PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
10764744-4	2000	Sodium azide, an inhibitor of catalase, reduced the increased sensitivity of mC5 and C33 cells to TNF-alpha to the level of toxicity found with control Hp cells.	Sodium Azide	0-12	hemolytic complement	Mus musculus	77-80
11867678-1	2002	Leukotriene B(4) (LTB(4)) is an easily diffusible proinflammatory chemotactic factor that has been posited to prime the initial inflammatory response for the action of other mediators, including C5a.	Leukotriene B4	0-13	hemolytic complement	Mus musculus	195-198
11867678-3	2002	Pretreatment of C5- mice with the specific 5-lipoxygenase inhibitor, zileuton, reduced peritoneal leukocytosis to almost unstimulated levels, suggesting that LTB(4) can act independently of C5a.	zileuton	69-77	hemolytic complement	Mus musculus	190-193
11867678-4	2002	Previously, LTB(4) and C5a have been shown in vitro to be inactivated by metabolites of superoxide.	Superoxides	88-98	hemolytic complement	Mus musculus	23-26
11867678-9	2002	These data suggest that LTB(4) and C5a have separate but overlapping roles in thioglycollate-elicited peritonitis, and at least the leukotriene component is, in turn, regulated by reactive oxidants.	Thioglycolates	78-92	hemolytic complement	Mus musculus	35-38
11165368-7	2001	The C-5-propyne-modified phosphorothioate probe showed pronounced tissue penetration and cellular uptake as soon as 30 min after injection which was still detectable after 24 h. Immediately after injection of the highest dose, long-lasting hind-limb paralysis was observed.	Parathion	25-41	hemolytic complement	Mus musculus	4-7
10764744-5	2000	Azide also decreased the elevated caspase-3 activity of mC5 cells.	Azides	0-5	hemolytic complement	Mus musculus	56-59
10764744-8	2000	TNF-alpha plus cycloheximide increased ATP levels, with higher levels in C33 and mC5 cells compared with Hp cells.	Cycloheximide	15-28	hemolytic complement	Mus musculus	81-84
10764744-8	2000	TNF-alpha plus cycloheximide increased ATP levels, with higher levels in C33 and mC5 cells compared with Hp cells.	Adenosine Triphosphate	39-42	hemolytic complement	Mus musculus	81-84
10496894-6	1999	K-76 monocarboxylic acid, an inhibitor of complement C5, effectively prevented the KO3-S LPS-induced degradation (but not accumulation) of platelets and the ensuing rapid shock in BALB/c mice.	monocarboxylic acid	5-24	hemolytic complement	Mus musculus	42-55
11125474-7	2000	C5a activates local mast cells to release serotonin (5-HT) and TNF alpha to induce endothelial ICAM-1 and VCAM-1, leading to T cell recruitment.	Serotonin	42-51	hemolytic complement	Mus musculus	0-3
10336122-3	1999	In response to intraventricular kainic acid injection, there was marked increase in the C5a receptor messenger RNA expression, particularly in hippocampal formation and cerebral cortex.	Kainic Acid	32-43	hemolytic complement	Mus musculus	88-91
10224363-5	1999	IgM forms complexes with challenge Ag, activating the classical complement (C) pathway, generating C5a, to activate endothelium directly, or indirectly via C5a receptors (R) on mast cells and platelets, that release vasoactive amines (serotonin) and cytokines (TNF-alpha).	Amines	227-233	hemolytic complement	Mus musculus	156-159
10224363-5	1999	IgM forms complexes with challenge Ag, activating the classical complement (C) pathway, generating C5a, to activate endothelium directly, or indirectly via C5a receptors (R) on mast cells and platelets, that release vasoactive amines (serotonin) and cytokines (TNF-alpha).	Serotonin	235-244	hemolytic complement	Mus musculus	156-159
10321830-2	1999	In the present study, we tested the hypothesis that the C5-derived anaphylatoxin C5a protects against kainic acid (KA)-induced neurodegeneration and investigated the mechanism of C5a neuronal activity in vitro.	Kainic Acid	102-113	hemolytic complement	Mus musculus	81-84
10321830-5	1999	In vitro studies confirmed C5a neuroprotection: treatment of primary murine corticohippocampal neurons with human or mouse recombinant C5a reduced glutamate neurotoxicity, as measured by trypan blue exclusion assay.	Glutamic Acid	147-156	hemolytic complement	Mus musculus	27-30
10321830-5	1999	In vitro studies confirmed C5a neuroprotection: treatment of primary murine corticohippocampal neurons with human or mouse recombinant C5a reduced glutamate neurotoxicity, as measured by trypan blue exclusion assay.	Glutamic Acid	147-156	hemolytic complement	Mus musculus	135-138
10321830-5	1999	In vitro studies confirmed C5a neuroprotection: treatment of primary murine corticohippocampal neurons with human or mouse recombinant C5a reduced glutamate neurotoxicity, as measured by trypan blue exclusion assay.	Trypan Blue	187-198	hemolytic complement	Mus musculus	27-30
10321830-5	1999	In vitro studies confirmed C5a neuroprotection: treatment of primary murine corticohippocampal neurons with human or mouse recombinant C5a reduced glutamate neurotoxicity, as measured by trypan blue exclusion assay.	Trypan Blue	187-198	hemolytic complement	Mus musculus	135-138
10321830-7	1999	Our studies indicate that C5a may inhibit glutamate-mediated neuronal death through partial inhibition of caspase-3 activity.	Glutamic Acid	42-51	hemolytic complement	Mus musculus	26-29
9736572-4	1998	The inclusion of a group at the C-5" position of amodiaquine reduced or eliminated bioactivation, as determined by glutathione conjugate formation in vivo.	Amodiaquine	49-60	hemolytic complement	Mus musculus	32-35
9736572-4	1998	The inclusion of a group at the C-5" position of amodiaquine reduced or eliminated bioactivation, as determined by glutathione conjugate formation in vivo.	Glutathione	115-126	hemolytic complement	Mus musculus	32-35
9736572-5	1998	This can be seen in two series of C-5"-substituted compounds: the bis-Mannich antimalarial agents, including cycloquine and pyronaridine, and mono-Mannich antimalarial agents containing a 5"-chlorophenyl group (tebuquine and 5"-ClPAQ).	bis-mannich	66-77	hemolytic complement	Mus musculus	34-37
9736572-5	1998	This can be seen in two series of C-5"-substituted compounds: the bis-Mannich antimalarial agents, including cycloquine and pyronaridine, and mono-Mannich antimalarial agents containing a 5"-chlorophenyl group (tebuquine and 5"-ClPAQ).	cycloquine	109-119	hemolytic complement	Mus musculus	34-37
9736572-5	1998	This can be seen in two series of C-5"-substituted compounds: the bis-Mannich antimalarial agents, including cycloquine and pyronaridine, and mono-Mannich antimalarial agents containing a 5"-chlorophenyl group (tebuquine and 5"-ClPAQ).	pyronaridine	124-136	hemolytic complement	Mus musculus	34-37
9736572-5	1998	This can be seen in two series of C-5"-substituted compounds: the bis-Mannich antimalarial agents, including cycloquine and pyronaridine, and mono-Mannich antimalarial agents containing a 5"-chlorophenyl group (tebuquine and 5"-ClPAQ).	mono-mannich	142-154	hemolytic complement	Mus musculus	34-37
9736572-5	1998	This can be seen in two series of C-5"-substituted compounds: the bis-Mannich antimalarial agents, including cycloquine and pyronaridine, and mono-Mannich antimalarial agents containing a 5"-chlorophenyl group (tebuquine and 5"-ClPAQ).	tebuquine	211-220	hemolytic complement	Mus musculus	34-37
9736572-5	1998	This can be seen in two series of C-5"-substituted compounds: the bis-Mannich antimalarial agents, including cycloquine and pyronaridine, and mono-Mannich antimalarial agents containing a 5"-chlorophenyl group (tebuquine and 5"-ClPAQ).	5"-clpaq	225-233	hemolytic complement	Mus musculus	34-37
9736572-6	1998	Chemical substitution at the C-5" position also resulted in compounds which underwent slower elimination (<5% of the dose excreted into bile and urine, compared with 50% for amodiaquine) and increased levels of accumulation in tissue (10% of the dose in the liver at 48 h compared with 1% with amodiaquine).	Amodiaquine	177-188	hemolytic complement	Mus musculus	29-32
9736572-6	1998	Chemical substitution at the C-5" position also resulted in compounds which underwent slower elimination (<5% of the dose excreted into bile and urine, compared with 50% for amodiaquine) and increased levels of accumulation in tissue (10% of the dose in the liver at 48 h compared with 1% with amodiaquine).	Amodiaquine	297-308	hemolytic complement	Mus musculus	29-32
9736572-8	1998	The alteration in the disposition following the introduction of the C-5" substituent resulted in an increased duration of antimalarial activity in the mouse compared with that for amodiaquine.	Amodiaquine	180-191	hemolytic complement	Mus musculus	68-71
9086140-3	1997	Administration of human C5 to C5-deficient mice caused a significant increase in PMNL recruitment following infection with C5a-ase-negative GBS.	gbs	140-143	hemolytic complement	Mus musculus	123-126
9086140-4	1997	GBS C5a-ase did not reduce PMNL accumulation in C5-sufficient mice but reduced PMNL recruitment in C5-deficient mice reconstituted with human C5.	gbs	0-3	hemolytic complement	Mus musculus	4-7
9086140-6	1997	Reduction of the acute inflammatory response by C5a-ase likely contributes to GBS virulence in human neonates.	gbs	78-81	hemolytic complement	Mus musculus	48-51
8809827-4	1996	The acute application of complement 5a (C5a) immediately induced intense ruffling of microglial membranes followed by lamellipodia extension within few seconds, while formyl-Met-Leu-Phe-OH, bacterial endotoxin (lipopolysaccharide) or inflammatory cytokines did not increase motility.	N-FORMYLMETHIONYL-LEUCYLPHENYLALANINE	167-188	hemolytic complement	Mus musculus	40-43
9047380-0	1996	Two chemotactic factors, C5a and MIP-1alpha, dramatically alter the mortality from zymosan-induced multiple organ dysfunction syndrome (MODS): C5a contributes to MODS while MIP-1alpha has a protective role.	Zymosan	83-90	hemolytic complement	Mus musculus	25-28
9047380-0	1996	Two chemotactic factors, C5a and MIP-1alpha, dramatically alter the mortality from zymosan-induced multiple organ dysfunction syndrome (MODS): C5a contributes to MODS while MIP-1alpha has a protective role.	Zymosan	83-90	hemolytic complement	Mus musculus	143-146
8809827-6	1996	A GTP-binding protein was involved in the signal cascade, since pertussis toxin inhibited motility and actin assembly in response to C5a.	Guanosine Triphosphate	2-5	hemolytic complement	Mus musculus	133-136
8809827-8	1996	The C5a-induced motility reaction was accompanied by an increase in intracellular calcium ([Ca2+]i) as measured by a Fluo-3 based imaging system.	Calcium	82-89	hemolytic complement	Mus musculus	4-7
8809827-8	1996	The C5a-induced motility reaction was accompanied by an increase in intracellular calcium ([Ca2+]i) as measured by a Fluo-3 based imaging system.	Fluo-3	117-123	hemolytic complement	Mus musculus	4-7
8809828-0	1996	Complement factor C5a and epidermal growth factor trigger the activation of outward potassium currents in cultured murine microglia.	Potassium	84-93	hemolytic complement	Mus musculus	18-21
7768675-1	1995	We investigated the in vivo selective anti-inflammatory effect of L-156,602, which was first identified as a preferential delayed-type hypersensitivity-suppressant in our screening program and first reported to be a C5a antagonist.	Linopirdine dihydrochloride	66-71	hemolytic complement	Mus musculus	216-219
7989321-7	1994	When the concentration of free Ca2+ ([Ca2+]i) was set to approximately 15 nM with 1.1 or 11 mM EGTA, a "slow"Ca2+ buffer, 10 nM C5a induced a large GkOR (11 nS at 1.1 mM EGTA versus 13.4 nS at 11 mM EGTA).	Egtazic Acid	95-99	hemolytic complement	Mus musculus	128-131
7989321-7	1994	When the concentration of free Ca2+ ([Ca2+]i) was set to approximately 15 nM with 1.1 or 11 mM EGTA, a "slow"Ca2+ buffer, 10 nM C5a induced a large GkOR (11 nS at 1.1 mM EGTA versus 13.4 nS at 11 mM EGTA).	Egtazic Acid	170-174	hemolytic complement	Mus musculus	128-131
7989321-7	1994	When the concentration of free Ca2+ ([Ca2+]i) was set to approximately 15 nM with 1.1 or 11 mM EGTA, a "slow"Ca2+ buffer, 10 nM C5a induced a large GkOR (11 nS at 1.1 mM EGTA versus 13.4 nS at 11 mM EGTA).	Egtazic Acid	170-174	hemolytic complement	Mus musculus	128-131
7989321-8	1994	Surprisingly, when [Ca2+]i was buffered at 15 nM with 10 mM BAPTA, a "rapid" Ca2+ buffer, C5a elicited a much smaller although significant K+ conductance (approximately 3 nS).	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	60-65	hemolytic complement	Mus musculus	90-93
7996541-3	1994	The 5-halo-6-alkoxy(or azido)-5,6-dihydro-3"-azido-3"-deoxythymidines, which differ in configuration at the C-5 and C-6 positions, were synthesized by the regiospecific addition of XR (X = Br, Cl, I; R = alkoxy, azido) to the 5,6-olefinic bond of AZT.	5-halo-6-alkoxy(or azido)-5,6-dihydro-3"-azido-3"-deoxythymidines	4-69	hemolytic complement	Mus musculus	108-111
