Cdk5 and Foxc2--a new relationship in the lymphatic vasculature.
Identifieur interne : 000C84 ( PubMed/Curation ); précédent : 000C83; suivant : 000C85Cdk5 and Foxc2--a new relationship in the lymphatic vasculature.
Auteurs : Johanna Liebl [Allemagne]Source :
- Oncotarget [ 1949-2553 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- cytologie : Vaisseaux lymphatiques.
- métabolisme : Facteurs de transcription Forkhead.
- physiologie : Kinase-5 cycline-dépendante, Lymphangiogenèse, Vaisseaux lymphatiques.
- Animaux, Souris, Souris knockout.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Forkhead Transcription Factors.
- chemical , physiology : Cyclin-Dependent Kinase 5.
- cytology : Lymphatic Vessels.
- physiology : Lymphangiogenesis, Lymphatic Vessels.
- Animals, Mice, Mice, Knockout.
Abstract
Lymphatic vessel dysfunction is associated with various pathologic conditions, including immunologic disorders, lymphedema, as well as tumor dissemination. Yet, the knowledge about the regulation of lymphatic vessel development is still limited. Our study elucidates cyclin dependent kinase 5 (Cdk5) as an essential player in the development of lymphatic vessels. Deletion of Cdk5 in the mouse endothelium results in severe lymphedema formation and embryonic lethality. On the mechanistic level, we show that Cdk5 phosphorylates the forkhead transcription factor Foxc2 which regulates Foxc2-dependent transcription. In summary, our study elucidates the Cdk5-Foxc2 interaction as a critical regulator of lymphatic vessel development.
DOI: 10.18632/oncotarget.4848
PubMed: 26327394
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pubmed:26327394Le document en format XML
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Yet, the knowledge about the regulation of lymphatic vessel development is still limited. Our study elucidates cyclin dependent kinase 5 (Cdk5) as an essential player in the development of lymphatic vessels. Deletion of Cdk5 in the mouse endothelium results in severe lymphedema formation and embryonic lethality. On the mechanistic level, we show that Cdk5 phosphorylates the forkhead transcription factor Foxc2 which regulates Foxc2-dependent transcription. In summary, our study elucidates the Cdk5-Foxc2 interaction as a critical regulator of lymphatic vessel development.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26327394</PMID><DateCreated><Year>2015</Year><Month>09</Month><Day>23</Day></DateCreated><DateCompleted><Year>2016</Year><Month>06</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1949-2553</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><Issue>26</Issue><PubDate><Year>2015</Year><Month>Sep</Month><Day>08</Day></PubDate></JournalIssue><Title>Oncotarget</Title><ISOAbbreviation>Oncotarget</ISOAbbreviation></Journal><ArticleTitle>Cdk5 and Foxc2--a new relationship in the lymphatic vasculature.</ArticleTitle><Pagination><MedlinePgn>21799-801</MedlinePgn></Pagination><Abstract><AbstractText>Lymphatic vessel dysfunction is associated with various pathologic conditions, including immunologic disorders, lymphedema, as well as tumor dissemination. Yet, the knowledge about the regulation of lymphatic vessel development is still limited. Our study elucidates cyclin dependent kinase 5 (Cdk5) as an essential player in the development of lymphatic vessels. Deletion of Cdk5 in the mouse endothelium results in severe lymphedema formation and embryonic lethality. On the mechanistic level, we show that Cdk5 phosphorylates the forkhead transcription factor Foxc2 which regulates Foxc2-dependent transcription. In summary, our study elucidates the Cdk5-Foxc2 interaction as a critical regulator of lymphatic vessel development.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liebl</LastName><ForeName>Johanna</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Ludwig Maximilians-University Munich, Department of Pharmacy, Pharmaceutical Biology, Munich, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Oncotarget</MedlineTA><NlmUniqueID>101532965</NlmUniqueID><ISSNLinking>1949-2553</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C082078">mesenchyme fork head 1 protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051360">Cyclin-Dependent Kinase 5</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Dev Cell. 2012 Feb 14;22(2):430-45</RefSource><PMID Version="1">22306086</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell Biol. 2013 Oct;33(19):3749-61</RefSource><PMID Version="1">23878394</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2001 May 15;10(11):1185-9</RefSource><PMID Version="1">11371511</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Med. 2004 Sep;10(9):974-81</RefSource><PMID Version="1">15322537</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10069-74</RefSource><PMID 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Version="1">26027726</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051360" MajorTopicYN="N">Cyclin-Dependent Kinase 5</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051858" MajorTopicYN="N">Forkhead Transcription Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000502" 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