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Search results 201 to 269 out of 269 for C3ar1

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Type Details Score
Publication
- | J:293217
       
First Author: GemPharmatech
Year: 2020
Title: GemPharmatech Website.
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Publication
- | J:326541
       
First Author: Cyagen Biosciences Inc.
Year: 2022
Title: Cyagen Biosciences Website.
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Publication
- | J:60000
       
First Author: UniProt-GOA
Year: 2012
Title: Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
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Publication
- | J:342605
       
First Author: GOA curators
Year: 2016
Title: Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
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Publication
- | J:68900
     
First Author: The Jackson Laboratory Mouse Radiation Hybrid Database
Year: 2004
Journal: Database Release
Title: Mouse T31 Radiation Hybrid Data Load
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Publication
12466851 | J:80000
First Author: Okazaki Y
Year: 2002
Journal: Nature
Title: Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs.
Volume: 420
Issue: 6915
Pages: 563-73
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Publication
- | J:164563
       
First Author: The Gene Ontology Consortium
Year: 2010
Title: Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
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Publication
- | J:75000
       
First Author: Mouse Genome Informatics Scientific Curators
Year: 2002
Title: Mouse Genome Informatics Computational Sequence to Gene Associations
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Publication
- | J:157972
     
First Author: Mouse Genome Informatics Scientific Curators
Year: 2010
Journal: Database Download
Title: Mouse Microarray Data Integration in Mouse Genome Informatics, the Affymetrix GeneChip Mouse Genome U74 Array Platform (A, B, C v2).
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Publication
- | J:57747
     
First Author: MGI Genome Annotation Group and UniGene Staff
Year: 2015
Journal: Database Download
Title: MGI-UniGene Interconnection Effort
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Publication
- | J:161428
       
First Author: Marc Feuermann, Huaiyu Mi, Pascale Gaudet, Dustin Ebert, Anushya Muruganujan, Paul Thomas
Year: 2010
Title: Annotation inferences using phylogenetic trees
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Publication
- | J:63103
     
First Author: Mouse Genome Database and National Center for Biotechnology Information
Year: 2000
Journal: Database Release
Title: Entrez Gene Load
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Publication
- | J:262123
     
First Author: Allen Institute for Brain Science
Year: 2004
Journal: Allen Institute
Title: Allen Brain Atlas: mouse riboprobes
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Publication
- | J:144086
     
First Author: Mouse Genome Informatics Scientific Curators
Year: 2009
Journal: Database Download
Title: Mouse Microarray Data Integration in Mouse Genome Informatics, the Affymetrix GeneChip Mouse Gene 1.0 ST Array Platform
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Publication
- | J:155721
     
First Author: Mouse Genome Informatics (MGI) and The National Center for Biotechnology Information (NCBI)
Year: 2010
Journal: Database Download
Title: Consensus CDS project
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Publication
- | J:85324
     
First Author: Mouse Genome Informatics Group
Year: 2003
Journal: Database Procedure
Title: Automatic Encodes (AutoE) Reference
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Publication
- | J:53168
     
First Author: Bairoch A
Year: 1999
Journal: Database Release
Title: SWISS-PROT Annotated protein sequence database
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Publication
- | J:91388
       
First Author: Mouse Genome Informatics Scientific Curators
Year: 2005
Title: Obtaining and Loading Genome Assembly Coordinates from Ensembl Annotations
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Publication
- | J:155221
     
First Author: Mouse Genome Informatics
Year: 2010
Journal: Database Release
Title: Protein Ontology Association Load.
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Publication
- | J:90438
       
First Author: Mouse Genome Informatics Scientific Curators
Year: 2005
Title: Obtaining and loading genome assembly coordinates from NCBI annotations
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Publication
- | J:144087
     