7996541-3	1994	The 5-halo-6-alkoxy(or azido)-5,6-dihydro-3"-azido-3"-deoxythymidines, which differ in configuration at the C-5 and C-6 positions, were synthesized by the regiospecific addition of XR (X = Br, Cl, I; R = alkoxy, azido) to the 5,6-olefinic bond of AZT.	3',5-diazido-2',3'-dideoxyuridine	23-28	hemolytic complement	Mus musculus	108-111
7996541-12	1994	The configuration at the C-5 and C-6 positions also influenced potency where the activity of the 5R,6R-diastereomer was generally greater than that of the corresponding 5S,6S-diastereomer.	S 6	171-174	hemolytic complement	Mus musculus	25-28
8023953-0	1994	Inhibition of C5a des Arg-induced neutrophil alveolitis in transgenic mice expressing C-reactive protein.	Arginine	22-25	hemolytic complement	Mus musculus	14-17
7980570-1	1994	The murine C-5 cytosine DNA methyltransferase (MTase, E.C.2.1.1.37) containing a hexahistidine affinity leader peptide has been expressed at levels which are at least 50-fold higher than previously reported.	His-His-His-His-His-His	81-94	hemolytic complement	Mus musculus	11-14
8023953-4	1994	After direct instillation of a known inflammatory agent (C5a des Arg) into the airways, transgenic mice with high plasma levels of CRP showed significantly diminished infiltration of neutrophils into bronchoalveolar lavage fluid (BALF) and a significant reduction of BALF total protein levels compared with normal mice.	Arginine	65-68	hemolytic complement	Mus musculus	57-60
7684573-3	1993	The goals of this study were to determine whether 1) cardiac mast cell activation accompanies the C5a response, 2) inhibition of mast cell degranulation inhibits the response, and 3) histamine release plays a role in the C5a-induced myocardial ischemia.	Histamine	183-192	hemolytic complement	Mus musculus	221-224
7684573-7	1993	Intracoronary C5a (500 ng) decreased coronary blood flow (45% of preinfusion levels) and LAD %SS (65% of preinfusion) and was accompanied by increases in coronary venous TxB2 (delta 63.3 ng/ml) and histamine (delta 200 nM).	Histamine	198-207	hemolytic complement	Mus musculus	14-17
34768949-1	2021	Mild hypercortisolism (mHC) is defined as an excessive cortisol secretion, without the classical manifestations of clinically overt Cushing"s syndrome.	Hydrocortisone	55-63	hemolytic complement	Mus musculus	23-26
1712820-5	1991	Release induced by rC5a was calcium-dependent, and peaked at 30 degrees C. These results indicate that functional heterogeneity exists between the CMC and the PMC of BALB/c mice, that C5a is a relevant stimulus for characterization of this heterogeneity, and that CMC from these animals can serve as a convenient in vitro model for the study of human C5a-mast cell interactions.	Calcium	28-35	hemolytic complement	Mus musculus	20-23
1712820-8	1991	The C5a-induced vasopermeability was markedly enhanced in animals that had been previously treated with an inhibitor of serum carboxypeptidase, which converts C5a to the less potent derivative, C5a des Arg.	Arginine	202-205	hemolytic complement	Mus musculus	4-7
33799167-0	2021	MK801 regulates the expression of key osteoarthritis factors in osteoarthritis synovial fibroblasts through complement C5.	Dizocilpine Maleate	0-5	hemolytic complement	Mus musculus	108-121
33799167-4	2021	This study aims to investigate complement C5"s influence on the effect of MK801 on osteoarthritis synovial fibroblasts (OA-SFs).	Dizocilpine Maleate	74-79	hemolytic complement	Mus musculus	31-44
33799167-10	2021	Meanwhile, MK801 can significantly inhibit the expression of complement C5 (C5) in OA-SFs.	Dizocilpine Maleate	11-16	hemolytic complement	Mus musculus	61-74
2009583-3	1991	7-Cl-BA and 7-Br-BA were metabolized considerably at C-3 and C-4, C-5 and C-6, C-8 and C-9, and C-10 and C-11.	7-chlorobenz(a)anthracene	0-7	hemolytic complement	Mus musculus	66-69
2009583-3	1991	7-Cl-BA and 7-Br-BA were metabolized considerably at C-3 and C-4, C-5 and C-6, C-8 and C-9, and C-10 and C-11.	7-bromobenzanthracene	12-19	hemolytic complement	Mus musculus	66-69
1691142-2	1990	Fresh human serum was incubated with zymosan to produce C5a.	Zymosan	37-44	hemolytic complement	Mus musculus	56-59
34768949-4	2021	Measuring cortisol after a 1 mg overnight dexamethasone suppression test is the first-line test for searching for mHC, and the degree of cortisol suppression is associated with the presence of cortisol-related consequences and mortality.	Hydrocortisone	10-18	hemolytic complement	Mus musculus	114-117
34768949-4	2021	Measuring cortisol after a 1 mg overnight dexamethasone suppression test is the first-line test for searching for mHC, and the degree of cortisol suppression is associated with the presence of cortisol-related consequences and mortality.	Dexamethasone	42-55	hemolytic complement	Mus musculus	114-117
35488279-6	2022	In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent.	Reactive Oxygen Species	80-103	hemolytic complement	Mus musculus	34-37
34675657-9	2021	Furthermore, the effect of C5a over-expression on RCC cells" proliferation, migration, and invasion could be blocked by Stattic, a STAT3-specific inhibitor.	stattic	120-127	hemolytic complement	Mus musculus	27-30
34356477-5	2021	Further analysis showed a trend towards an increase in complement component C5a independent of component C3, observed to be tightly regulated by complement factor H. Interestingly, we found that thrombin, a serine protease enzyme, was involved in enhancing the terminal pathway producing C5a, independent of C3.	Serine	207-213	hemolytic complement	Mus musculus	76-79
34356477-5	2021	Further analysis showed a trend towards an increase in complement component C5a independent of component C3, observed to be tightly regulated by complement factor H. Interestingly, we found that thrombin, a serine protease enzyme, was involved in enhancing the terminal pathway producing C5a, independent of C3.	Serine	207-213	hemolytic complement	Mus musculus	288-310
33942437-6	2021	An isomer of trihydroxycholanoyl-taurine was detected in brain tissue samples from both rats and mice with induced HE; however, this isomer was not detected in the brains of healthy rats and mice.	trihydroxycholanoyl-taurine	13-40	hemolytic complement	Mus musculus	115-117
35488279-6	2022	In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent.	Reactive Oxygen Species	105-108	hemolytic complement	Mus musculus	34-37
35488279-6	2022	In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent.	Reactive Oxygen Species	175-178	hemolytic complement	Mus musculus	34-37
35488279-6	2022	In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent.	Reactive Oxygen Species	175-178	hemolytic complement	Mus musculus	153-156
35488279-6	2022	In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent.	mito-ros	180-188	hemolytic complement	Mus musculus	34-37
35488279-6	2022	In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent.	mito-ros	180-188	hemolytic complement	Mus musculus	153-156
35488279-7	2022	Furthermore, we found that C5a induced the production of Mito-ROS by inhibiting mitochondrial STAT3 activity.	mito-ros	57-65	hemolytic complement	Mus musculus	27-30
35488279-8	2022	CONCLUSIONS: By inhibiting mitochondrial STAT3 to elicit Mito-ROS generation, C5a triggers the generation of NETs to promote the development of arterial thrombosis.	mito-ros	57-65	hemolytic complement	Mus musculus	78-81
34655413-6	2022	Furthermore, the plasma levels of proinflammatory molecules (C5a, ICAM-1, IL-6, MCP-1, IL-1beta and TNF-alpha) were found to be elevated (3-fold) in dAGE-fed mice.	dage	149-153	hemolytic complement	Mus musculus	61-64
35509858-16	2022	In the control group, the concentration of Glu in the C5aR-/- group was significantly higher than that in the WT group, and the C5a group was significantly lower than the C5a+C5aRA group.	Glutamic Acid	43-46	hemolytic complement	Mus musculus	171-174
35387346-6	2022	Furthermore, GHI and its major components hydroxysafflower yellow A (HSYA) and aceglutamide (AG) enhanced cell viability and reduced LDH level and C5AR1 expression in a C5A-induced Neuro-2a cell damage model.	aceglutamide	79-91	hemolytic complement	Mus musculus	169-172
35007559-7	2022	In vitro, C5ar2-/- neutrophils exhibited significantly reduced (Ca2+)i flux, reactive oxygen species release, and migratory capacity when activated with immune complexes or exposed to C5a.	Reactive Oxygen Species	77-100	hemolytic complement	Mus musculus	184-187
3397990-5	1988	Reaction with a monoalkylhydrazine gave a 5-nitrobenzothiopyranoindazole adduct, which was catalytically reduced to a corresponding C-5 anilino intermediate.	monoalkylhydrazine	16-34	hemolytic complement	Mus musculus	132-135
2809211-8	1989	All mRNA species studied (SAP, SAA and the complement components C3, C5 and factor B) were induced more rapidly by the thioglycollate stimulus and reached higher peak concentrations.	Thioglycolates	119-133	hemolytic complement	Mus musculus	69-84
2604288-2	1989	The chemotactic responses to autologous zymosan-activated serum (C5a) by neutrophils obtained from uninfected digoxin-treated and control animals were similar; comparable observations were made with circulating granulocytes isolated from animals at 24 or 48 h after intratracheal challenge with 5 x 10(5) colony-forming units (cfu) of bacteria.	Zymosan	40-47	hemolytic complement	Mus musculus	65-68
2604288-2	1989	The chemotactic responses to autologous zymosan-activated serum (C5a) by neutrophils obtained from uninfected digoxin-treated and control animals were similar; comparable observations were made with circulating granulocytes isolated from animals at 24 or 48 h after intratracheal challenge with 5 x 10(5) colony-forming units (cfu) of bacteria.	Digoxin	110-117	hemolytic complement	Mus musculus	65-68
2760478-7	1989	SDS-polyacrylamide gel electrophoresis revealed that mouse C3 and C5 had apparent Mrs of 170,000 and 190,000, respectively.	sds-polyacrylamide	0-18	hemolytic complement	Mus musculus	59-68
3397990-5	1988	Reaction with a monoalkylhydrazine gave a 5-nitrobenzothiopyranoindazole adduct, which was catalytically reduced to a corresponding C-5 anilino intermediate.	5-nitrobenzothiopyranoindazole	42-72	hemolytic complement	Mus musculus	132-135
3397990-8	1988	Described also is the synthesis of selected benzothiopyranoindazole congeners with proximal acylamino side chains at C-5 and B-ring sulfone functionality at S-6.	benzothiopyranoindazole	44-67	hemolytic complement	Mus musculus	117-120
2436653-9	1987	A four-residue basic sequence (Arg-Ser-Lys-Arg) was identified upstream of the amino-terminal Asn of C5a, thereby specifying a beta alpha-chain orientation for the promolecule form of murine C5.	Arginine	31-34	hemolytic complement	Mus musculus	101-104
3669020-4	1987	The N-oxide 7 cannot be converted to a pyrrole in vivo because of the gem-dimethyl substitution at C-5.	n-oxide	4-11	hemolytic complement	Mus musculus	99-102
2434565-8	1987	C5a at 1 nM resulted in contractions equivalent to approximately 50% of the maximal KCl response; normal and mast cell-deficient tissues responded in a similar manner.	Potassium Chloride	84-87	hemolytic complement	Mus musculus	0-3
2434565-9	1987	C5a also released histamine from the normal mouse ileum, in addition to causing contraction of the tissues.	Histamine	18-27	hemolytic complement	Mus musculus	0-3
2436653-9	1987	A four-residue basic sequence (Arg-Ser-Lys-Arg) was identified upstream of the amino-terminal Asn of C5a, thereby specifying a beta alpha-chain orientation for the promolecule form of murine C5.	Serine	35-38	hemolytic complement	Mus musculus	101-104
2436653-9	1987	A four-residue basic sequence (Arg-Ser-Lys-Arg) was identified upstream of the amino-terminal Asn of C5a, thereby specifying a beta alpha-chain orientation for the promolecule form of murine C5.	Lysine	39-42	hemolytic complement	Mus musculus	101-104
2436653-9	1987	A four-residue basic sequence (Arg-Ser-Lys-Arg) was identified upstream of the amino-terminal Asn of C5a, thereby specifying a beta alpha-chain orientation for the promolecule form of murine C5.	Arginine	43-46	hemolytic complement	Mus musculus	101-104
2436653-9	1987	A four-residue basic sequence (Arg-Ser-Lys-Arg) was identified upstream of the amino-terminal Asn of C5a, thereby specifying a beta alpha-chain orientation for the promolecule form of murine C5.	Asparagine	94-97	hemolytic complement	Mus musculus	101-104
6216123-5	1982	Both the response to SRBC and the mixed lymphocyte reaction are enhanced by C5a.	srbc	21-25	hemolytic complement	Mus musculus	76-79
3033240-0	1987	Effect of low dose methotrexate on neutrophil chemotaxis induced by leukotriene B4 and complement C5a.	Methotrexate	19-31	hemolytic complement	Mus musculus	98-101
