left lane run alongside purified sheep COX-1 protein (right right lane in a Western blot that has 
14511332COX-1COX-15.4Western blot that has been incubated with the same polyclonal COX-1 antibody as that used for immunohistochemistry 
14511332COX-1COX-15.475 kDa consistent with the reported molecular mass of human COX-1 protein in the literature (74 74 kDa ( Vane et 
14511332COX-1COX-15.4the two COX isoforms we determined the specifity with purified COX-1 and COX-2 protein by Western blotting 
14511332COX-1COX-15.4Figure 1C shows that the goat antihuman polyclonal COX-1 antibody exclusively detected COX-1 protein and not COX-2 protein 
14511332COX-1COX-15.4shows that the goat antihuman polyclonal COX-1 antibody exclusively detected COX-1 protein and not COX-2 protein 
14511332COX-1COX-15.4antihuman polyclonal COX-2 antibody detected only COX-2 protein and not COX-1 protein 
14511332COX-1COX-15.4Expression of COX-1 protein was predominantly confined to some small cells with the 
14511332COX-1COX-15.4This could also be demonstrated by the costaining of COX-1 with the microglial marker MAC-1 ( Fig 2L 
14511332COX-1COX-15.4Thirdly COX-1 expression was predominately confined to glial cells 
14511332COX-1COX-15.4Furthermore no study has yet investigated the cellular expression of COX-1 in sALS 
14511332COX-1COX-15.4neurons and predominantly in astroglia although no apparent differences in COX-1 expression were seen between mSOD1 mice and controls 
14511332COX-1COX-15.4. 2003 and were shown to be specific for the COX-1 and COX-2 protein respectively 
14511332COX-1COX-15.4have intentionally focused on the in situ expression of both COX-1 and COX-2 proteins in human ALS spinal cords 
14511332COX-1COX-15.4Expression of COX-1 protein 
14511332COX-1COX-15.4In contrast to the COX-2 protein COX-1 expression was predominantly found in microglia cells and showed no 
14511332COX-1COX-15.4Expression of COX-1 in microglia is consistent with our previous animal study and 
14511332COX-1COX-15.4(2001 2001 who reported a similar content of COX-1 mRNA in sALS and controls 
14511332COX-1COX-15.4The unaltered expression of COX-1 in sALS implies that there is no or only a 
14511332COX-1COX-15.4was detected between controls and sALS with regard to the COX-1 protein 
15081582COX-1COX-11.3There are two distinct COX isoenzymes known as COX-1 and COX-2 that are 65% homologous 
15081582COX-1COX-11.3COX-1 is constitutively expressed in most tissues and produces prostaglandins that 
15081582COX-1COX-11.3The COX enzymes (COX-1 COX-1 and COX-2 are more completely termed prostaglandin G/H G H 
15081582COX-1COX-11.3permit us to form a hypothesis regarding the roles of COX-1 and -2 under normal conditions and during disease 
15081582COX-1COX-11.3COX-1 is constitutively expressed throughout the normal brain ( Kawasaki et 
15081582COX-1COX-11.3is attenuated by a COX-2 inhibitor but not with a COX-1 selective inhibitor ( Hewett et al. 2000 
15081582COX-1COX-11.3There is no correlate change in COX-1 mRNA 
15081582COX-1COX-11.3types in the CNS microglia appear to predominantly express the COX-1 isoform ( Yermakova et al. 1999 
15081582COX-1COX-11.3In addition COX-1 positive microglia accumulate at sites of neuronal degeneration including traumatic 
15081582COX-1COX-11.3Although increased COX-1 in microglia is observed injury paradigms there are little data 
15081582COX-1COX-11.3in which the significance of the differential expression of the COX-1 and COX-2 isoforms may arise 
15081582COX-1COX-11.3Since COX-1 increases in activated microglia and is not regulated by NF-_amp_#x3ba 