First Author: Mouse Genome Informatics Scientific Curators
Year: 2009
Journal: Database Download
Title: Mouse Microarray Data Integration in Mouse Genome Informatics, the Affymetrix GeneChip Mouse Genome 430 2.0 Array Platform
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Allele
C3ar1<em2Smoc> | MGI:7288575
Name: complement component 3a receptor 1; endonuclease-mediated mutation 2, Shanghai Model Organisms Center
Allele Type: Endonuclease-mediated
Attribute String: Null/knockout
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Publication
25456411 | -
First Author: Cero C
Year: 2014
Journal: Structure
Title: The TLQP-21 peptide activates the G-protein-coupled receptor C3aR1 via a folding-upon-binding mechanism.
Volume: 22
Issue: 12
Pages: 1744-1753
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Strain
MGI:6770603 | C57BL/6JSmoc-C3ar1<em2Smoc>/Smoc
Attribute String: coisogenic, endonuclease-mediated mutation, mutant strain
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Allele
C3ar1<em1Smoc> | MGI:7288574
Name: complement component 3a receptor 1; endonuclease-mediated mutation 1, Shanghai Model Organisms Center
Allele Type: Endonuclease-mediated
Attribute String: Conditional ready, No functional change
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Allele
C3ar1<tm1.1Kohl> | MGI:7782580
Name: complement component 3a receptor 1; targeted mutation 1.1, Jorg Kohl
Allele Type: Targeted
Attribute String: Conditional ready, Null/knockout, Reporter
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Publication
36110094 | J:328924
 
First Author: Wang S
Year: 2022
Journal: Front Neurosci
Title: Complement C3a receptor inactivation attenuates retinal degeneration induced by oxidative damage.
Volume: 16
Pages: 951491
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Publication
36402750 | J:331409
First Author: Farini A
Year: 2022
Journal: Cell Death Dis
Title: Inhibition of the immunoproteasome modulates innate immunity to ameliorate muscle pathology of dysferlin-deficient BlAJ mice.
Volume: 13
Issue: 11
Pages: 975
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Publication
31484069 | J:288398
First Author: Sahu BS
Year: 2019
Journal: Cell Rep
Title: Peptide/Receptor Co-evolution Explains the Lipolytic Function of the Neuropeptide TLQP-21.
Volume: 28
Issue: 10
Pages: 2567-2580.e6
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Publication
9108406 | -
First Author: Hartmann K
Year: 1997
Journal: Blood
Title: C3a and C5a stimulate chemotaxis of human mast cells.
Volume: 89
Issue: 8
Pages: 2863-70
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Publication
22500977 | -
First Author: Bellows-Peterson ML
Year: 2012
Journal: J Med Chem
Title: De novo peptide design with C3a receptor agonist and antagonist activities: theoretical predictions and experimental validation.
Volume: 55
Issue: 9
Pages: 4159-68
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Publication
8156000 | -
First Author: Takafuji S
Year: 1994
Journal: Int Arch Allergy Immunol
Title: Degranulation from human eosinophils stimulated with C3a and C5a.
Volume: 104 Suppl 1
Issue: 1
Pages: 27-9
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Publication
19265162 | -
First Author: Schraufstatter IU
Year: 2009
Journal: J Immunol
Title: C3a and C5a are chemotactic factors for human mesenchymal stem cells, which cause prolonged ERK1/2 phosphorylation.
Volume: 182
Issue: 6
Pages: 3827-36
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Protein Domain
IPR001644 | Anaphtx_C3AR1
Type: Family
Description: The activation of the complement cascade produces a number of small fragments that are bioactive: potent chemoattractants and secretagogues that act on immune and non-immune cells []. Similar peptides can also be released by the actions of non-complement proteases, for instance during clotting []. Initially these were termed anaphylatoxins because of their effect on mast cell histamine release, but were reclassified as complement component peptides. They include C3a and C5a, which are involved immune response [], neural development and organ regeneration [, ]. A third peptide, C4a, has a similar structure, but it is inactive in humans []. Since the primary function of complement component peptides is in inflammation, they are important targets for the development of anti-inflammatory therapies [].The anaphylatoxin chemotactic receptors (also known as complement peptide receptors) are a group of rhodopsin-like G-protein coupled receptors (GPCRs) [, , , ]. There are three subtypes: C3a anaphylatoxin chemotactic receptor (C3AR1) [], C5a anaphylatoxin chemotactic receptor (C5AR1) []and C5a anaphylatoxin chemotactic receptor C5L2 (C5AR2) []. Both C3AR1 and C5AR1 receptors are classical GPCRs. However, C5AR2 appears to be permanently uncoupled from G proteins but can associate with beta-arrestin []. Nevertheless, it has been shown that activation of both C5AR1 and C5AR2 is required for a full pro-inflammatory response, particularly in mice []. Several receptor antagonists have been reported [, , , ], although none, so far, have been show to be effective in humans. This entry represents C3AR1, also known as complement component 3a receptor 1 and C3aR []. It appears to be widely expressed in different lymphoid tissues, providing evidence for a central role in inflammatory processes []. This receptor stimulates chemotaxis [], granule enzyme release [, ]and increases phosphorylated-ERK1/2 production []. C3AR1 may provide a theraputic avenue for the treatment of asthma [], retinal degeneration [], and rheumatoid arthritis [].
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Publication
37624843 | J:339369
First Author: Kaur G
Year: 2023
Journal: PLoS One
Title: Helicase-like transcription factor (Hltf)-deletion activates Hmgb1-Rage axis and granzyme A-mediated killing of pancreatic β cells resulting in neonatal lethality.
Volume: 18
Issue: 8
Pages: e0286109
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Publication
27041370 | J:274454
First Author: López-González I
Year: 2017
Journal: Mol Neurobiol
Title: Inflammation in Lafora Disease: Evolution with Disease Progression in Laforin and Malin Knock-out Mouse Models.
Volume: 54
Issue: 5
Pages: 3119-3130
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Publication
15833747 | -
First Author: Kalant D
Year: 2005
Journal: J Biol Chem
Title: C5L2 is a functional receptor for acylation-stimulating protein.
Volume: 280
Issue: 25
Pages: 23936-44
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Publication
8702752 | -
First Author: Ames RS
Year: 1996
Journal: J Biol Chem
Title: Molecular cloning and characterization of the human anaphylatoxin C3a receptor.
Volume: 271
Issue: 34
Pages: 20231-4
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Publication
17603557 | -
First Author: Monk PN
Year: 2007
Journal: Br J Pharmacol
Title: Function, structure and therapeutic potential of complement C5a receptors.
Volume: 152
Issue: 4
Pages: 429-48
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Publication
19025115 | -
 