3033240-2	1987	Pretreatment of mice with low doses of methotrexate inhibits leukotriene B4 or C5a induced neutrophil migration into the air pouch.	Methotrexate	39-51	hemolytic complement	Mus musculus	79-82
6470622-1	1984	Sexual dimorphism of mouse complement component 5 (C5) was detected by isoelectric focusing of desialated ethylenediamine tetraacetic acid (EDTA)-plasma on agarose gel, followed by immunofixation with anti-mouse C5.	Edetic Acid	106-138	hemolytic complement	Mus musculus	51-53
6470622-1	1984	Sexual dimorphism of mouse complement component 5 (C5) was detected by isoelectric focusing of desialated ethylenediamine tetraacetic acid (EDTA)-plasma on agarose gel, followed by immunofixation with anti-mouse C5.	Edetic Acid	140-144	hemolytic complement	Mus musculus	51-53
6470622-1	1984	Sexual dimorphism of mouse complement component 5 (C5) was detected by isoelectric focusing of desialated ethylenediamine tetraacetic acid (EDTA)-plasma on agarose gel, followed by immunofixation with anti-mouse C5.	Sepharose	156-163	hemolytic complement	Mus musculus	51-53
6699874-0	1984	Antiviral activity of C-5 substituted tubercidin analogues.	Tubercidin	38-48	hemolytic complement	Mus musculus	22-25
6699874-7	1984	This study demonstrates the significance of structural modification at C-5 and the potential of C-5 substituted analogues of tubercidin as biologically active agents.	Tubercidin	125-135	hemolytic complement	Mus musculus	96-99
6300969-5	1982	Although resident peritoneal macrophages incubated with chemotactic peptides did not generate O-2, these cells did secrete significant levels of PGE2, PGF2 alpha, and TXB2 in response to C5a.	Dinoprostone	145-149	hemolytic complement	Mus musculus	187-190
6300969-5	1982	Although resident peritoneal macrophages incubated with chemotactic peptides did not generate O-2, these cells did secrete significant levels of PGE2, PGF2 alpha, and TXB2 in response to C5a.	Dinoprost	151-155	hemolytic complement	Mus musculus	187-190
6300969-7	1982	Elicited macrophages generated increased levels of PGE2 and PGF2 alpha when incubated with C5a.	Dinoprostone	51-55	hemolytic complement	Mus musculus	91-94
6300969-7	1982	Elicited macrophages generated increased levels of PGE2 and PGF2 alpha when incubated with C5a.	Dinoprost	60-64	hemolytic complement	Mus musculus	91-94
7310817-1	1981	Hydrogenolysis of 3-(benzyloxy)cyclophosphamide (10) using Pd/C catalyst and ethyl acetate as solvent leads to the formation of 3-hydroxycyclophosphamide (3, approximately 20%) and cyclophosphamide (1, approximately 10%), accompanied by regioselective hydrogen-exchange reactions at the C-4 and C-5 positions in 3 and 1.	3-hydroxycyclophosphamide	128-153	hemolytic complement	Mus musculus	295-298
7182841-5	1982	A good solubility-activity relationship depending on bromine substituents at C-4 and C-5 in the pyridazine-3, 6-dione group was observed.	Bromine	53-60	hemolytic complement	Mus musculus	85-88
7182841-5	1982	A good solubility-activity relationship depending on bromine substituents at C-4 and C-5 in the pyridazine-3, 6-dione group was observed.	pyridazine-3, 6-dione	96-117	hemolytic complement	Mus musculus	85-88
7182841-6	1982	The activity of soluble, pyridazine-3,6-diones depended proportionally on the number of bromine substituents at C-4 and C-5 -contrary to solubility inversely proportional to the number of bromine atoms.	pyridazine-3,6-diones	25-46	hemolytic complement	Mus musculus	120-123
7182841-6	1982	The activity of soluble, pyridazine-3,6-diones depended proportionally on the number of bromine substituents at C-4 and C-5 -contrary to solubility inversely proportional to the number of bromine atoms.	Bromine	88-95	hemolytic complement	Mus musculus	120-123
7310817-1	1981	Hydrogenolysis of 3-(benzyloxy)cyclophosphamide (10) using Pd/C catalyst and ethyl acetate as solvent leads to the formation of 3-hydroxycyclophosphamide (3, approximately 20%) and cyclophosphamide (1, approximately 10%), accompanied by regioselective hydrogen-exchange reactions at the C-4 and C-5 positions in 3 and 1.	3-(benzyloxy)cyclophosphamide	18-47	hemolytic complement	Mus musculus	295-298
7310817-1	1981	Hydrogenolysis of 3-(benzyloxy)cyclophosphamide (10) using Pd/C catalyst and ethyl acetate as solvent leads to the formation of 3-hydroxycyclophosphamide (3, approximately 20%) and cyclophosphamide (1, approximately 10%), accompanied by regioselective hydrogen-exchange reactions at the C-4 and C-5 positions in 3 and 1.	Cyclophosphamide	31-47	hemolytic complement	Mus musculus	295-298
33144519-5	2020	We also observed that p101VVKR777AAAA neutrophils showed enhanced p84-dependent ROS responses to fMLP and C5a, suggesting that competition may exist between p101/p110gamma and p84/p110gamma for Gbetagamma subunits downstream of GPCR activation.	ros	80-83	hemolytic complement	Mus musculus	106-109
7310817-1	1981	Hydrogenolysis of 3-(benzyloxy)cyclophosphamide (10) using Pd/C catalyst and ethyl acetate as solvent leads to the formation of 3-hydroxycyclophosphamide (3, approximately 20%) and cyclophosphamide (1, approximately 10%), accompanied by regioselective hydrogen-exchange reactions at the C-4 and C-5 positions in 3 and 1.	ethyl acetate	77-90	hemolytic complement	Mus musculus	295-298
34027271-10	2021	Excessive complement expression in alcohol-fed PRMT1 knockout mice resulted in further complement activation and an increase in serum C3a and C5a levels, which correlated with inflammation in multiple organs including lung and adipose tissue.	Alcohols	35-42	hemolytic complement	Mus musculus	142-145
34027271-13	2021	C3a and C5a play a role in this liver-lung and liver-adipose interaction in alcohol-fed mice deficient in liver arginine methylation.	Alcohols	76-83	hemolytic complement	Mus musculus	8-11
34027271-13	2021	C3a and C5a play a role in this liver-lung and liver-adipose interaction in alcohol-fed mice deficient in liver arginine methylation.	Arginine	112-120	hemolytic complement	Mus musculus	8-11
33858424-6	2021	RESULTS: To achieve this goal, a traditional nanoantioxidant of nanoceria was surface conjugated with the anti-C5a aptamers (Ceria@Apt) to scavenge the ROS and reduce C5a-mediated inflammation.	Reactive Oxygen Species	152-155	hemolytic complement	Mus musculus	111-114
33852847-6	2021	Stimulation of C5aR+ LysoDCs by C5a increases reactive oxygen species levels, leading to efficient antigen cross-presentation, which elicits an antigen-specific CD8+ T cell response.	Reactive Oxygen Species	46-69	hemolytic complement	Mus musculus	15-18
33551801-10	2020	This translated to a functional outcome in both human and mouse primary macrophages, where SB290157 significantly dampened C5a-induced ERK signaling.	SB 290157	91-99	hemolytic complement	Mus musculus	123-126
32868671-4	2020	Macrophages have previously also been suggested to be pathogenic in mice via binding of C5a to their C5a-receptor, producing reactive oxygen species (ROS), which damages the pulmonary endothelium.	Reactive Oxygen Species	125-148	hemolytic complement	Mus musculus	88-113
32868671-4	2020	Macrophages have previously also been suggested to be pathogenic in mice via binding of C5a to their C5a-receptor, producing reactive oxygen species (ROS), which damages the pulmonary endothelium.	Reactive Oxygen Species	150-153	hemolytic complement	Mus musculus	88-113
32557852-0	2020	C5a/C5aR1 mediates IMQ-induced psoriasiform skin inflammation by promoting IL-17A production from gammadelta-T cells.	Imiquimod	19-22	hemolytic complement	Mus musculus	0-3
32306687-18	2020	Conclusion: The regulation of C5a on the expression of MCP-1 and NGAL may participate in TCE- induced mice kidney damage, and pharmacological inhibition of C5a seems to be an effective way to protect the kidney injury in TCE-sensitized mice.	Trichloroethylene	89-92	hemolytic complement	Mus musculus	30-33
32306687-18	2020	Conclusion: The regulation of C5a on the expression of MCP-1 and NGAL may participate in TCE- induced mice kidney damage, and pharmacological inhibition of C5a seems to be an effective way to protect the kidney injury in TCE-sensitized mice.	Trichloroethylene	89-92	hemolytic complement	Mus musculus	156-159
32306687-18	2020	Conclusion: The regulation of C5a on the expression of MCP-1 and NGAL may participate in TCE- induced mice kidney damage, and pharmacological inhibition of C5a seems to be an effective way to protect the kidney injury in TCE-sensitized mice.	Trichloroethylene	221-224	hemolytic complement	Mus musculus	30-33
32306687-18	2020	Conclusion: The regulation of C5a on the expression of MCP-1 and NGAL may participate in TCE- induced mice kidney damage, and pharmacological inhibition of C5a seems to be an effective way to protect the kidney injury in TCE-sensitized mice.	Trichloroethylene	221-224	hemolytic complement	Mus musculus	156-159
31510052-8	2019	Reactive oxygen species (ROS) formation was detected in C5a-treated mouse KECs; however, W-54011 or NAC pretreatment inhibited high-dose rmC5a-induced ROS formation and also reduced cytochrome c release, apoptotic cell formation, and apoptotic DNA fragmentation.	Reactive Oxygen Species	0-23	hemolytic complement	Mus musculus	56-59
31510052-8	2019	Reactive oxygen species (ROS) formation was detected in C5a-treated mouse KECs; however, W-54011 or NAC pretreatment inhibited high-dose rmC5a-induced ROS formation and also reduced cytochrome c release, apoptotic cell formation, and apoptotic DNA fragmentation.	Reactive Oxygen Species	25-28	hemolytic complement	Mus musculus	56-59
31510052-9	2019	These factors determined the apoptosis of mouse KECs treated with high-dose C5a through C5aR and subsequently led to apoptosis via ROS regeneration and cytochrome c release.	Reactive Oxygen Species	131-134	hemolytic complement	Mus musculus	76-79
31510052-10	2019	The results showed that high concentrations of C5a induced mouse KEC apoptosis via a C5aR/ROS/mitochondria-dependent pathway.	Reactive Oxygen Species	90-93	hemolytic complement	Mus musculus	47-50
31111056-5	2019	Furthermore, C5a and C5aR expression in the cisplatin-treated group was notably increased compared with the control group, and this increase could be significantly inhibited by NAC.	Cisplatin	44-53	hemolytic complement	Mus musculus	13-16
30403186-8	2018	In addition, C5a also increased the Abeta-induced neuro-inflammatory response, and these effects were blocked by the C5aR antagonist, PMX205.	UNII-042A8N37WH	36-41	hemolytic complement	Mus musculus	13-16
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	Trifluoroacetic Acid	237-240	hemolytic complement	Mus musculus	63-66
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	Trifluoroacetic Acid	237-240	hemolytic complement	Mus musculus	77-80
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	cls026	271-277	hemolytic complement	Mus musculus	63-66
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	cls026	271-277	hemolytic complement	Mus musculus	77-80
30536348-3	2018	3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to detect effect of C5a and C5aR antagonists on vitality of microglial cells.	3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide	0-65	hemolytic complement	Mus musculus	107-110
30403186-11	2018	CONCLUSION: The complement protein C5a could exaggerate the Abeta-induced neuroinflammatory response in microglia, and C5aR may be a potential therapeutic tool for AD treatment.	UNII-042A8N37WH	60-65	hemolytic complement	Mus musculus	35-38
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	SB 290157	193-235	hemolytic complement	Mus musculus	63-66
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	SB 290157	193-235	hemolytic complement	Mus musculus	77-80
30507785-5	2019	Knockout of TRPV1 or pretreatment with the TRPV1 antagonists, AMG9810 or 5"-iodoresiniferatoxin (5"-IRTX), significantly reduced C5a-induced mechanical sensitization.	3-(4-t-butylphenyl)-N-(2,3-dihydrobenzo(b)(1,4)dioxin-6-yl)acrylamide	62-69	hemolytic complement	Mus musculus	129-132
30507785-5	2019	Knockout of TRPV1 or pretreatment with the TRPV1 antagonists, AMG9810 or 5"-iodoresiniferatoxin (5"-IRTX), significantly reduced C5a-induced mechanical sensitization.	iodoresiniferatoxin	73-95	hemolytic complement	Mus musculus	129-132
30507785-5	2019	Knockout of TRPV1 or pretreatment with the TRPV1 antagonists, AMG9810 or 5"-iodoresiniferatoxin (5"-IRTX), significantly reduced C5a-induced mechanical sensitization.	iodoresiniferatoxin	97-104	hemolytic complement	Mus musculus	129-132
30507785-6	2019	Notably, local administration of 5"-IRTX 90 minutes after C5a injection resulted in a slow, but complete, reversal of mechanical sensitization, indicating that TRPV1 activity was required for maintaining C5a-induced mechanical hypersensitivity.	iodoresiniferatoxin	33-40	hemolytic complement	Mus musculus	58-61
