Differential Receptor Binding and Regulatory Mechanisms for the Lymphangiogenic Growth Factors Vascular Endothelial Growth Factor (VEGF)-C and -D.
Identifieur interne : 000516 ( PubMed/Corpus ); précédent : 000515; suivant : 000517Differential Receptor Binding and Regulatory Mechanisms for the Lymphangiogenic Growth Factors Vascular Endothelial Growth Factor (VEGF)-C and -D.
Auteurs : Natalia Davydova ; Nicole C. Harris ; Sally Roufail ; Sophie Paquet-Fifield ; Musarat Ishaq ; Victor A. Streltsov ; Steven P. Williams ; Tara Karnezis ; Steven A. Stacker ; Marc G. AchenSource :
- The Journal of biological chemistry [ 1083-351X ] ; 2016.
English descriptors
- KwdEn :
- Animals, Antibodies, Neutralizing, Cells, Cultured, Dermis (metabolism), Dermis (pathology), Endothelium, Vascular (metabolism), Endothelium, Vascular (pathology), Female, Humans, Lymphangiogenesis, Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Mice, Inbred NOD, Mice, SCID, Mutagenesis, Site-Directed, Mutation (genetics), Neovascularization, Pathologic (metabolism), Neovascularization, Pathologic (pathology), Signal Transduction, Vascular Endothelial Growth Factor C (chemistry), Vascular Endothelial Growth Factor C (genetics), Vascular Endothelial Growth Factor C (metabolism), Vascular Endothelial Growth Factor D (chemistry), Vascular Endothelial Growth Factor D (genetics), Vascular Endothelial Growth Factor D (metabolism), Vascular Endothelial Growth Factor Receptor-2 (genetics), Vascular Endothelial Growth Factor Receptor-2 (metabolism), Vascular Endothelial Growth Factor Receptor-3 (genetics), Vascular Endothelial Growth Factor Receptor-3 (metabolism).
- MESH :
- chemical , chemistry : Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D.
- chemical , genetics : Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-2, Vascular Endothelial Growth Factor Receptor-3.
- chemical , metabolism : Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D, Vascular Endothelial Growth Factor Receptor-2, Vascular Endothelial Growth Factor Receptor-3.
- chemical : Antibodies, Neutralizing.
- genetics : Mutation.
- metabolism : Dermis, Endothelium, Vascular, Lymphatic Vessels, Neovascularization, Pathologic.
- pathology : Dermis, Endothelium, Vascular, Lymphatic Vessels, Neovascularization, Pathologic.
- Animals, Cells, Cultured, Female, Humans, Lymphangiogenesis, Mice, Inbred NOD, Mice, SCID, Mutagenesis, Site-Directed, Signal Transduction.
Abstract
VEGF-C and VEGF-D are secreted glycoproteins that induce angiogenesis and lymphangiogenesis in cancer, thereby promoting tumor growth and spread. They exhibit structural homology and activate VEGFR-2 and VEGFR-3, receptors on endothelial cells that signal for growth of blood vessels and lymphatics. VEGF-C and VEGF-D were thought to exhibit similar bioactivities, yet recent studies indicated distinct signaling mechanisms (e.g. tumor-derived VEGF-C promoted expression of the prostaglandin biosynthetic enzyme COX-2 in lymphatics, a response thought to facilitate metastasis via the lymphatic vasculature, whereas VEGF-D did not). Here we explore the basis of the distinct bioactivities of VEGF-D using a neutralizing antibody, peptide mapping, and mutagenesis to demonstrate that the N-terminal α-helix of mature VEGF-D (Phe(93)-Arg(108)) is critical for binding VEGFR-2 and VEGFR-3. Importantly, the N-terminal part of this α-helix, from Phe(93) to Thr(98), is required for binding VEGFR-3 but not VEGFR-2. Surprisingly, the corresponding part of the α-helix in mature VEGF-C did not influence binding to either VEGFR-2 or VEGFR-3, indicating distinct determinants of receptor binding by these growth factors. A variant of mature VEGF-D harboring a mutation in the N-terminal α-helix, D103A, exhibited enhanced potency for activating VEGFR-3, was able to promote increased COX-2 mRNA levels in lymphatic endothelial cells, and had enhanced capacity to induce lymphatic sprouting in vivo This mutant may be useful for developing protein-based therapeutics to drive lymphangiogenesis in clinical settings, such as lymphedema. Our studies shed light on the VEGF-D structure/function relationship and provide a basis for understanding functional differences compared with VEGF-C.