First Author: Amara U
Year: 2008
Journal: Adv Exp Med Biol
Title: Interaction between the coagulation and complement system.
Volume: 632
Pages: 71-9
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Publication
19601884 | -
First Author: Peng Q
Year: 2009
Journal: Inflamm Allergy Drug Targets
Title: The role of anaphylatoxins C3a and C5a in regulating innate and adaptive immune responses.
Volume: 8
Issue: 3
Pages: 236-46
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Publication
22118769 | -
First Author: Carmona-Fontaine C
Year: 2011
Journal: Dev Cell
Title: Complement fragment C3a controls mutual cell attraction during collective cell migration.
Volume: 21
Issue: 6
Pages: 1026-37
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Publication
19477527 | -
First Author: Klos A
Year: 2009
Journal: Mol Immunol
Title: The role of the anaphylatoxins in health and disease.
Volume: 46
Issue: 14
Pages: 2753-66
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Publication
9725198 | J:49259
First Author: Lienenklaus S
Year: 1998
Journal: J Immunol
Title: Human anaphylatoxin C4a is a potent agonist of the guinea pig but not the human C3a receptor.
Volume: 161
Issue: 5
Pages: 2089-93
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Publication
2528484 | -
 
First Author: Fukuoka Y
Year: 1989
Journal: Dermatologica
Title: Characterization of receptors to the anaphylatoxins on isolated cells.
Volume: 179 Suppl 1
Pages: 35-40
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Publication
11165367 | -
First Author: Lee DK
Year: 2001
Journal: Brain Res Mol Brain Res
Title: Identification of four novel human G protein-coupled receptors expressed in the brain.
Volume: 86
Issue: 1-2
Pages: 13-22
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Publication
8011297 | -
 