30507785-6	2019	Notably, local administration of 5"-IRTX 90 minutes after C5a injection resulted in a slow, but complete, reversal of mechanical sensitization, indicating that TRPV1 activity was required for maintaining C5a-induced mechanical hypersensitivity.	iodoresiniferatoxin	33-40	hemolytic complement	Mus musculus	204-207
30403186-8	2018	In addition, C5a also increased the Abeta-induced neuro-inflammatory response, and these effects were blocked by the C5aR antagonist, PMX205.	hydrocinnamate-cyclo(ornithyl-prolyl-cyclohexylalanyl-tryptophyl-arginyl)	134-140	hemolytic complement	Mus musculus	13-16
29881374-4	2018	Here, we demonstrate the impact of C5a blockade on Treg induction and microvascular restoration in rejecting mouse airway allografts.	treg	51-55	hemolytic complement	Mus musculus	35-38
29294056-8	2018	In db/db mice, administration of a novel C5a inhibitor, NOX-D21, reduced the serum triglyceride level and attenuated the upregulation of diacylglycerolacyltransferase-1 and sterol-regulatory element binding protein-1 expression and lipid accumulation in diabetic kidney.	Triglycerides	83-95	hemolytic complement	Mus musculus	41-44
29602515-6	2018	Then, C5a/C5aR1 induces the release of leukotriene B4 (LTB4) from the arrested neutrophils.	Leukotriene B4	39-53	hemolytic complement	Mus musculus	6-9
28315675-8	2017	Although no effect of CCL2 inhibition was detected, treatment with the C5a inhibitor, NOX-D21, rescued the phenotype of nonexercised mdx mice, but not of exercised ones.	nicotine 1-N-oxide	86-89	hemolytic complement	Mus musculus	71-74
29017823-6	2018	The reduction of early erythroblast numbers in spleen was enhanced by the phenylhydrazine-induced pernicious anemia model knock-in mice and was rescued by a functional analogue of RP S19 dimer S-tagged C5a/RP S19.	phenylhydrazine	74-89	hemolytic complement	Mus musculus	202-205
29285167-0	2017	Effectiveness of C5a aptamers in a TNBS-induced colitis mouse model.	Trinitrobenzenesulfonic Acid	35-39	hemolytic complement	Mus musculus	17-20
28477014-8	2017	These results demonstrated that anti-C5 antibody targeting MG4 domain inhibited CNV in neovascular AMD.	mg4	59-62	hemolytic complement	Mus musculus	37-39
27543123-8	2016	In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent.	Reactive Oxygen Species	123-146	hemolytic complement	Mus musculus	50-53
28052346-7	2017	Complement became activated in mice receiving 5-FU, indicated by increased intestinal levels of C3a and C5a.	Fluorouracil	46-50	hemolytic complement	Mus musculus	104-107
27974594-7	2017	Macrophage depletion reversed C5a agonist peptide-induced TNF-alpha up-regulation and APN down-regulation in the PVAT of DOCA mice.	Desoxycorticosterone Acetate	121-125	hemolytic complement	Mus musculus	30-33
28167912-0	2017	C5a Regulates IL-1beta Production and Leukocyte Recruitment in a Murine Model of Monosodium Urate Crystal-Induced Peritonitis.	Uric Acid	81-97	hemolytic complement	Mus musculus	0-3
28167912-7	2017	Mechanistic studies revealed that C5a most likely increased NLRP3 inflammasome activation via production of reactive oxygen species (ROS), and not through increased transcription of inflammasome components.	Reactive Oxygen Species	108-131	hemolytic complement	Mus musculus	34-37
28167912-7	2017	Mechanistic studies revealed that C5a most likely increased NLRP3 inflammasome activation via production of reactive oxygen species (ROS), and not through increased transcription of inflammasome components.	Reactive Oxygen Species	133-136	hemolytic complement	Mus musculus	34-37
28167912-8	2017	Therefore we conclude that C5a generated upon MSU-induced complement activation increases neutrophil recruitment in vivo by promoting IL-1 production via the generation of ROS, which activate the NLRP3 inflammasome.	Reactive Oxygen Species	172-175	hemolytic complement	Mus musculus	27-30
28107529-7	2017	The CS was found to be activated early in the diabetic wounds as demonstrated by increased anaphylatoxin C5a in wound fluid and C3-fragment deposition by immunostaining.	Cesium	4-6	hemolytic complement	Mus musculus	105-108
27939824-10	2017	(i) Catecholamines may stimulate macrophages and release complement C5 via alpha2-receptors.	Catecholamines	4-18	hemolytic complement	Mus musculus	57-70
27253992-6	2017	Moreover, the DEN-induced tumors overexpressed mRNAs for the oncogene-induced senescence (OIS) markers such as p15Ink4b and p19Arf as well as pro-survival/pro-proliferative cytokines/chemokines such as complement C5/C5a, ICAM-1, IL-1 receptor antagonist and CXCL9, suggesting that the BrafV637E mutation influences the expression of genes involved in either OIS or cellular growth/survival.	Diethylnitrosamine	14-17	hemolytic complement	Mus musculus	216-219
28028363-14	2016	Moreover, inhibition of p38-MAPK activity with SB203580 reduced SphK1 protein production significantly in PEMs after C5a stimulation.	SB 203580	47-55	hemolytic complement	Mus musculus	117-120
27543123-8	2016	In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent.	Reactive Oxygen Species	123-146	hemolytic complement	Mus musculus	56-59
27543123-8	2016	In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent.	Reactive Oxygen Species	148-151	hemolytic complement	Mus musculus	50-53
27543123-8	2016	In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent.	Reactive Oxygen Species	148-151	hemolytic complement	Mus musculus	56-59
27147658-8	2016	Macrophage depletion in transgenic macrophage Fas-induced apoptosis mice abolished C5a-dependent thermal hyperalgesia.	ammonium ferrous sulfate	46-49	hemolytic complement	Mus musculus	83-86
27531651-5	2016	We discovered a unique role for p110beta in supporting synergistic PIP3 formation in response to the coactivation of macrophages by macrophage colony-stimulating factor (M-CSF) and the complement protein C5a.	PIP3	67-71	hemolytic complement	Mus musculus	204-207
27480930-4	2016	The responses for C5a and ADP were abolished by pertussis toxin (PTX), but not rho-associated protein kinase inhibitor, Y-27632, indicating that C5a and ADP elicited responses through the Galphai pathway.	Adenosine Diphosphate	26-29	hemolytic complement	Mus musculus	145-148
27480930-4	2016	The responses for C5a and ADP were abolished by pertussis toxin (PTX), but not rho-associated protein kinase inhibitor, Y-27632, indicating that C5a and ADP elicited responses through the Galphai pathway.	Adenosine Diphosphate	153-156	hemolytic complement	Mus musculus	18-21
26095957-0	2016	Complement C5a-C5aR interaction enhances MAPK signaling pathway activities to mediate renal injury in trichloroethylene sensitized BALB/c mice.	Trichloroethylene	102-119	hemolytic complement	Mus musculus	11-14
26095957-3	2016	The present study tested the hypothesis that anaphylatoxin C5a binding to its receptor C5aR mediates renal injury in TCE-sensitized BALB/c mice.	Trichloroethylene	117-120	hemolytic complement	Mus musculus	59-62
26095957-6	2016	TCE sensitization up-regulated C5a and C5aR expressions in kidney tissue, generated inflammatory infiltration, renal tubule damage, glomerular hypercellularity and impaired renal function.	Trichloroethylene	0-3	hemolytic complement	Mus musculus	31-34
26095957-10	2016	These data identify C5a binding to C5aR, MAP kinase activation, and inflammatory cytokine release as a novel mechanism for complement-mediated renal injury by sensitization with TCE or other environmental chemicals.	Trichloroethylene	178-181	hemolytic complement	Mus musculus	20-23
25736459-5	2015	Deficiency in key components of complement (e.g., C3, C5, or C5a receptor) rendered tumor repression in mice subjected to AOM/DSS.	Dextran Sulfate	126-129	hemolytic complement	Mus musculus	61-64
26475925-5	2015	In neutrophils, complement 5a (C5a) inspires strong ER stress through inositol-requiring kinase 1a and, to a less extent, the protein kinase R-like ER kinase signaling pathway.	Inositol	70-78	hemolytic complement	Mus musculus	31-34
27382187-8	2016	C5a"s suppressive effects were negated during phosphoinositide 3-kinase (PI3K) inhibition by wortmannin but were largely preserved in the absence of C5aR1.	Wortmannin	93-103	hemolytic complement	Mus musculus	0-3
25982331-1	2015	Combination of the Suzuki cross-coupling and nucleophilic aromatic substitution of hydrogen (SN(H)) reactions proved to be a convenient method for the synthesis of C(4) and/or C(5) mono(thienyl) and di(thienyl) substituted pyrimidines from commercially available 5-bromopyrimidine.	Hydrogen	83-91	hemolytic complement	Mus musculus	176-180
25981118-2	2015	METHODS: In C57BL/6 J mice CNV was induced by argon-laser, C5a-inhibitor (NOX-D20) was intravitreally injected in three concentrations: 0.3, 3.0, and 30 mg/ml.	NOX-D20	74-81	hemolytic complement	Mus musculus	59-62
25790939-7	2015	Significantly, application of Rho-associated kinase inhibitor, Y27632, prevented the protein leaking effects observed in both C5a-treated purified endothelial cells and mice.	Y 27632	63-69	hemolytic complement	Mus musculus	126-129
25982331-1	2015	Combination of the Suzuki cross-coupling and nucleophilic aromatic substitution of hydrogen (SN(H)) reactions proved to be a convenient method for the synthesis of C(4) and/or C(5) mono(thienyl) and di(thienyl) substituted pyrimidines from commercially available 5-bromopyrimidine.	sn(h)	93-98	hemolytic complement	Mus musculus	176-180
25982331-1	2015	Combination of the Suzuki cross-coupling and nucleophilic aromatic substitution of hydrogen (SN(H)) reactions proved to be a convenient method for the synthesis of C(4) and/or C(5) mono(thienyl) and di(thienyl) substituted pyrimidines from commercially available 5-bromopyrimidine.	5-bromopyrimidine	263-280	hemolytic complement	Mus musculus	176-180
25822713-11	2015	Treating Lsecs with a physiological level of LPA significantly enhanced the protein levels of angiogenesis related proteins (cyr61 and TIMP-1), cytokines (C5/C5a, M-CSF, and SDF-1), and chemokines (MCP-5, gp130, CCL28, and CXCL16).	lysophosphatidic acid	45-48	hemolytic complement	Mus musculus	155-161
25901944-6	2015	Finally, our structural model provides the molecular basis for the Spiegelmer affinity improvement through positional L-ribonucleotide to L-deoxyribonucleotide exchanges and for its inhibition of the C5a:C5aR interaction.	l-ribonucleotide	118-134	hemolytic complement	Mus musculus	200-203
25901944-6	2015	Finally, our structural model provides the molecular basis for the Spiegelmer affinity improvement through positional L-ribonucleotide to L-deoxyribonucleotide exchanges and for its inhibition of the C5a:C5aR interaction.	l-deoxyribonucleotide	138-159	hemolytic complement	Mus musculus	200-203
25822713-12	2015	The LPAR1 and LPAR3 antagonist ki16425 significantly inhibited the LPA-enhanced expression of cyr61, TIMP-1, SDF-1, MCP-5, gp130, CCL28, and CXCL16, but not that of C5/C5a or M-CSF.	3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acid	31-38	hemolytic complement	Mus musculus	165-171
23837638-8	2014	The accumulated silver ions in the kidney not only interacted with the kidney cells membrane but also induced a rapid increase of complement fraction C3 followed by a significant consumption and C3a and C5a production significantly in the serum, which resulted in kidney oxidative damage and eventually led to the morphological changes and filtration function impairment of the glomerulus.	Silver	16-22	hemolytic complement	Mus musculus	203-206
25822713-12	2015	The LPAR1 and LPAR3 antagonist ki16425 significantly inhibited the LPA-enhanced expression of cyr61, TIMP-1, SDF-1, MCP-5, gp130, CCL28, and CXCL16, but not that of C5/C5a or M-CSF.	lysophosphatidic acid	4-7	hemolytic complement	Mus musculus	165-171
25822713-13	2015	LPA-induced C5/C5a and M-CSF expression may have been through an indirect regulation mechanism.	lysophosphatidic acid	0-3	hemolytic complement	Mus musculus	12-18
25573852-6	2015	Furthermore, we identified the complement 5a (C5a) as the major C3 activation product that was involved in macrophage polarization and DOCA-salt-induced vascular injury.	Desoxycorticosterone Acetate	135-139	hemolytic complement	Mus musculus	46-49
25573852-6	2015	Furthermore, we identified the complement 5a (C5a) as the major C3 activation product that was involved in macrophage polarization and DOCA-salt-induced vascular injury.	Salts	140-144	hemolytic complement	Mus musculus	46-49
25573852-8	2015	CONCLUSIONS: The presence and activation of bone marrow-derived macrophages in PVAT are crucial for complement activation in hypertensive vascular inflammation, and C5a plays a critical role in DOCA-salt-induced vascular injury by stimulating macrophage polarization toward a proinflammatory M1 phenotype in PVAT.	Desoxycorticosterone Acetate	194-198	hemolytic complement	Mus musculus	165-168