DOI: 10.1074/jbc.M116.736801
PubMed: 27852824
Links to Exploration step
pubmed:27852824Le document en format XML
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Harris</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Roufail, Sally" sort="Roufail, Sally" uniqKey="Roufail S" first="Sally" last="Roufail">Sally Roufail</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Paquet Fifield, Sophie" sort="Paquet Fifield, Sophie" uniqKey="Paquet Fifield S" first="Sophie" last="Paquet-Fifield">Sophie Paquet-Fifield</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Ishaq, Musarat" sort="Ishaq, Musarat" uniqKey="Ishaq M" first="Musarat" last="Ishaq">Musarat Ishaq</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Streltsov, Victor A" sort="Streltsov, Victor A" uniqKey="Streltsov V" first="Victor A" last="Streltsov">Victor A. Streltsov</name><affiliation><nlm:affiliation>the Florey Institute of Neuroscience and Mental Health, 30 Royal Parade, Parkville, Victoria 3052, and.</nlm:affiliation></affiliation></author><author><name sortKey="Williams, Steven P" sort="Williams, Steven P" uniqKey="Williams S" first="Steven P" last="Williams">Steven P. Williams</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Karnezis, Tara" sort="Karnezis, Tara" uniqKey="Karnezis T" first="Tara" last="Karnezis">Tara Karnezis</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A" last="Stacker">Steven A. 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Achen</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, marc.achen@petermac.org.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27852824</idno><idno type="pmid">27852824</idno><idno type="doi">10.1074/jbc.M116.736801</idno><idno type="wicri:Area/PubMed/Corpus">000516</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000516</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Differential Receptor Binding and Regulatory Mechanisms for the Lymphangiogenic Growth Factors Vascular Endothelial Growth Factor (VEGF)-C and -D.</title><author><name sortKey="Davydova, Natalia" sort="Davydova, Natalia" uniqKey="Davydova N" first="Natalia" last="Davydova">Natalia Davydova</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Harris, Nicole C" sort="Harris, Nicole C" uniqKey="Harris N" first="Nicole C" last="Harris">Nicole C. Harris</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Roufail, Sally" sort="Roufail, Sally" uniqKey="Roufail S" first="Sally" last="Roufail">Sally Roufail</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Paquet Fifield, Sophie" sort="Paquet Fifield, Sophie" uniqKey="Paquet Fifield S" first="Sophie" last="Paquet-Fifield">Sophie Paquet-Fifield</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Ishaq, Musarat" sort="Ishaq, Musarat" uniqKey="Ishaq M" first="Musarat" last="Ishaq">Musarat Ishaq</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Streltsov, Victor A" sort="Streltsov, Victor A" uniqKey="Streltsov V" first="Victor A" last="Streltsov">Victor A. Streltsov</name><affiliation><nlm:affiliation>the Florey Institute of Neuroscience and Mental Health, 30 Royal Parade, Parkville, Victoria 3052, and.</nlm:affiliation></affiliation></author><author><name sortKey="Williams, Steven P" sort="Williams, Steven P" uniqKey="Williams S" first="Steven P" last="Williams">Steven P. Williams</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Karnezis, Tara" sort="Karnezis, Tara" uniqKey="Karnezis T" first="Tara" last="Karnezis">Tara Karnezis</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A" last="Stacker">Steven A. Stacker</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</nlm:affiliation></affiliation></author><author><name sortKey="Achen, Marc G" sort="Achen, Marc G" uniqKey="Achen M" first="Marc G" last="Achen">Marc G. Achen</name><affiliation><nlm:affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, marc.achen@petermac.org.</nlm:affiliation></affiliation></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="eISSN">1083-351X</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Neutralizing</term><term>Cells, Cultured</term><term>Dermis (metabolism)</term><term>Dermis (pathology)</term><term>Endothelium, Vascular (metabolism)</term><term>Endothelium, Vascular (pathology)</term><term>Female</term><term>Humans</term><term>Lymphangiogenesis</term><term>Lymphatic Vessels (metabolism)</term><term>Lymphatic Vessels (pathology)</term><term>Mice, Inbred NOD</term><term>Mice, SCID</term><term>Mutagenesis, Site-Directed</term><term>Mutation (genetics)</term><term>Neovascularization, Pathologic (metabolism)</term><term>Neovascularization, Pathologic (pathology)</term><term>Signal Transduction</term><term>Vascular Endothelial Growth Factor C (chemistry)</term><term>Vascular Endothelial Growth Factor C (genetics)</term><term>Vascular