First Author: Gerard C
Year: 1994
Journal: Annu Rev Immunol
Title: C5A anaphylatoxin and its seven transmembrane-segment receptor.
Volume: 12
Pages: 775-808
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Publication
8605247 | -
First Author: Roglic A
Year: 1996
Journal: Biochim Biophys Acta
Title: cDNA cloning of a novel G protein-coupled receptor with a large extracellular loop structure.
Volume: 1305
Issue: 1-2
Pages: 39-43
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Publication
1847994 | -
First Author: Gerard NP
Year: 1991
Journal: Nature
Title: The chemotactic receptor for human C5a anaphylatoxin.
Volume: 349
Issue: 6310
Pages: 614-7
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Publication
12429062 | -
First Author: Joost P
Year: 2002
Journal: Genome Biol
Title: Phylogenetic analysis of 277 human G-protein-coupled receptors as a tool for the prediction of orphan receptor ligands.
Volume: 3
Issue: 11
Pages: RESEARCH0063
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Publication
17322907 | J:279795
First Author: Chen NJ
Year: 2007
Journal: Nature
Title: C5L2 is critical for the biological activities of the anaphylatoxins C5a and C3a.
Volume: 446
Issue: 7132
Pages: 203-7
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Publication
11342658 | -
First Author: Ames RS
Year: 2001
Journal: J Immunol
Title: Identification of a selective nonpeptide antagonist of the anaphylatoxin C3a receptor that demonstrates antiinflammatory activity in animal models.
Volume: 166
Issue: 10
Pages: 6341-8
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Publication
16154494 | -
First Author: Mathieu MC
Year: 2005
Journal: Immunol Lett
Title: The C3a receptor antagonist SB 290157 has agonist activity.
Volume: 100
Issue: 2
Pages: 139-45
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Publication
14570896 | -
First Author: Otto M
Year: 2004
Journal: J Biol Chem
Title: C5a mutants are potent antagonists of the C5a receptor (CD88) and of C5L2: position 69 is the locus that determines agonism or antagonism.
Volume: 279
Issue: 1
Pages: 142-51
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Protein Domain
IPR002234 | Anphylx_rcpt_C3a/C5a1-2
Type: Family
Description: The activation of the complement cascade produces a number of small fragments that are bioactive: potent chemoattractants and secretagogues that act on immune and non-immune cells []. Similar peptides can also be released by the actions of non-complement proteases, for instance during clotting []. Initially these were termed anaphylatoxins because of their effect on mast cell histamine release, but were reclassified as complement component peptides. They include C3a and C5a, which are involved immune response [], neural development and organ regeneration [, ]. A third peptide, C4a, has a similar structure, but it is inactive in humans []. Since the primary function of complement component peptides is in inflammation, they are important targets for the development of anti-inflammatory therapies [].The anaphylatoxin chemotactic receptors (also known as complement peptide receptors) are a group of rhodopsin-like G-protein coupled receptors (GPCRs) [, , , ]. There are three subtypes: C3a anaphylatoxin chemotactic receptor (C3AR1) [], C5a anaphylatoxin chemotactic receptor (C5AR1) []and C5a anaphylatoxin chemotactic receptor C5L2 (C5AR2) []. Both C3AR1 and C5AR1 receptors are classical GPCRs. However, C5AR2 appears to be permanently uncoupled from G proteins but can associate with beta-arrestin []. Nevertheless, it has been shown that activation of both C5AR1 and C5AR2 is required for a full pro-inflammatory response, particularly in mice []. Several receptor antagonists have been reported [, , , ], although none, so far, have been show to be effective in humans. This entry represents C3a anaphylatoxin chemotactic receptors and C5a anaphylatoxin chemotactic receptor 1/2.
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Protein Domain
IPR027809 | Anaphtx_C5AR2
Type: Family
Description: The activation of the complement cascade produces a number of small fragments that are bioactive: potent chemoattractants and secretagogues that act on immune and non-immune cells []. Similar peptides can also be released by the actions of non-complement proteases, for instance during clotting []. Initially these were termed anaphylatoxins because of their effect on mast cell histamine release, but were reclassified as complement component peptides. They include C3a and C5a, which are involved immune response [], neural development and organ regeneration [, ]. A third peptide, C4a, has a similar structure, but it is inactive in humans []. Since the primary function of complement component peptides is in inflammation, they are important targets for the development of anti-inflammatory therapies [].The anaphylatoxin chemotactic receptors (also known as complement peptide receptors) are a group of rhodopsin-like G-protein coupled receptors (GPCRs) [, , , ]. There are three subtypes: C3a anaphylatoxin chemotactic receptor (C3AR1) [], C5a anaphylatoxin chemotactic receptor (C5AR1) []and C5a anaphylatoxin chemotactic receptor C5L2 (C5AR2) []. Both C3AR1 and C5AR1 receptors are classical GPCRs. However, C5AR2 appears to be permanently uncoupled from G proteins but can associate with beta-arrestin []. Nevertheless, it has been shown that activation of both C5AR1 and C5AR2 is required for a full pro-inflammatory response, particularly in mice []. Several receptor antagonists have been reported [, , , ], although none, so far, have been show to be effective in humans. This entry represents C5AR2, also known as complement component 5a receptor 2.
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Publication
34069842 | J:311236
 