25573852-8	2015	CONCLUSIONS: The presence and activation of bone marrow-derived macrophages in PVAT are crucial for complement activation in hypertensive vascular inflammation, and C5a plays a critical role in DOCA-salt-induced vascular injury by stimulating macrophage polarization toward a proinflammatory M1 phenotype in PVAT.	Salts	199-203	hemolytic complement	Mus musculus	165-168
24397921-7	2014	Addition of C5a completely blocked ASP signaling and activity in both C5aRKO and WT adipocytes as well as 3T3-L1 adipocytes.	Aspartic Acid	35-38	hemolytic complement	Mus musculus	12-15
24604562-7	2014	In vitro C5a administration accelerates MHV-3-induced Fgl2 secretion by macrophages.	mhv-3	40-45	hemolytic complement	Mus musculus	9-12
24604562-9	2014	CONCLUSION: These data provide evidence that mouse susceptibility to MHV-3-induced FH may rely on C5a/C5aR interactions, for which ERK1/2 and p38 pathways participate in up-regulating Fgl2 expression.	mhv-3	69-74	hemolytic complement	Mus musculus	98-101
25169086-0	2014	[Levels of complement components C3a and C5a in renal injury among trichloroethylene-sensitized BALB/c mice].	Trichloroethylene	67-84	hemolytic complement	Mus musculus	41-44
25169086-1	2014	OBJECTIVE: To determine the levels of complement components C3a and C5a in the kidneys of trichloroethylene (TCE)-sensitized BALB/c mice, and to investigate the role of complement components in TCE-induced renal injury among BALB/c mice.	Trichloroethylene	90-107	hemolytic complement	Mus musculus	68-71
25169086-1	2014	OBJECTIVE: To determine the levels of complement components C3a and C5a in the kidneys of trichloroethylene (TCE)-sensitized BALB/c mice, and to investigate the role of complement components in TCE-induced renal injury among BALB/c mice.	Trichloroethylene	109-112	hemolytic complement	Mus musculus	68-71
25169086-13	2014	Levels of complement components C3a and C5a are elevated in the kidneys of sensitized mice, indicating that C3a and C5a may be involved in the renal injury induced by TCE sensitization.	Trichloroethylene	167-170	hemolytic complement	Mus musculus	40-43
25169086-13	2014	Levels of complement components C3a and C5a are elevated in the kidneys of sensitized mice, indicating that C3a and C5a may be involved in the renal injury induced by TCE sensitization.	Trichloroethylene	167-170	hemolytic complement	Mus musculus	116-119
24574221-4	2014	METHODS: An anti-C5a vaccine was generated by incorporating the unnatural amino acid p-nitrophenylalanine (4NPA) into selected sites in the murine C5a molecule.	amino acid p-nitrophenylalanine	74-105	hemolytic complement	Mus musculus	17-20
24574221-4	2014	METHODS: An anti-C5a vaccine was generated by incorporating the unnatural amino acid p-nitrophenylalanine (4NPA) into selected sites in the murine C5a molecule.	amino acid p-nitrophenylalanine	74-105	hemolytic complement	Mus musculus	147-150
24574221-4	2014	METHODS: An anti-C5a vaccine was generated by incorporating the unnatural amino acid p-nitrophenylalanine (4NPA) into selected sites in the murine C5a molecule.	4npa	107-111	hemolytic complement	Mus musculus	17-20
24574221-4	2014	METHODS: An anti-C5a vaccine was generated by incorporating the unnatural amino acid p-nitrophenylalanine (4NPA) into selected sites in the murine C5a molecule.	4npa	107-111	hemolytic complement	Mus musculus	147-150
24574221-8	2014	RESULTS: Replacing a single tyrosine residue in position 35 (Y(35) ) with 4NPA allowed the generation of an anti-C5a vaccine, which partly protected mice against the development of CIA while strongly ameliorating the severity of clinical disease.	Tyrosine	28-36	hemolytic complement	Mus musculus	113-116
24631530-4	2014	Abrogation of C5a-induced receptor internalization by treatment with the dynamin inhibitor dynasore(TM) impaired C5a-induced MEK and ERK signaling.	N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide	91-99	hemolytic complement	Mus musculus	14-17
24631530-4	2014	Abrogation of C5a-induced receptor internalization by treatment with the dynamin inhibitor dynasore(TM) impaired C5a-induced MEK and ERK signaling.	N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide	91-99	hemolytic complement	Mus musculus	113-116
23911420-1	2013	BACKGROUND: Complement component C5-derived C5a locally generated in the brain has been shown to protect against glutamate-induced neuronal apoptosis and beta-amyloid (Abeta) toxicity, but the mechanism is not clear.	Glutamic Acid	113-122	hemolytic complement	Mus musculus	44-47
24184716-8	2014	Increased glutamate release was observed in cortical neurons in culture exposed to C5a.	Glutamic Acid	10-19	hemolytic complement	Mus musculus	83-86
24218268-5	2014	Here, we describe three assays to assess C5a-mediated effector functions: (1) increase in (Ca(2+))i in bone marrow-derived neutrophils using the intracellular fluorescent Ca(2+)-sensitive indicator Fluo-4 AM and flow cytometry-based methods; (2) in vitro migration of murine, bone marrow-derived neutrophils using a modified Boyden chamber; and (3) in vivo migration of neutrophils from the circulation into the peritoneal cavity.	fluo-4 am	198-207	hemolytic complement	Mus musculus	41-44
24044938-0	2013	Synthesis and in vitro/in vivo antibacterial activity of oxazolidinones having thiocarbamate at C-5 on the A-ring and an amide- or urea-substituted [1,2,5]triazepane or [1,2,5]oxadiazepane as the C-ring.	Oxazolidinones	57-71	hemolytic complement	Mus musculus	96-99
24044938-0	2013	Synthesis and in vitro/in vivo antibacterial activity of oxazolidinones having thiocarbamate at C-5 on the A-ring and an amide- or urea-substituted [1,2,5]triazepane or [1,2,5]oxadiazepane as the C-ring.	Thiocarbamates	79-92	hemolytic complement	Mus musculus	96-99
24203680-7	2013	The concentrations of serum complement components C3a-desArg, C5a-desArg, and C5b-9 were significantly increased in 24-hour, 48-hour, and 72-hour sensitization-positive groups treated with TCE and peaked in the 72-hour sensitization-positive group.	Trichloroethylene	189-192	hemolytic complement	Mus musculus	62-65
23802687-1	2013	We examined the effects of six furocoumarins with alkoxy groups at the C-5 or C-8 position isolated from Umbelliferae medicinal plants on cell proliferation, and their mechanisms of action against B16F10 melanoma cells or in melanin-possessing hairless mice implanted with B16F10 cells, under UVA irradiation.	Furocoumarins	31-44	hemolytic complement	Mus musculus	71-74
23802687-2	2013	Three furocoumarins with an alkoxy group at C-5, isoimperatorin (1), oxypeucedanin (2) and oxypeucedanin hydrate (3), showed antiproliferative activity and caused G2/M arrest at concentrations of 0.1-10.0 mum.	Furocoumarins	6-19	hemolytic complement	Mus musculus	44-47
23802687-6	2013	We suggest that the antitumor actions of UVA plus furocoumarins with an alkoxy group at C-5 or C-8 were due to G2/M arrest of the cell cycle by an increase in phosphor-Chk1 and decrease in phospho-cdc2.	Furocoumarins	50-63	hemolytic complement	Mus musculus	88-91
23442682-2	2012	The polygalacturonic acid (AE-CWI) contained 95% GalA and its (13)C NMR spectrum showed signals at delta 98.9, 78.0, 71.4, 69.1, 68.4, and 175.1 from C-1, C-4, C-5, C-3, C-2, and C-6 respectively, from (1 4)-linked alpha-GalpA units.	polygalacturonic acid	4-25	hemolytic complement	Mus musculus	160-163
25436577-1	2013	The methylation of the C-5 position of deoxycytidine (dC) in the promoter regions of tumor suppressor genes is often observed in cancer cells.	Deoxycytidine	39-52	hemolytic complement	Mus musculus	23-26
25436577-1	2013	The methylation of the C-5 position of deoxycytidine (dC) in the promoter regions of tumor suppressor genes is often observed in cancer cells.	Deoxycytidine	54-56	hemolytic complement	Mus musculus	23-26
23675299-9	2013	SB203580, a receptor-interacting protein 2 (RIP2) inhibitor downstream of NOD2, reduced C5a generation by enhancing CD55 expression on neutrophils, resulting in attenuation of polymicrobial sepsis.	SB 203580	0-8	hemolytic complement	Mus musculus	88-91
23071133-8	2013	C5a most likely exerts its function via mast cell activation since the mast cell inhibitor cromolyn totally blocked C5a-enhanced vein graft disease.	Cromolyn Sodium	91-99	hemolytic complement	Mus musculus	0-3
23071133-8	2013	C5a most likely exerts its function via mast cell activation since the mast cell inhibitor cromolyn totally blocked C5a-enhanced vein graft disease.	Cromolyn Sodium	91-99	hemolytic complement	Mus musculus	116-119
23093649-9	2013	We identified a serine protease from the midgut of tenebrio molitor larvae in CDEs which was able to induce the release of biologically active C5a in murine BAL.	ACE protocol 1	78-82	hemolytic complement	Mus musculus	143-146
23442682-2	2012	The polygalacturonic acid (AE-CWI) contained 95% GalA and its (13)C NMR spectrum showed signals at delta 98.9, 78.0, 71.4, 69.1, 68.4, and 175.1 from C-1, C-4, C-5, C-3, C-2, and C-6 respectively, from (1 4)-linked alpha-GalpA units.	ae-cwi	27-33	hemolytic complement	Mus musculus	160-163
24634797-5	2013	Long-term treatment with muramyl dipeptide (MDP), a NOD2 ligand, enhanced C5a-mediated expression of chemokine mRNAs in RAW 264.7 cells.	Acetylmuramyl-Alanyl-Isoglutamine	25-42	hemolytic complement	Mus musculus	74-77
24634797-5	2013	Long-term treatment with muramyl dipeptide (MDP), a NOD2 ligand, enhanced C5a-mediated expression of chemokine mRNAs in RAW 264.7 cells.	Acetylmuramyl-Alanyl-Isoglutamine	44-47	hemolytic complement	Mus musculus	74-77
23630572-4	2013	RESULTS: In Ctl mice, WAT C5L2 and C5a receptor mRNA increased (up to 10-fold) both over time and with DIO.	3,3'-Dioctadecyloxacarbocyanine perchlorate	103-106	hemolytic complement	Mus musculus	35-38
22924972-2	2013	The purpose of this study was to further build on this evidence by examining the efficacy, mechanism and specificity of a potent, non-competitive and orally active C5a receptor (CD88) antagonist, PMX205, in the dextran sulphate sodium (DSS) model of murine innate colitis.	dextran sulphate sodium	211-234	hemolytic complement	Mus musculus	164-167
22406418-15	2012	Based on these results we propose that estradiol may differentially modulate C5a-induced Ca(2+)-influx via L-VGCCs in neurons depending on the expression of the two ER isotypes.	Estradiol	39-48	hemolytic complement	Mus musculus	77-80
22535677-3	2012	We found that cDCs lack C5a receptor (C5aR) and do not respond to C5a directly.	Chenodeoxycholate 3-sulphate	14-18	hemolytic complement	Mus musculus	24-27
22430971-5	2012	We demonstrate in this in vitro study that the combination of two matrices with different subliming properties ((hexamethylcyclotrisiloxane [HMCS] and cyclododecane [CDD]) containing 10% labile C5A yielded the best results in terms of controlled release and preserved anti-HIV activity of the peptide when pre-exposed to cell-free medium or cell culture at body temperature for up to 2 months.	CYCLODODECANE	151-164	hemolytic complement	Mus musculus	194-197
21802065-2	2011	STUDY DESIGN: C5a peptidase was encapsulated in semipermeable microspheres of poly(lactide-coglycolide) (PLGA).	Polyglactin 910	78-103	hemolytic complement	Mus musculus	14-17
22503964-2	2012	Here we show that complement C5a exhibits anxiolytic-like activity via the PGD(2) system.	Prostaglandin D2	75-81	hemolytic complement	Mus musculus	29-32
22503964-4	2012	C5a-induced anxiolytic-like activity was inhibited by indomethacin, a cyclooxygenase inhibitor, or BWA868C, an antagonist of DP(1) receptor for PGD(2), respectively.	Indomethacin	54-66	hemolytic complement	Mus musculus	0-3
22503964-4	2012	C5a-induced anxiolytic-like activity was inhibited by indomethacin, a cyclooxygenase inhibitor, or BWA868C, an antagonist of DP(1) receptor for PGD(2), respectively.	BW A868C	99-106	hemolytic complement	Mus musculus	0-3
22503964-4	2012	C5a-induced anxiolytic-like activity was inhibited by indomethacin, a cyclooxygenase inhibitor, or BWA868C, an antagonist of DP(1) receptor for PGD(2), respectively.	Prostaglandins D	144-147	hemolytic complement	Mus musculus	0-3
22503964-5	2012	The anxiolytic effect of C5a was also blocked by SCH58261 or bicuculline, antagonists of adenosine A(2A) and GABA(A) receptors, respectively, which were activated downstream of PGD(2)-DP(1) receptor.	5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine	49-57	hemolytic complement	Mus musculus	25-28
22503964-5	2012	The anxiolytic effect of C5a was also blocked by SCH58261 or bicuculline, antagonists of adenosine A(2A) and GABA(A) receptors, respectively, which were activated downstream of PGD(2)-DP(1) receptor.	Bicuculline	61-72	hemolytic complement	Mus musculus	25-28