15081582COX-1COX-11.3mSOD1 mice there is increased expression of COX-2 but not COX-1 mRNA 
15081582COX-1COX-11.3slowly in COX-2 inhibitor-treated animals possibly through the slower microglial COX-1 upregulation and likely through multiple additional regulatory mechanisms 
15453089COX-1COX-12.3Besides a constitutive isoform (COX-1), COX-1 which is widely distributed in virtually all cell types and 
15453089COX-1COX-12.3COX-1 and COX-2 are coded by 2 distinct genes located on 
15453089COX-1COX-12.3On the contrary the COX-1 gene represents a classical _amp_#147 housekeeping_amp_#148 gene lacking of a 
15453089COX-1COX-12.32 isoenzymes which could account for the different sensitivities of COX-1 and COX-2 to specific inhibitors ( 5 
15453089COX-1COX-12.3insert near the COX-2 C-terminus which is not present in COX-1 and has allowed the production of specific antibodies 
15453089COX-1COX-12.3In the majority of the tissues COX-1 appears to be the only isoform constitutively expressed confirming the 
15453089COX-1COX-12.3However in brain testes and kidney macula densa cells both COX-1 and COX-2 are expressed under physiological conditions ( 2 
15453089COX-1COX-12.3In rat brain COX-1 and COX-2 immunoreactivities are present in discrete neuronal populations distributed 
15453089COX-1COX-12.3In other regions such as midbrain pons and medulla COX-1 immunoreactivity prevails ( 6 7 
15453089COX-1COX-12.3Similarly mRNAs for both COX-1 and COX-2 are present in several regions of human brain 
15453089COX-1COX-12.3The relative contribution of COX-1 and COX-2 activity to brain pathology and physiology has been 
15453089COX-1COX-12.3On one side it has been argued that COX-1 activity in brain diseases has been overlooked on the other 
15453089COX-1COX-12.3studies it is clear that the popular paradigm by which COX-1 serves physiological functions and COX-2 is responsible for _amp_#147 pathological_amp_#148 
15453089COX3COX-30.3Recently a third variant of COX named COX-3 and 2 partial COX-1 proteins (PCOX-1 PCOX-1 proteins have been 
15453089COX-1COX-12.3a third variant of COX named COX-3 and 2 partial COX-1 proteins (PCOX-1 PCOX-1 proteins have been identified from canine and 
15453089PCOX1PCOX-10.8of COX named COX-3 and 2 partial COX-1 proteins (PCOX-1 PCOX-1 proteins have been identified from canine and human cerebral cortex 
15453089COX3COX-30.3COX-3 and one of the PCOX-1 are products of the COX-1 
15453089PCOX1PCOX-10.8COX-3 and one of the PCOX-1 are products of the COX-1 gene but retain intron 1 
15453089COX-1COX-12.3COX-3 and one of the PCOX-1 are products of the COX-1 gene but retain intron 1 in their mRNA 
15453089COX-1COX-12.3in the in cerebral cortex where the expression of the COX-1 variant gene accounts for ~5_amp_#37 of COX-1 
15453089COX-1COX-12.3expression of the COX-1 variant gene accounts for ~5_amp_#37 of COX-1 
15453089COX-1COX-12.3As its counterpart COX-1 COX-3 is not induced by acute inflammatory stimulation ( 13 
15453089COX3COX-30.3As its counterpart COX-1 COX-3 is not induced by acute inflammatory stimulation ( 13 
15453089COX3COX-30.3COX-3 but not PCOX-1 exhibits enzymatic activity that is glycosylation-dependent and 
15453089PCOX1PCOX-10.8COX-3 but not PCOX-1 exhibits enzymatic activity that is glycosylation-dependent and especially sensitive to 
15453089COX3COX-30.3Thus COX-3 could represent the brain-specific COX isoform the existence of which 
15453089COX3COX-30.3Nonetheless the functional role of COX-3 is largely unknown and more intense research is required to 
15453089COX3COX-30.3more intense research is required to elucidate the contribution of COX-3 to the overall PG production in brain 