First Author: Tajmim A
Year: 2021
Journal: Nutrients
Title: (-)-Oleocanthal Nutraceuticals for Alzheimer's Disease Amyloid Pathology: Novel Oral Formulations, Therapeutic, and Molecular Insights in 5xFAD Transgenic Mice Model.
Volume: 13
Issue: 5
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Publication
8765043 | -
First Author: Crass T
Year: 1996
Journal: Eur J Immunol
Title: Expression cloning of the human C3a anaphylatoxin receptor (C3aR) from differentiated U-937 cells.
Volume: 26
Issue: 8
Pages: 1944-50
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Publication
38591068 | J:347081
 
First Author: Speers AB
Year: 2024
Journal: Front Neurosci
Title: Mode of administration influences plasma levels of active Centella asiatica compounds in 5xFAD mice while markers of neuroinflammation remain unaltered.
Volume: 18
Pages: 1277626
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Protein
O09047
Organism: Mus musculus/domesticus
Length: 477  
Fragment?: false
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Protein
Q5U7A4
Organism: Mus musculus/domesticus
Length: 477  
Fragment?: false
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Protein
Q8C6R2
Organism: Mus musculus/domesticus
Length: 477  
Fragment?: false
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Protein
Q3U4N3
Organism: Mus musculus/domesticus
Length: 226  
Fragment?: true
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Protein
Q8BW93
Organism: Mus musculus/domesticus
Length: 344  
Fragment?: false
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Protein
E9QQ21
Organism: Mus musculus/domesticus
Length: 358  
Fragment?: false
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Protein
E9PVQ2
Organism: Mus musculus/domesticus
Length: 358  
Fragment?: false
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Protein
P30993
Organism: Mus musculus/domesticus
Length: 351  
Fragment?: false
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Protein
Q3UCS9
Organism: Mus musculus/domesticus
Length: 301  
Fragment?: true
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Protein
A0A1B0GT01
Organism: Mus musculus/domesticus
Length: 181  
Fragment?: true
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MouseMine is a collaboration between MGI at The Jackson Laboratory and the InterMine project at the Cambridge Systems Biology Centre. MouseMine is funded through a grant from the NIH/NHGRI.The Jackson Laboratory makes no representation about the suitability or accuracy of this software or data for any purpose, and makes no warranties, either express or implied, including merchantability and fitness for a particular purpose or that the use of this software or data will not infringe any third party patents, copyrights, trademarks, or other rights. the software and data are provided "as is". This software and data are provided to enhance knowledge and encourage progress in the scientific community and are to be used only for research and educational purposes. Any reproduction or use for commercial purpose is prohibited without the prior express written permission of the Jackson Laboratory.

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