22503964-6	2012	These results suggest that C5a exhibits anxiolytic-like activity via the PGD(2)-DP(1) receptor system coupled to the activation of adenosine A(2A) and GABA(A) receptors.	adenosine a	131-142	hemolytic complement	Mus musculus	27-30
21421909-10	2011	Together, these studies indicate that PQ-induced ALI is mediated through receptor signaling by the C3a and C5a complement activation products that are generated via the alternative complement pathway, and that complement inhibition may be an effective clinical intervention for postexposure treatment of PQ-induced ALI.	Paraquat	38-40	hemolytic complement	Mus musculus	107-110
21421909-10	2011	Together, these studies indicate that PQ-induced ALI is mediated through receptor signaling by the C3a and C5a complement activation products that are generated via the alternative complement pathway, and that complement inhibition may be an effective clinical intervention for postexposure treatment of PQ-induced ALI.	Paraquat	304-306	hemolytic complement	Mus musculus	107-110
21859896-6	2011	In vitro signaling studies indicated that LPS or C5a, or the combination, caused phosphorylation of Akt occurring at threonine 308 but not at serine 473.	Threonine	117-126	hemolytic complement	Mus musculus	49-52
21859896-6	2011	In vitro signaling studies indicated that LPS or C5a, or the combination, caused phosphorylation of Akt occurring at threonine 308 but not at serine 473.	Serine	142-148	hemolytic complement	Mus musculus	49-52
21106540-9	2011	The actions of C5a were sensitive to pertussis toxin and PD98059, suggesting a role of G protein-mediated activation of the Erk1/2 pathway.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	57-64	hemolytic complement	Mus musculus	15-18
21736743-12	2011	PMX53 blocked sensitization of C-fiber afferents to heat by C5a but did not by itself influence ongoing activity or heat sensitivity in afferents innervating control or incised skin.	AcPhe(ornithine-Pro-cyclohexylamine-Trp-Arg)	0-5	hemolytic complement	Mus musculus	60-63
21273683-4	2010	The time courses of protection by bergapten, imperatorin, oxypeucedanin and xanthotoxin against maximal electroshock-induced seizures revealed that 300 mg/kg imperatorin and xanthotoxin (C-8 substituted derivatives of psoralen) exerted strong anticonvulsant activity, whereas 300 mg/kg bergapten and oxypeucedanin (C-5 substituted derivatives of psoralen) did not produce any anticonvulsant activity in this model.	Methoxsalen	174-185	hemolytic complement	Mus musculus	315-318
20723031-11	2010	The plasma concentrations of C5a, factor D and transforming growth factor-beta1 were increased in TAFI/ApoE double-deficient mice treated with stz compared with the mice of the same genotype treated with saline.	Streptozocin	143-146	hemolytic complement	Mus musculus	29-79
20723031-11	2010	The plasma concentrations of C5a, factor D and transforming growth factor-beta1 were increased in TAFI/ApoE double-deficient mice treated with stz compared with the mice of the same genotype treated with saline.	Sodium Chloride	204-210	hemolytic complement	Mus musculus	29-79
20813409-0	2010	CNS-specific expression of C3a and C5a exacerbate demyelination severity in the cuprizone model.	Cuprizone	80-89	hemolytic complement	Mus musculus	35-38
19800413-7	2009	These results suggest that C5a stimulates food intake via a PGD(2)- and NPY-dependent mechanism.	Prostaglandin D2	60-66	hemolytic complement	Mus musculus	27-30
20153643-1	2010	Analog 8, a 3-pyridinecarbonitrile with an (E)-2-[6-[(4-methylpiperazin-1-yl)methyl]pyridin-2-yl]vinyl group at C-5, had an IC(50) value of 1.1 nM for the inhibition of PKCtheta and potently blocked the production of IL-2 in both stimulated murine T cells (IC(50)=34 nM) and human whole blood (IC(50)=500 nM).	3-cyanopyridine	12-34	hemolytic complement	Mus musculus	112-115
20153643-1	2010	Analog 8, a 3-pyridinecarbonitrile with an (E)-2-[6-[(4-methylpiperazin-1-yl)methyl]pyridin-2-yl]vinyl group at C-5, had an IC(50) value of 1.1 nM for the inhibition of PKCtheta and potently blocked the production of IL-2 in both stimulated murine T cells (IC(50)=34 nM) and human whole blood (IC(50)=500 nM).	[(4-methylpiperazin-1-yl)methyl]pyridin-2-yl	52-96	hemolytic complement	Mus musculus	112-115
20031321-10	2010	C5a and C3a application elevated [Ca(2+)](i) and facilitated capsaicin-induced [Ca(2+)](i) responses in DRG neurons.	Capsaicin	61-70	hemolytic complement	Mus musculus	0-3
20606325-2	2010	CPR removes the C-terminal arginine from inflammatory peptides such as C3a and C5a, bradykinin, enkephalin, and the thrombin-cleaved N-terminal fragment osteopontin (cleaved N-OPN).	Arginine	27-35	hemolytic complement	Mus musculus	79-82
19800413-0	2009	Complement C5a stimulates food intake via a prostaglandin D(2)- and neuropeptide Y-dependent mechanism in mice.	Prostaglandin D2	44-62	hemolytic complement	Mus musculus	11-14
19800413-2	2009	Here we show that complement C5a stimulates food intake by activating the orexigenic PGD(2) system.	Prostaglandin D2	85-91	hemolytic complement	Mus musculus	29-32
20718497-0	2010	Inhibition of mycobacterial replication by pyrimidines possessing various C-5 functionalities and related 2"-deoxynucleoside analogues using in vitro and in vivo models.	Pyrimidines	43-54	hemolytic complement	Mus musculus	74-77
20664064-2	2010	Here, we show that macrophages navigate in a gradient of the chemoattractant C5a through the release of adenosine triphosphate (ATP) and autocrine "purinergic feedback loops" that involve receptors for ATP (P2Y(2)), adenosine diphosphate (ADP) (P2Y(12)), and adenosine (A2a, A2b, and A3).	Adenosine Triphosphate	104-126	hemolytic complement	Mus musculus	77-80
20664064-2	2010	Here, we show that macrophages navigate in a gradient of the chemoattractant C5a through the release of adenosine triphosphate (ATP) and autocrine "purinergic feedback loops" that involve receptors for ATP (P2Y(2)), adenosine diphosphate (ADP) (P2Y(12)), and adenosine (A2a, A2b, and A3).	Adenosine Triphosphate	128-131	hemolytic complement	Mus musculus	77-80
20664064-2	2010	Here, we show that macrophages navigate in a gradient of the chemoattractant C5a through the release of adenosine triphosphate (ATP) and autocrine "purinergic feedback loops" that involve receptors for ATP (P2Y(2)), adenosine diphosphate (ADP) (P2Y(12)), and adenosine (A2a, A2b, and A3).	Adenosine Triphosphate	202-205	hemolytic complement	Mus musculus	77-80
20664064-2	2010	Here, we show that macrophages navigate in a gradient of the chemoattractant C5a through the release of adenosine triphosphate (ATP) and autocrine "purinergic feedback loops" that involve receptors for ATP (P2Y(2)), adenosine diphosphate (ADP) (P2Y(12)), and adenosine (A2a, A2b, and A3).	Adenosine Diphosphate	216-237	hemolytic complement	Mus musculus	77-80
20664064-2	2010	Here, we show that macrophages navigate in a gradient of the chemoattractant C5a through the release of adenosine triphosphate (ATP) and autocrine "purinergic feedback loops" that involve receptors for ATP (P2Y(2)), adenosine diphosphate (ADP) (P2Y(12)), and adenosine (A2a, A2b, and A3).	Adenosine Diphosphate	239-242	hemolytic complement	Mus musculus	77-80
20664064-2	2010	Here, we show that macrophages navigate in a gradient of the chemoattractant C5a through the release of adenosine triphosphate (ATP) and autocrine "purinergic feedback loops" that involve receptors for ATP (P2Y(2)), adenosine diphosphate (ADP) (P2Y(12)), and adenosine (A2a, A2b, and A3).	Adenosine	104-113	hemolytic complement	Mus musculus	77-80
20473789-2	2010	Class IB PI3K plays a major role in the initial generation of PtdIns(3,4,5)P3 by Gi-coupled G-protein coupled receptors (GPCRs) (e.g., receptors for fMLP, C5a, LTB4).	phosphatidylinositol 3,4,5-triphosphate	62-77	hemolytic complement	Mus musculus	155-158
19800413-4	2009	The orexigenic activity of C5a was blocked by co-administration of a DP(1) receptor antagonist, BWA868C.	BW A868C	96-103	hemolytic complement	Mus musculus	27-30
19800413-8	2009	C5a is the first example of orexigenic peptides acting through the PGD(2)-NPY system in the central nervous system.	Prostaglandin D2	67-73	hemolytic complement	Mus musculus	0-3
19800413-5	2009	Central administration of C5a elevated the hypothalamic mRNA expression of COX-2 but not COX-1, and the food intake stimulation of C5a was inhibited by pretreatment with a COX-2 inhibitor, celecoxib, suggesting that C5a activates COX-2 upstream of the PGD(2)-DP(1) system.	Celecoxib	189-198	hemolytic complement	Mus musculus	26-29
19800413-5	2009	Central administration of C5a elevated the hypothalamic mRNA expression of COX-2 but not COX-1, and the food intake stimulation of C5a was inhibited by pretreatment with a COX-2 inhibitor, celecoxib, suggesting that C5a activates COX-2 upstream of the PGD(2)-DP(1) system.	Celecoxib	189-198	hemolytic complement	Mus musculus	131-134
19800413-5	2009	Central administration of C5a elevated the hypothalamic mRNA expression of COX-2 but not COX-1, and the food intake stimulation of C5a was inhibited by pretreatment with a COX-2 inhibitor, celecoxib, suggesting that C5a activates COX-2 upstream of the PGD(2)-DP(1) system.	Celecoxib	189-198	hemolytic complement	Mus musculus	131-134
19717511-9	2009	XO and NOS inhibitors and NOS-3 KO mice injected with LPS had decreased levels of C5a in spleens of septic mice, indicating peroxynitrite as a possible cause for CPB1 functional alteration.	Peroxynitrous Acid	124-137	hemolytic complement	Mus musculus	82-85
19800413-5	2009	Central administration of C5a elevated the hypothalamic mRNA expression of COX-2 but not COX-1, and the food intake stimulation of C5a was inhibited by pretreatment with a COX-2 inhibitor, celecoxib, suggesting that C5a activates COX-2 upstream of the PGD(2)-DP(1) system.	pgd(2)-dp	252-261	hemolytic complement	Mus musculus	26-29
19800413-5	2009	Central administration of C5a elevated the hypothalamic mRNA expression of COX-2 but not COX-1, and the food intake stimulation of C5a was inhibited by pretreatment with a COX-2 inhibitor, celecoxib, suggesting that C5a activates COX-2 upstream of the PGD(2)-DP(1) system.	pgd(2)-dp	252-261	hemolytic complement	Mus musculus	131-134
19800413-5	2009	Central administration of C5a elevated the hypothalamic mRNA expression of COX-2 but not COX-1, and the food intake stimulation of C5a was inhibited by pretreatment with a COX-2 inhibitor, celecoxib, suggesting that C5a activates COX-2 upstream of the PGD(2)-DP(1) system.	pgd(2)-dp	252-261	hemolytic complement	Mus musculus	131-134
19800413-6	2009	The orexigenic activity of C5a was also inhibited by an antagonist for neuropeptide Y (NPY) Y(1) receptor, which was activated downstream of the PGD(2)-DP(1) system.	pgd(2)-dp	145-154	hemolytic complement	Mus musculus	27-30
19346296-0	2009	Resveratrol attenuates C5a-induced inflammatory responses in vitro and in vivo by inhibiting phospholipase D and sphingosine kinase activities.	Resveratrol	0-11	hemolytic complement	Mus musculus	23-26
19346296-1	2009	The anti-inflammatory activity of the phytoalexin resveratrol (RSV) was evaluated in C5 anaphylatoxin (C5a)-stimulated primary neutrophils and in a mouse model of acute peritonitis.	Resveratrol	50-61	hemolytic complement	Mus musculus	103-106
19346296-8	2009	Indeed, prior injection of RSV virtually completely attenuated the effects of C5a on vascular permeability, neutrophil migration, release of interleukin 1beta, tumor necrosis factor alpha, interleukin 6, and the chemokine MIP-1alpha.	Resveratrol	27-30	hemolytic complement	Mus musculus	78-81
19767107-1	2009	C5L2 is a recently identified receptor for C5a/C5adesArg, C3a and C3adesArg (ASP).	Aspartic Acid	77-80	hemolytic complement	Mus musculus	43-46
19416544-11	2009	RESULTS: Tyrphostin AG-490 attenuated the early phase of zymosan-induced shock via inhibition of MIP-1alpha, RANTES and C5a plasma levels and via elevation of IL-10 in plasma.	Tyrphostins	9-19	hemolytic complement	Mus musculus	120-123
19416544-15	2009	These beneficial effects of AG-490 were related to lowered levels of circulating IL-6, MIP-1alpha and C5a, and to inhibited expression of STAT1, STAT3 and C5aR in kidneys.	alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide	28-34	hemolytic complement	Mus musculus	102-105
18607531-3	2009	In terms of structural specificity, the methoxyl group on C-5 and C-7 and the short alkyl chain (1-5 carbons) on C-6 may be essential for the potent activities.	Carbon	101-108	hemolytic complement	Mus musculus	58-61
19414808-9	2009	These studies describe for the first time a complete deficiency of CPN and demonstrate 1) that CPN plays a requisite role in regulating the lethal effects of anaphylatoxin-mediated shock, 2) that these lethal effects are mediated predominantly by C5a-induced histamine release, and 3) that C3a does not contribute significantly to shock following acute complement activation.	Histamine	259-268	hemolytic complement	Mus musculus	247-250