15453089COX-1COX-12.3first post-natal week showed decreased levels of COX-2 but not COX-1 in the hippocampus at adulthood 
15453089COX-1COX-12.3COX-2 inhibitors but not COX-1 selective inhibitors administered systemically shortly after training in the Morris 
15453089COX-1COX-12.3formed during the enzymatic activity of COX-2 rather than of COX-1 could participate to synaptic plasticity through several mechanisms including modulation 
15453089COX-1COX-12.3In addition significant compensatory effects of COX-1 and possibly COX-3 cannot be ruled out 
15453089COX3COX-30.3In addition significant compensatory effects of COX-1 and possibly COX-3 cannot be ruled out 
15453089COX-1COX-12.3Macrophage/ Macrophage microglia-like cells expressing COX-1 were disseminated throughout the brain parenchyma of control animals 
15453089COXCOX-1-positive0.0In EAE the number of COX-1-positive macrophages increased along with that of COX-2-positive cellsJunguk Hur
15453089COX-1COX-12.3In contrast COX-1 immunoreactivity was confined to some microglial cells and there was 
15453089COX-1COX-12.3Moderate COX-1 immunoreactivity was observed in some neuronal somata and processes and 
15453089COX-1COX-12.3that MPTP neurodegeneration was mitigated in COX-2 but not in COX-1 knock out mice 
15453089COXCOX-1-positive0.0Few scattered COX-1-positive microglia-like cells were found in control and infected brains (Junguk Hur
15453089COX-1COX-12.3results were reported in a recent study in which both COX-1 and COX-2 were increased in sporadic CJD cortex ( 58 
15453089COX-1COX-12.3COX-1 immunoreactivity was present in macrophages/microglial macrophages microglial cells whereas COX-2 
15453089COX-1COX-12.3in neuroblastoma cells PrP peptides increase PGE 2 levels and COX-1 inhibitors protect against PrP toxicity ( 62 
15453089COX-1COX-12.3Over the last 10 years several analyses of COX-1 and COX-2 expressions have been carried out in animal models 
15453089COX-1COX-12.3In contrast to COX-2 the levels of COX-1 mRNA and protein were not significantly altered in AD brains 
15453089COX-1COX-12.3COX-1 appeared to be mainly expressed by microglial cells found in 
16101543COX-1COX-10.3by two isoforms of the cyclooxygenase (COX) COX enzyme namely COX-1 and COX-2 
16647138COX-1COX-14.9Three forms of COX enzymes designated as COX-1 COX-2 and COX-3 occur in mammalian tissues 
16647138COX-1COX-14.9COX-1 is a constitutively expressed in brain tissue and is responsible 
16647138COX-1COX-14.9COX-1 and COX-2 are homodimers 
16647138COX-1COX-14.9COX-1 contains Val at the 434 and 523 positions whereas COX-2 
16647138COX-1COX-14.9flexible substrate and inhibitor binding sites in COX-2 than in COX-1 ( Kurumbail et al. 1996 
16647138COX-1COX-14.9The amino acid sequences of COX-1 and COX-2 also differ from each other at the N- 
16647138COX-1COX-14.9of COX-2 is larger and more accommodating than that of COX-1 and COX-1 displays negative allosterism at low concentrations of AA 
16647138COX-1COX-14.9of COX-2 is larger and more accommodating than that of COX-1 and COX-1 displays negative allosterism at low concentrations of AA 
16647138COX-1COX-14.9is larger and more accommodating than that of COX-1 and COX-1 displays negative allosterism at low concentrations of AA 
16647138COX-1COX-14.9AA is the preferred substrate for COX-1 and COX-2 
16647138COX-1COX-14.9The COX-2 gene is 8.3 kb whereas the COX-1 gene is much larger (22 22 kb ( Vane et 
16647138COX-1COX-14.9COX-1 mRNA is approximately 2.8 kb while COX-2 mRNA is approximately 
16647138COX-1COX-14.9Analysis of the 5_amp_#x2032 -flanking untranslated regions of COX-1 and COX-2 indicates that the COX-1 gene is associated with 