Endothelial Growth Factor C (metabolism)</term><term>Vascular Endothelial Growth Factor D (chemistry)</term><term>Vascular Endothelial Growth Factor D (genetics)</term><term>Vascular Endothelial Growth Factor D (metabolism)</term><term>Vascular Endothelial Growth Factor Receptor-2 (genetics)</term><term>Vascular Endothelial Growth Factor Receptor-2 (metabolism)</term><term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term><term>Vascular Endothelial Growth Factor Receptor-3 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor D</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor D</term><term>Vascular Endothelial Growth Factor Receptor-2</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor D</term><term>Vascular Endothelial Growth Factor Receptor-2</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Antibodies, Neutralizing</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dermis</term><term>Endothelium, Vascular</term><term>Lymphatic Vessels</term><term>Neovascularization, Pathologic</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dermis</term><term>Endothelium, Vascular</term><term>Lymphatic Vessels</term><term>Neovascularization, Pathologic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Lymphangiogenesis</term><term>Mice, Inbred NOD</term><term>Mice, SCID</term><term>Mutagenesis, Site-Directed</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">VEGF-C and VEGF-D are secreted glycoproteins that induce angiogenesis and lymphangiogenesis in cancer, thereby promoting tumor growth and spread. They exhibit structural homology and activate VEGFR-2 and VEGFR-3, receptors on endothelial cells that signal for growth of blood vessels and lymphatics. VEGF-C and VEGF-D were thought to exhibit similar bioactivities, yet recent studies indicated distinct signaling mechanisms (e.g. tumor-derived VEGF-C promoted expression of the prostaglandin biosynthetic enzyme COX-2 in lymphatics, a response thought to facilitate metastasis via the lymphatic vasculature, whereas VEGF-D did not). Here we explore the basis of the distinct bioactivities of VEGF-D using a neutralizing antibody, peptide mapping, and mutagenesis to demonstrate that the N-terminal α-helix of mature VEGF-D (Phe(93)-Arg(108)) is critical for binding VEGFR-2 and VEGFR-3. Importantly, the N-terminal part of this α-helix, from Phe(93) to Thr(98), is required for binding VEGFR-3 but not VEGFR-2. Surprisingly, the corresponding part of the α-helix in mature VEGF-C did not influence binding to either VEGFR-2 or VEGFR-3, indicating distinct determinants of receptor binding by these growth factors. A variant of mature VEGF-D harboring a mutation in the N-terminal α-helix, D103A, exhibited enhanced potency for activating VEGFR-3, was able to promote increased COX-2 mRNA levels in lymphatic endothelial cells, and had enhanced capacity to induce lymphatic sprouting in vivo This mutant may be useful for developing protein-based therapeutics to drive lymphangiogenesis in clinical settings, such as lymphedema. Our studies shed light on the VEGF-D structure/function relationship and provide a basis for understanding functional differences compared with VEGF-C.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27852824</PMID><DateCreated><Year>2016</Year><Month>11</Month><Day>17</Day></DateCreated><DateCompleted><Year>2017</Year><Month>07</Month><Day>20</Day></DateCompleted><DateRevised><Year>2017</Year><Month>07</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN><JournalIssue CitedMedium="Internet"><Volume>291</Volume><Issue>53</Issue><PubDate><Year>2016</Year><Month>Dec</Month><Day>30</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J. Biol. Chem.</ISOAbbreviation></Journal><ArticleTitle>Differential Receptor Binding and Regulatory Mechanisms for the Lymphangiogenic Growth Factors Vascular Endothelial Growth Factor (VEGF)-C and -D.</ArticleTitle><Pagination><MedlinePgn>27265-27278</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.M116.736801</ELocationID><Abstract><AbstractText>VEGF-C and VEGF-D are secreted glycoproteins that induce angiogenesis and lymphangiogenesis in cancer, thereby promoting tumor growth and spread. They exhibit structural homology and activate VEGFR-2 and VEGFR-3, receptors on endothelial cells that signal for growth of blood vessels and lymphatics. VEGF-C and VEGF-D were thought to exhibit similar bioactivities, yet recent studies indicated distinct signaling mechanisms (e.g. tumor-derived VEGF-C promoted expression of the prostaglandin biosynthetic enzyme COX-2 in lymphatics, a response thought to facilitate metastasis via the lymphatic vasculature, whereas VEGF-D did not). Here we explore the basis of the distinct bioactivities of VEGF-D using a neutralizing