19144695-0	2009	Anaphylatoxin C5a contributes to the pathogenesis of cisplatin-induced nephrotoxicity.	Cisplatin	53-62	hemolytic complement	Mus musculus	14-17
19144695-2	2009	In this study, we investigated the role of anaphylatoxin C5a in the pathogenesis of cisplatin-mediated nephrotoxicity.	Cisplatin	84-93	hemolytic complement	Mus musculus	57-60
19144695-4	2009	However, pretreatment with C5 or C5a restores sensitivity to cisplatin-induced nephrotoxicity in C5-deficient mice.	Cisplatin	61-70	hemolytic complement	Mus musculus	33-36
19144695-8	2009	In conclusion, our findings suggest that C5a plays an important role in the pathogenesis of cisplatin nephrotoxicity.	Cisplatin	92-101	hemolytic complement	Mus musculus	41-44
18706698-3	2008	We have recently shown that CPB is catalytically more efficient than plasma CPN, the major plasma anaphylatoxin inhibitor, in inhibiting bradykinin, activated complement C3a, C5a, and thrombin-cleaved osteopontin in vitro.	cpb	28-31	hemolytic complement	Mus musculus	175-178
18639891-8	2008	We present evidence that C5a represents the effector molecule because C57Bl/6 mice treated with a C5a receptor antagonist displayed limited intestinal injury (injury score = 0.88), leukotriene B4 (13.16 pg/mg tissue), and myeloperoxidase (115.6 pg/mg tissue) production compared with hemorrhaged C57Bl/6 mice (P < 0.05).	Leukotrienes	181-192	hemolytic complement	Mus musculus	25-28
18639891-8	2008	We present evidence that C5a represents the effector molecule because C57Bl/6 mice treated with a C5a receptor antagonist displayed limited intestinal injury (injury score = 0.88), leukotriene B4 (13.16 pg/mg tissue), and myeloperoxidase (115.6 pg/mg tissue) production compared with hemorrhaged C57Bl/6 mice (P < 0.05).	Leukotrienes	181-192	hemolytic complement	Mus musculus	98-101
18706698-3	2008	We have recently shown that CPB is catalytically more efficient than plasma CPN, the major plasma anaphylatoxin inhibitor, in inhibiting bradykinin, activated complement C3a, C5a, and thrombin-cleaved osteopontin in vitro.	cpn	76-79	hemolytic complement	Mus musculus	175-178
18706698-7	2008	By specific cleavage of the carboxyl terminal arginines from C3a, C5a, bradykinin and thrombin-cleaved osteopontin, it inactivates these active inflammatory mediators.	Arginine	46-55	hemolytic complement	Mus musculus	66-69
18411281-0	2008	Signaling and cross-talk by C5a and UDP in macrophages selectively use PLCbeta3 to regulate intracellular free calcium.	Calcium	111-118	hemolytic complement	Mus musculus	28-31
18818727-3	2008	We analyze the effects of the two signaling molecules complement factors 5a (C5a) and uridine diphosphate (UDP) on the intracellular second messenger calcium to elucidate the principles that govern the processing of multiple signals by GPCRs.	Calcium	150-157	hemolytic complement	Mus musculus	77-80
18818727-6	2008	When the model is also used as a tool in the design of experiments, it predicts a synergistic region in the calcium peak height dose response that results when cells are simultaneously stimulated by C5a and UDP.	Calcium	108-115	hemolytic complement	Mus musculus	199-202
18818727-7	2008	An analysis of the model reveals a potential mechanism for crosstalk between the Galphai-coupled C5a receptor and the Galphaq-coupled UDP receptor signaling systems that results in synergistic calcium release.	Calcium	193-200	hemolytic complement	Mus musculus	97-100
18411281-3	2008	We found a synergistic response to complement component 5a (C5a) in combination with uridine 5"-diphosphate (UDP), platelet activating factor (PAF), or lysophosphatidic acid (LPA).	lysophosphatidic acid	175-178	hemolytic complement	Mus musculus	60-63
18411281-5	2008	Synergy between C5a and UDP, mediated by the C5a and P2Y6 receptors, required dual receptor occupancy, and affected the initial release of Ca(2+) from intracellular stores as well as sustained Ca(2+) levels.	Uridine Diphosphate	24-27	hemolytic complement	Mus musculus	45-48
18411281-6	2008	C5a and UDP synergized in generating inositol 1,4,5-trisphosphate, suggesting synergy in activating phospholipase C (PLC) beta.	Inositol 1,4,5-Trisphosphate	37-65	hemolytic complement	Mus musculus	0-3
18411281-13	2008	In contrast to Ca(2+), PI 3-kinase activation by C5a was inhibited by UDP, as was macropinocytosis, which depends on PI 3-kinase.	Uridine Diphosphate	70-73	hemolytic complement	Mus musculus	49-52
17996333-0	2008	Estrogen enhances expression of the complement C5a receptor and the C5a-agonist evoked calcium influx in hormone secreting neurons of the hypothalamus.	Calcium	87-94	hemolytic complement	Mus musculus	47-50
18559098-5	2008	MC required approximately 4 h of stimulation with Ag (DNP-albumin, following preincubation with IgE anti-DNP), ionomycin, or PMA to enable a strong chemotactic response towards C5a, paralleled by a distinct C5aR upregulation.	2,4-Dinitrophenol	54-57	hemolytic complement	Mus musculus	177-180
18559098-5	2008	MC required approximately 4 h of stimulation with Ag (DNP-albumin, following preincubation with IgE anti-DNP), ionomycin, or PMA to enable a strong chemotactic response towards C5a, paralleled by a distinct C5aR upregulation.	Tetradecanoylphorbol Acetate	125-128	hemolytic complement	Mus musculus	177-180
18559098-6	2008	Likewise, C5a induced intracellular calcium fluxes solely in activated MC.	Calcium	36-43	hemolytic complement	Mus musculus	10-13
17996333-0	2008	Estrogen enhances expression of the complement C5a receptor and the C5a-agonist evoked calcium influx in hormone secreting neurons of the hypothalamus.	Calcium	87-94	hemolytic complement	Mus musculus	68-71
18230183-2	2008	We previously reported that pre-treatment of murine cortico-hippocampal neuronal cultures with the complement derived anaphylatoxin C5a, protects against glutamate mediated apoptosis.	Glutamic Acid	154-163	hemolytic complement	Mus musculus	132-135
19025114-3	2008	We have recently shown that CPB is catalytically more efficient than plasma CPN, the major plasma anaphylatoxin inhibitor, in inhibiting bradykinin, activated complement C3a, C5a, and thrombin-cleaved osteopontin in vitro.	cpb	28-31	hemolytic complement	Mus musculus	175-178
19025114-3	2008	We have recently shown that CPB is catalytically more efficient than plasma CPN, the major plasma anaphylatoxin inhibitor, in inhibiting bradykinin, activated complement C3a, C5a, and thrombin-cleaved osteopontin in vitro.	cpn	76-79	hemolytic complement	Mus musculus	175-178
19025114-6	2008	By specific cleavage of the carboxyl terminal arginines from C3a, C5a, bradykinin and thrombin-cleaved osteopontin, it inactivates these active inflammatory mediators.	Arginine	46-55	hemolytic complement	Mus musculus	66-69
17471173-6	2007	KEY RESULTS: RAW264.7 cell migration towards C5a (1 microg ml(-1)) was significantly inhibited by cryptotanshinone (1, 3, 10 and 30 microM) in a concentration-dependent manner.	cryptotanshinone	98-114	hemolytic complement	Mus musculus	45-48
17905172-1	2008	OBJECTIVE: The purpose of the study was to test whether C5a peptidase encapsulated within a biodegradable polymer can act as a vaccine and elicit an immune response to prevent group B streptococci (GBS) infection in mice and provide protection to pups.	Polymers	106-113	hemolytic complement	Mus musculus	56-59
17905172-1	2008	OBJECTIVE: The purpose of the study was to test whether C5a peptidase encapsulated within a biodegradable polymer can act as a vaccine and elicit an immune response to prevent group B streptococci (GBS) infection in mice and provide protection to pups.	gbs	198-201	hemolytic complement	Mus musculus	56-59
17905172-2	2008	STUDY DESIGN: C5a peptidase was encapsulated in semipermeable microspheres of poly(lactide-co-glycolide).	Polyglactin 910	78-103	hemolytic complement	Mus musculus	14-17
17905172-12	2008	CONCLUSION: Encapsulated C5a peptidase elicited significant immune responses and protection against GBS challenge.	gbs	100-103	hemolytic complement	Mus musculus	25-28
17905172-13	2008	C5a peptidase microsphere encapsulation has potential as a GBS vaccine.	gbs	59-62	hemolytic complement	Mus musculus	0-3
17471173-8	2007	C5a-evoked migration in RAW264.7 cells was significantly suppressed by wortmannin (phosphatidylinositol 3-kinase (PI3K) inhibitor), PD98059 (MEK1/2 inhibitor) and SB203580 (p38 mitogen-activated protein kinase (MAPK) inhibitor), but not by SP600125 (c-Jun N-terminal kinase (JNK) inhibitor), suggesting that activation of PI3K, ERK1/2 and p38 MAPK signal pathways was involved in responses to C5a.	Wortmannin	71-81	hemolytic complement	Mus musculus	0-3
17471173-8	2007	C5a-evoked migration in RAW264.7 cells was significantly suppressed by wortmannin (phosphatidylinositol 3-kinase (PI3K) inhibitor), PD98059 (MEK1/2 inhibitor) and SB203580 (p38 mitogen-activated protein kinase (MAPK) inhibitor), but not by SP600125 (c-Jun N-terminal kinase (JNK) inhibitor), suggesting that activation of PI3K, ERK1/2 and p38 MAPK signal pathways was involved in responses to C5a.	Wortmannin	71-81	hemolytic complement	Mus musculus	393-396
17471173-8	2007	C5a-evoked migration in RAW264.7 cells was significantly suppressed by wortmannin (phosphatidylinositol 3-kinase (PI3K) inhibitor), PD98059 (MEK1/2 inhibitor) and SB203580 (p38 mitogen-activated protein kinase (MAPK) inhibitor), but not by SP600125 (c-Jun N-terminal kinase (JNK) inhibitor), suggesting that activation of PI3K, ERK1/2 and p38 MAPK signal pathways was involved in responses to C5a.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	132-139	hemolytic complement	Mus musculus	0-3
17471173-8	2007	C5a-evoked migration in RAW264.7 cells was significantly suppressed by wortmannin (phosphatidylinositol 3-kinase (PI3K) inhibitor), PD98059 (MEK1/2 inhibitor) and SB203580 (p38 mitogen-activated protein kinase (MAPK) inhibitor), but not by SP600125 (c-Jun N-terminal kinase (JNK) inhibitor), suggesting that activation of PI3K, ERK1/2 and p38 MAPK signal pathways was involved in responses to C5a.	pyrazolanthrone	240-248	hemolytic complement	Mus musculus	0-3
17471173-9	2007	Western blotting revealed that cryptotanshinone significantly inhibited PI3K-p110gamma membrane translocation and phosphorylation of Akt (PI3K downstream effector protein) and ERK1/2 induced by C5a.	cryptotanshinone	31-47	hemolytic complement	Mus musculus	194-197
17471173-11	2007	Wortmannin significantly attenuated C5a-induced PI3K-p110gamma translocation, Akt and ERK1/2 phosphorylation.	Wortmannin	0-10	hemolytic complement	Mus musculus	36-39
16988251-1	2006	The streptococcal C5a peptidase (ScpB) of group B streptococci (GBS) is found in virtually all clinical GBS isolates and is required for mucosal colonization in a neonatal mouse model.	gbs	64-67	hemolytic complement	Mus musculus	18-21
16980298-11	2006	Initial challenge with UTP also reduced Ca2+ mobilization by complement component C5a (and vice versa).	Uridine Triphosphate	23-26	hemolytic complement	Mus musculus	82-85
17154261-5	2007	We have treated mice with zymosan, resulting in significant leukocyte (primarily neutrophil) accumulation in the peritoneum at 4 h. Zymosan-mediated leukocyte recruitment was TLR2 independent, but was predominantly dependent on the complement components, C3 and C5a with a minor contribution from LTB4.	Zymosan	26-33	hemolytic complement	Mus musculus	262-265
17154261-5	2007	We have treated mice with zymosan, resulting in significant leukocyte (primarily neutrophil) accumulation in the peritoneum at 4 h. Zymosan-mediated leukocyte recruitment was TLR2 independent, but was predominantly dependent on the complement components, C3 and C5a with a minor contribution from LTB4.	Zymosan	132-139	hemolytic complement	Mus musculus	262-265
16988251-1	2006	The streptococcal C5a peptidase (ScpB) of group B streptococci (GBS) is found in virtually all clinical GBS isolates and is required for mucosal colonization in a neonatal mouse model.	gbs	104-107	hemolytic complement	Mus musculus	18-21
16548688-15	2006	Inhibition of C5a may provide a potential therapeutic approach to limit the inflammation associated with PGA-derived materials following implantation.	Polyglycolic Acid	105-108	hemolytic complement	Mus musculus	14-17
16034133-0	2005	Opposing regulatory roles of complement factor 5 in the development of bleomycin-induced pulmonary fibrosis.	Bleomycin	71-80	hemolytic complement	Mus musculus	29-48
16275622-7	2005	Activity analysis of total lung p38 MAPK revealed that p38 activity was increased at 4 h after C5a-instillation and that SB203580-treated C5a-instilled mouse lungs had lower p38 activity than did the C5a-instilled control.	SB 203580	121-129	hemolytic complement	Mus musculus	138-141