16647138COX-1COX-14.9-flanking untranslated regions of COX-1 and COX-2 indicates that the COX-1 gene is associated with housekeeping activities whereas the COX-2 gene 
16647138COX-1COX-14.9Tazawa et al. 1994 whereas the same region in the COX-1 gene has no canonic TATA box ( Wu 1995 
16647138COX-1COX-14.9The COX-1 gene also has some putative regulatory sites such as Sp-1 
16647138COX-1COX-14.9COX-1 does not respond to NF-_amp_#x3ba B as intensely as COX-2 
16647138COX-1COX-14.9In rat and ovine brain COX-1 and COX-2 immunoreactivities are present in discrete neuronal populations distributed 
16647138COX-1COX-14.9COX-1 immunoreactivity is enriched in midbrain pons and medulla ( Breder 
16647138COX-1COX-14.9different pharmacological properties have been described for COX-3 compared with COX-1 or COX-2 enzymes many investigators consider it to be a 
16647138COX-1COX-14.9many investigators consider it to be a splice variant of COX-1 ( Chandrasekharan et al. 2002 and Davies et al. 2004 
16647138COX-1COX-14.9Thus COX-3 is a product of the COX-1 gene but retains intron 1 in its mRNA 
16647138COX-1COX-14.9Comparison of canine COX-3 activity with murine COX-1 and COX-2 demonstrates that analgesic/antipyretic analgesic antipyretic drugs such as 
16647138COX-1COX-14.9Sequence analysis indicated that the 98-base-pair intron 1 of COX-1 gene remains unprocessed in COX-3 inducing a frameshift mutation and 
16647138COX-1COX-14.9of affecting the cerebral circulation in a comparable manner to COX-1 and 2 pathways 
16647138COX-1COX-14.9COX-1 and COX-2 play a central role in the induction of 
16647138COX-1COX-14.9the most abundant prostaglandins generated in the brain through COX-1/COX-2 COX-1 COX-2 pathways (PGE PGE 2 PGF 2a and PGD 2 
16647138COX-1COX-14.9s and both the non-selective inhibitor indomethacin and the selective COX-1 inhibitor SC-560 reduced photolysis-induced hyperemia 
16647138COX-1COX-14.9not play a significant role in vasodilation as compared to COX-1 metabolites 
16647138COX-1COX-14.9(2006) 2006 observed dense immunohistochemical staining for COX-1 but not COX-2 in the astrocytic endfeet that ensheath cortical 
16647138COX-1COX-14.9that is initiated by neural activity using a mechanism involving COX-1 metabolites 
16647138COX-1COX-14.9of long-term potentiation in hippocampal dentate granule neurons whereas a COX-1 inhibitor was not effective ( Chen et al. 2002 
16647138COX-1COX-14.9is a profound difference between NSAIDs with different selectivities for COX-1 and COX-2 with regard to their effects on the synthesis 
16647138COX-1COX-14.9NSAIDs displaying an inhibitory action on COX-1 increased brain KYNA formation whereas COX-2 selective inhibitors had the 
16647138COX-1COX-14.9acid formation induced by NSAIDs displaying an inhibitory action on COX-1 could possibly contribute to a reduction in glutamatergic transmission along 
16647138COX-1COX-14.9because of the well-known analgesic and temperature-reducing effects of COX-1/-2 COX-1 -2 inhibitors on patients experiencing these conditions 
16647138COX-1COX-14.9has allowed investigators to study the individual roles of the COX-1 and COX-2 isoforms 
16647138COX-1COX-14.9At 30 to 40 min after IL-1_amp_#x3b2 COX-1 KO mice showed a smaller reduction in milk intake in 
16647138COX-1COX-14.9IL-1_amp_#x3b2 administration COX-2 KO mice showed only small responses while COX-1 KO mice responded normally 
16647138COX-1COX-14.9This result suggests that while COX-1 is primarily involved in the early phase of milk intake 