antibody, peptide mapping, and mutagenesis to demonstrate that the N-terminal α-helix of mature VEGF-D (Phe(93)-Arg(108)) is critical for binding VEGFR-2 and VEGFR-3. Importantly, the N-terminal part of this α-helix, from Phe(93) to Thr(98), is required for binding VEGFR-3 but not VEGFR-2. Surprisingly, the corresponding part of the α-helix in mature VEGF-C did not influence binding to either VEGFR-2 or VEGFR-3, indicating distinct determinants of receptor binding by these growth factors. A variant of mature VEGF-D harboring a mutation in the N-terminal α-helix, D103A, exhibited enhanced potency for activating VEGFR-3, was able to promote increased COX-2 mRNA levels in lymphatic endothelial cells, and had enhanced capacity to induce lymphatic sprouting in vivo This mutant may be useful for developing protein-based therapeutics to drive lymphangiogenesis in clinical settings, such as lymphedema. Our studies shed light on the VEGF-D structure/function relationship and provide a basis for understanding functional differences compared with VEGF-C.</AbstractText><CopyrightInformation>© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Davydova</LastName><ForeName>Natalia</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harris</LastName><ForeName>Nicole C</ForeName><Initials>NC</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roufail</LastName><ForeName>Sally</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paquet-Fifield</LastName><ForeName>Sophie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ishaq</LastName><ForeName>Musarat</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Streltsov</LastName><ForeName>Victor A</ForeName><Initials>VA</Initials><AffiliationInfo><Affiliation>the Florey Institute of Neuroscience and Mental Health, 30 Royal Parade, Parkville, Victoria 3052, and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Williams</LastName><ForeName>Steven P</ForeName><Initials>SP</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karnezis</LastName><ForeName>Tara</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stacker</LastName><ForeName>Steven A</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>the Sir Peter MacCallum Department of Oncology, University of Melbourne, Victoria 3010, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Achen</LastName><ForeName>Marc G</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, marc.achen@petermac.org.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>the Sir Peter MacCallum Department of Oncology, University of Melbourne, Victoria 3010, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>PDB</DataBankName><AccessionNumberList><AccessionNumber>2XV7</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>11</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D057134">Antibodies, Neutralizing</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467486">VEGFC protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C579459">VEGFD protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042582">Vascular Endothelial Growth Factor C</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042643">Vascular Endothelial Growth Factor 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MajorTopicYN="Y">Lymphangiogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016688" MajorTopicYN="N">Mice, Inbred NOD</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016513" MajorTopicYN="N">Mice, SCID</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016297" MajorTopicYN="N">Mutagenesis, Site-Directed</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009389" MajorTopicYN="N">Neovascularization, Pathologic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042582" MajorTopicYN="N">Vascular Endothelial Growth Factor C</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042643" MajorTopicYN="N">Vascular Endothelial Growth Factor D</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D040301" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D040321" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-3</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">angiogenesis</Keyword><Keyword MajorTopicYN="N">endothelial cell</Keyword><Keyword MajorTopicYN="N">lymphangiogenesis</Keyword><Keyword MajorTopicYN="N">mutagenesis in vitro</Keyword><Keyword MajorTopicYN="N">receptor</Keyword><Keyword MajorTopicYN="N">vascular endothelial growth factor (VEGF)</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>09</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27852824</ArticleId><ArticleId IdType="pii">M116.736801</ArticleId><ArticleId IdType="doi">10.1074/jbc.M116.736801</ArticleId><ArticleId IdType="pmc">PMC5207153</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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