16275622-7	2005	Activity analysis of total lung p38 MAPK revealed that p38 activity was increased at 4 h after C5a-instillation and that SB203580-treated C5a-instilled mouse lungs had lower p38 activity than did the C5a-instilled control.	SB 203580	121-129	hemolytic complement	Mus musculus	138-141
16034133-5	2005	C5-deficient mice had an exaggerated inflammatory phenotype compared with C5-sufficient mice during acute bleomycin-induced lung injury.	Bleomycin	106-115	hemolytic complement	Mus musculus	0-2
16034133-7	2005	In contrast, C5 had a detrimental effect during chronic stages of bleomycin-induced injury, indicating a profibrotic role for C5.	Bleomycin	66-75	hemolytic complement	Mus musculus	13-15
16034136-3	2005	Similar to the regulation of Ca2+ by cGKI in other cells, there was a cGMP-dependent decrease in Ca2+ transients in response to C5a in WT, but not cGKI-/- bone marrow neutrophils.	Cyclic GMP	70-74	hemolytic complement	Mus musculus	128-131
16101818-0	2005	Requisite role for complement C5 and the C5a receptor in granulomatous response to mycobacterial glycolipid trehalose 6,6"-dimycolate.	Glycolipids	97-107	hemolytic complement	Mus musculus	19-32
16101818-0	2005	Requisite role for complement C5 and the C5a receptor in granulomatous response to mycobacterial glycolipid trehalose 6,6"-dimycolate.	Trehalose	108-117	hemolytic complement	Mus musculus	19-32
16101818-0	2005	Requisite role for complement C5 and the C5a receptor in granulomatous response to mycobacterial glycolipid trehalose 6,6"-dimycolate.	6,6"-dimycolate	118-133	hemolytic complement	Mus musculus	19-32
15879148-3	2005	administration of C5a triggers a rapid neutropenic response, but pretreating mice with the SPHK inhibitor, N,N-dimethylsphingosine (DMS), 10 min before the C5a i.v.	N,N-dimethylsphingosine	107-130	hemolytic complement	Mus musculus	156-159
15905548-0	2005	C5a-mediated leukotriene B4-amplified neutrophil chemotaxis is essential in tumor immunotherapy facilitated by anti-tumor monoclonal antibody and beta-glucan.	Leukotrienes	13-24	hemolytic complement	Mus musculus	0-3
15905548-4	2005	Neutrophil recruitment by C5a in vivo required amplification via leukotriene B(4), because both C5a-mediated leukocyte recruitment into the peritoneal cavity and tumor regression were suppressed in leukotriene B(4)R-deficient (BLT-1(-/-)) mice.	Leukotriene B4	65-78	hemolytic complement	Mus musculus	96-99
15905548-4	2005	Neutrophil recruitment by C5a in vivo required amplification via leukotriene B(4), because both C5a-mediated leukocyte recruitment into the peritoneal cavity and tumor regression were suppressed in leukotriene B(4)R-deficient (BLT-1(-/-)) mice.	Leukotriene B4	198-211	hemolytic complement	Mus musculus	26-29
15905548-4	2005	Neutrophil recruitment by C5a in vivo required amplification via leukotriene B(4), because both C5a-mediated leukocyte recruitment into the peritoneal cavity and tumor regression were suppressed in leukotriene B(4)R-deficient (BLT-1(-/-)) mice.	Leukotriene B4	198-211	hemolytic complement	Mus musculus	96-99
15983374-6	2005	Similarly, C5a-mediated actin polymerization, C5a- and UTP-stimulated intracellular calcium mobilization, and the stimulation of cAMP formation by isoproterenol were all eliminated in the absence of the Gbeta-subunits.	Calcium	84-91	hemolytic complement	Mus musculus	46-49
15983374-6	2005	Similarly, C5a-mediated actin polymerization, C5a- and UTP-stimulated intracellular calcium mobilization, and the stimulation of cAMP formation by isoproterenol were all eliminated in the absence of the Gbeta-subunits.	Cyclic AMP	129-133	hemolytic complement	Mus musculus	11-14
15879148-3	2005	administration of C5a triggers a rapid neutropenic response, but pretreating mice with the SPHK inhibitor, N,N-dimethylsphingosine (DMS), 10 min before the C5a i.v.	N,N-dimethylsphingosine	132-135	hemolytic complement	Mus musculus	156-159
15879148-13	2005	In mice pretreated with DMS, there was a significant reduction on the C5a-triggered neutrophil and monocyte infiltration, as well as a marked reduction on the Evans blue influx.	N,N-dimethylsphingosine	24-27	hemolytic complement	Mus musculus	70-73
15827963-3	2005	We here demonstrate statistically significant synergy between regakine-1 and the neutrophil attractants C5a or IL-8/CXCL8 in inducing neutrophil shape change and migration under agarose.	Sepharose	178-185	hemolytic complement	Mus musculus	104-107
15805316-2	2005	The authors studied the role of complement C5 in the development of abnormal oxygen kinetics during sepsis in mice, arguing that as a pro-inflammatory event, complement activation might exacerbate disturbances in oxygen use during abdominal sepsis.	Oxygen	77-83	hemolytic complement	Mus musculus	32-45
15805316-2	2005	The authors studied the role of complement C5 in the development of abnormal oxygen kinetics during sepsis in mice, arguing that as a pro-inflammatory event, complement activation might exacerbate disturbances in oxygen use during abdominal sepsis.	Oxygen	213-219	hemolytic complement	Mus musculus	32-45
15383602-1	2004	Carboxypeptidase R (CPR) is a heat-labile enzyme found in serum in addition to stable carboxypeptidase N. CPR cleaves the C-terminal basic amino acids, arginine and lysine, from inflammatory peptides such as complement C3a and C5a, bradykinin, and enkephalin.	Amino Acids, Basic	133-150	hemolytic complement	Mus musculus	227-230
15383602-1	2004	Carboxypeptidase R (CPR) is a heat-labile enzyme found in serum in addition to stable carboxypeptidase N. CPR cleaves the C-terminal basic amino acids, arginine and lysine, from inflammatory peptides such as complement C3a and C5a, bradykinin, and enkephalin.	Arginine	152-160	hemolytic complement	Mus musculus	227-230
15383602-1	2004	Carboxypeptidase R (CPR) is a heat-labile enzyme found in serum in addition to stable carboxypeptidase N. CPR cleaves the C-terminal basic amino acids, arginine and lysine, from inflammatory peptides such as complement C3a and C5a, bradykinin, and enkephalin.	Lysine	165-171	hemolytic complement	Mus musculus	227-230
12954113-0	2003	Evaluation of C-5 propynyl pyrimidine-containing oligonucleotides in vitro and in vivo.	containing oligonucleotides	38-65	hemolytic complement	Mus musculus	14-17
15255929-2	2004	This correlated to an attenuated calcium signaling of complement (C5a) and purinergic (UTP) receptors as well as to the capacity for effective production of cytokines-chemokines.	Calcium	33-40	hemolytic complement	Mus musculus	66-69
15255929-8	2004	However, both the elevation in basal [Ca2+]i as well as the suppression of C5a- and UTP-evoked calcium signals are selectively and dose-dependently reversed by tyrphostin AG126, a PTK inhibitor that, moreover, blocks inducible nitric oxide and cytokine-chemokine release.	Calcium	95-102	hemolytic complement	Mus musculus	75-78
15255929-8	2004	However, both the elevation in basal [Ca2+]i as well as the suppression of C5a- and UTP-evoked calcium signals are selectively and dose-dependently reversed by tyrphostin AG126, a PTK inhibitor that, moreover, blocks inducible nitric oxide and cytokine-chemokine release.	tyrphostin AG 126	160-176	hemolytic complement	Mus musculus	75-78
15255929-8	2004	However, both the elevation in basal [Ca2+]i as well as the suppression of C5a- and UTP-evoked calcium signals are selectively and dose-dependently reversed by tyrphostin AG126, a PTK inhibitor that, moreover, blocks inducible nitric oxide and cytokine-chemokine release.	Nitric Oxide	227-239	hemolytic complement	Mus musculus	75-78
14678471-6	2004	The SiK213-induced 5HT decrease and shock were reduced by a complement-C5 inhibitor.	Serotonin	19-22	hemolytic complement	Mus musculus	60-73
14699051-5	2004	Similarly, the C5a-mediated calcium response of single cells is either absent or significantly delayed and weakened by G beta(2) knockdown.	Calcium	28-35	hemolytic complement	Mus musculus	15-18
14766418-2	2004	For instance, its derivatives C3a, C3b, iC3b, C5a, and C5b-9 independently induce the production by myeloid and non-myeloid cells of the cytokines interleukin (IL)-1(, IL-6 and tumor necrosis factor-(, and of prostaglandin (PG)E2, all putative mediators of fever.	Dinoprostone	209-229	hemolytic complement	Mus musculus	46-49
14766418-9	2004	The purpose of this article is to review the studies that have led us to conclude that C5a, Kc and Kc-generated PGE2 may be integrally involved in the pathogenesis of LPS fever.	Dinoprostone	112-116	hemolytic complement	Mus musculus	87-90
12899627-9	2003	Biophysical properties of the C5L2, including slow ligand on and off rates, absence of internalization, and relatively high affinity for the C5a des Arg metabolite, suggest that this receptor may serve to modulate C5a biological functions in vivo.	Arginine	149-152	hemolytic complement	Mus musculus	141-144
12899627-9	2003	Biophysical properties of the C5L2, including slow ligand on and off rates, absence of internalization, and relatively high affinity for the C5a des Arg metabolite, suggest that this receptor may serve to modulate C5a biological functions in vivo.	Arginine	149-152	hemolytic complement	Mus musculus	214-217
12421982-7	2002	Exposure of MDMEC to C5a or IL-6 did not result in changes in MIP-2 or MCP-1 production, but initial exposure of MDMEC to IL-6, followed by exposure to C5a, resulted in significantly enhanced production of MIP-2 and MCP-1 (but not TNF-alpha and MIP-1alpha).	mdmec	12-17	hemolytic complement	Mus musculus	21-24
12428251-8	2002	CII-stimulated spleen cells from anti-C5-treated mice produced lower levels of tumor necrosis factor alpha (TNFalpha) and interleukin-10 (IL-10) compared with those from mice treated with Crry-Ig.	N-[(1S)-2-methyl-1-(pyridin-4-ylcarbamoyl)propyl]cyclohexanecarboxamide	0-3	hemolytic complement	Mus musculus	38-40
12428251-9	2002	Lower steady-state messenger RNA (mRNA) levels for TNFalpha, interferon-gamma (IFNgamma), IL-18, and IL-6 were observed in the joints of anti-C5-treated mice, and for IFNgamma and IL-6 in mice receiving Crry-Ig, all in comparison with PBS-treated mice.	pbs	235-238	hemolytic complement	Mus musculus	142-144
12954113-1	2003	Inclusion of C-5 propynyl pyrimidines in phosphorothioate antisense oligonucleotides (ASOs) has been shown to significantly increase their potency for inhibiting gene expression in vitro.	Parathion	41-57	hemolytic complement	Mus musculus	13-16
12954113-1	2003	Inclusion of C-5 propynyl pyrimidines in phosphorothioate antisense oligonucleotides (ASOs) has been shown to significantly increase their potency for inhibiting gene expression in vitro.	Oligonucleotides	68-84	hemolytic complement	Mus musculus	13-16
12954113-1	2003	Inclusion of C-5 propynyl pyrimidines in phosphorothioate antisense oligonucleotides (ASOs) has been shown to significantly increase their potency for inhibiting gene expression in vitro.	Oligonucleotides, Antisense	86-90	hemolytic complement	Mus musculus	13-16
12954113-3	2003	Our results show that C-5 propynyl pyrimidine-modified oligonucleotides caused an increase in the melting temperature (T(m)) of both oligodeoxynucleotides (ODNs) and 2"-O-(2-methoxy)ethyl (2"-MOE)-modified oligonucleotides.	Oligonucleotides	55-71	hemolytic complement	Mus musculus	22-25
12954113-3	2003	Our results show that C-5 propynyl pyrimidine-modified oligonucleotides caused an increase in the melting temperature (T(m)) of both oligodeoxynucleotides (ODNs) and 2"-O-(2-methoxy)ethyl (2"-MOE)-modified oligonucleotides.	Oligodeoxyribonucleotides	133-154	hemolytic complement	Mus musculus	22-25
12954113-3	2003	Our results show that C-5 propynyl pyrimidine-modified oligonucleotides caused an increase in the melting temperature (T(m)) of both oligodeoxynucleotides (ODNs) and 2"-O-(2-methoxy)ethyl (2"-MOE)-modified oligonucleotides.	Oligodeoxyribonucleotides	156-160	hemolytic complement	Mus musculus	22-25
12954113-3	2003	Our results show that C-5 propynyl pyrimidine-modified oligonucleotides caused an increase in the melting temperature (T(m)) of both oligodeoxynucleotides (ODNs) and 2"-O-(2-methoxy)ethyl (2"-MOE)-modified oligonucleotides.	2"-o-(2-methoxy)ethyl (2"-moe)-modified oligonucleotides	166-222	hemolytic complement	Mus musculus	22-25
12954113-4	2003	The in vitro data show a moderate increase in potency for an antisense oligodeoxynucleotide containing C-5 propynyl pyrimidines targeting the murine PTEN (MMAC1) transcript.	Oligodeoxyribonucleotides	71-91	hemolytic complement	Mus musculus	103-106
12954113-10	2003	C-5 propynyl pyrimidine-modified chimeric oligonucleotides exhibited decreased hepatotoxicity compared with C-5 propynyl-modified ODNs but did not exhibit an increase in potency compared with unmodified chimeric oligonucleotides.	Oligonucleotides	42-58	hemolytic complement	Mus musculus	0-3