16647138COX-1COX-14.9assessed the febrile response to injection of intraperitoneal LPS in COX-1 and COX-2-deficient mice 
16647138COX-1COX-14.9The wild-type and COX-1 _amp_#x2212;/_amp_#x2212; _amp_#x2212 _amp_#x2212 mice responded to LPS with a 1_amp_#xb0 
16647138COX-1COX-14.9A persistent accumulation of microglial cells and macrophages expressing COX-1 was also observed in human and rat traumatic brain injuries 
16647138COX-1COX-14.9Studies on COX-1 and COX-2 gene deletion provided some information on the roles 
16647138COX-1COX-14.9were not able to confirm the harmful effect of losing COX-1 activity in a permanent endovascular middle cerebral artery occlusion (MCAO) 
16647138COX-1COX-14.9PLA 2 activation may be converted to prostaglandins by both COX-1 and COX-2 during the immediate response and predominantly by COX-2 
16647138COX-1COX-14.92000 and is functionally coupled with COX-2 but not with COX-1 ( Balsinde et al. 1998 
16647138COX-1COX-14.9In another human study COX-1 expressed intensely in microglia but weakly in neurons in control 
16647138COX-1COX-14.9Pretreatment with indomethacin an inhibitor of COX-1 and COX-2 reduced infarct size following focal ischemia with reperfusion 
16647138COX-1COX-14.9Ibuprofen which also inhibits both COX-1 and COX-2 reduced neuronal injury and improved cerebral blood flow 
16647138COX-1COX-14.9Selective inhibition of COX-1 by valerylsalicylate or of COX-2 by rofecoxib was used to 
16647138COX-1COX-14.9suppresses COX-2 at low nanomolar levels but does not affect COX-1 
16647138COX-1COX-14.9blocked by the infusion of NMDA antagonists as well as COX-1 and COX-2 inhibitors indicating that both COX-1 and COX-2 contribute 
16647138COX-1COX-14.9as well as COX-1 and COX-2 inhibitors indicating that both COX-1 and COX-2 contribute to the prostaglandin synthesis and oxidative damage 
16647138COX-1COX-14.9Induction of COX-2 but not COX-1 gene expression has been demonstrated to precede apoptosis in the 
16647138COX-1COX-14.9A marked increase of COX-1 and COX-2 expression and immunoreactivity in cerebral cortex and hippocampal 
16647138COX-1COX-14.9The neuroprotective effects of COX-1 and COX-2 inhibitors (NSAID) NSAID strongly support the view that 
16647138COX-1COX-14.9The molecular mechanism by which COX-1 and COX-2 promote amyloidogenic accumulation of _amp_#x3b2 -amyloid peptide is 
16647138COX-1COX-14.9COX-1 and COX-2 potentiate _amp_#x3b2 -amyloid peptide generation through mechanisms that 
16647138COX-1COX-14.9Using RT-PCR and Western blotting both COX-1 and COX-2 are significantly increased in brains from CJD patients 
16647138COX-1COX-14.9and in brain homogenates of scrapie-infected mice the upregulation of COX-1 and COX-2 is accompanied by a several-fold increase in concentrations 
16647138COX-1COX-14.9In contrast indomethacin a COX-1 and COX-2 inhibitor and baicalein a 12-LOX inhibitor do not 
16647138COX-1COX-14.9In astrocytes TGF_amp_#x3b2 1 upregulates COX-1 expression and serum increases COX-2 expression 
16647138COX-1COX-14.9Neither TGF_amp_#x3b2 1 nor serum affects COX-1 and COX-2 expression in neurons 
16647138COX-1COX-14.9Furthermore COX-1 compensates for the loss of COX-2 in the COX-2 knockout 
16647138COX-1COX-14.9COX-2 _amp_#x2212;/_amp_#x2212; _amp_#x2212 _amp_#x2212 shows a compensatory increase in brain COX-1 expression and activity (with with exogenous arachidonic acid in brain 
17574754COX-1COX-10.0signaling molecules derived from the metabolism of arachidonic acid by COX-1 and the inducible COX-2 
18040778COX-1COX-10.1Hypothetically by inhibiting microglial cell cyclooxygenases (COX-1 COX-1 or COX-2 the metabolism of arachadonic acid is curtailed and