LymphedemaV1, Pmc, Corpus, bibRecord, 003481

Update on the Molecular Genetics of Vascular Anomalies

Identifieur interne : 003481 ( Pmc/Corpus ); précédent : 003480; suivant : 003482

Update on the Molecular Genetics of Vascular Anomalies

Source :

Lymphatic research and biology [ 1539-6851 ] ; 2005.

RBID : PMC:1579841

Abstract

Genetic factors play a critical role in the pathogenesis of vascular anomalies. Significant advances have been made in recent years in identifying the genetic and molecular determinants of a variety of vascular anomalies using a molecular genetic approach. Several genes for vascular anomalies have been identified. These genes include AGGF1 for Klippel-Trenaunay syndrome, RASA1 for capillary malformations, KRIT1, MGC4607, PDCD10 for cerebral cavernous malformations, glomulin for glomuvenous malformations, TIE2 for multiple cutaneous and mucosal venous malformations, VEGFR-3, FOXC2, NEMO, SOX18 for lymphedema or related syndromes, ENG, ACVRLK1, MADH4 for HHT or related syndromes, NDP for Coats’ disease, Notch3 for CADASIL, and PTEN for Proteus Syndrome. These findings have made genetic testing possible in some clinical cases, and may lead to the development of therapeutic strategies for vascular anomalies. Furthermore, these studies have identified critical genes involved in vascular morphogenesis, and provided fundamental understanding of the molecular mechanisms underlying vasculogenesis and angiogenesis.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1579841

DOI: 10.1089/lrb.2005.3.226
PubMed: 16379592
PubMed Central: 1579841

Links to Exploration step

PMC:1579841

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Update on the Molecular Genetics of Vascular Anomalies</title>
<author><name sortKey="Wang, Qing K" sort="Wang, Qing K" uniqKey="Wang Q" first="Qing K." last="Wang">Qing K. Wang</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">16379592</idno>
<idno type="pmc">1579841</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1579841</idno>
<idno type="RBID">PMC:1579841</idno>
<idno type="doi">10.1089/lrb.2005.3.226</idno>
<date when="2005">2005</date>
<idno type="wicri:Area/Pmc/Corpus">003481</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003481</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Update on the Molecular Genetics of Vascular Anomalies</title>
<author><name sortKey="Wang, Qing K" sort="Wang, Qing K" uniqKey="Wang Q" first="Qing K." last="Wang">Qing K. Wang</name>
</author>
</analytic>
<series><title level="j">Lymphatic research and biology</title>
<idno type="ISSN">1539-6851</idno>
<imprint><date when="2005">2005</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="P1">Genetic factors play a critical role in the pathogenesis of vascular anomalies. Significant advances have been made in recent years in identifying the genetic and molecular determinants of a variety of vascular anomalies using a molecular genetic approach. Several genes for vascular anomalies have been identified. These genes include <italic>AGGF1</italic>
 for Klippel-Trenaunay syndrome, <italic>RASA1</italic>
 for capillary malformations, <italic>KRIT1</italic>
, <italic>MGC4607</italic>
, <italic>PDCD10</italic>
 for cerebral cavernous malformations, <italic>glomulin</italic>
 for glomuvenous malformations, <italic>TIE2</italic>
 for multiple cutaneous and mucosal venous malformations, <italic>VEGFR-3</italic>
, <italic>FOXC2</italic>
, <italic>NEMO</italic>
, <italic>SOX18</italic>
 for lymphedema or related syndromes, <italic>ENG</italic>
, <italic>ACVRLK1</italic>
, <italic>MADH4</italic>
 for HHT or related syndromes, NDP for Coats’ disease, <italic>Notch3</italic>
 for CADASIL, and <italic>PTEN</italic>
 for Proteus Syndrome. These findings have made genetic testing possible in some clinical cases, and may lead to the development of therapeutic strategies for vascular anomalies. Furthermore, these studies have identified critical genes involved in vascular morphogenesis, and provided fundamental understanding of the molecular mechanisms underlying vasculogenesis and angiogenesis.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <pmc-dir>properties manuscript</pmc-dir>
  <front><journal-meta><journal-id journal-id-type="nlm-journal-id">101163587</journal-id>
<journal-id journal-id-type="pubmed-jr-id">32169</journal-id>
<journal-id journal-id-type="nlm-ta">Lymphat Res Biol</journal-id>
<journal-title>Lymphatic research and biology</journal-title>
<issn pub-type="ppub">1539-6851</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">16379592</article-id>
<article-id pub-id-type="pmc">1579841</article-id>
<article-id pub-id-type="doi">10.1089/lrb.2005.3.226</article-id>
<article-id pub-id-type="manuscript">NIHMS12107</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Update on the Molecular Genetics of Vascular Anomalies</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>WANG</surname>
<given-names>QING K.</given-names>
</name>
<degrees>Ph.D., M.B.A.</degrees>
<xref rid="FN1" ref-type="author-notes"></xref>
</contrib>
<aff id="A1">Department of Molecular Cardiology and Center for Cardiovascular Genetics, The Cleveland Clinic Foundation, Cleveland, Ohio; Huazhong University of Science and Technology Human Genome Research Center, Wuhan, Hubei, People’s Republic of China.</aff>
</contrib-group>
<author-notes><corresp id="FN1"><bold>Address reprint requests to:</bold>
 Qing Wang, Ph.D., Lerner Research Institute/ND40, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, E-mail: <email>wangq2@ccf.org</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>22</day>
<month>9</month>
<year>2006</year>
</pub-date>
<pub-date pub-type="ppub"><year>2005</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>28</day>
<month>9</month>
<year>2006</year>
</pub-date>
<volume>3</volume>
<issue>4</issue>
<fpage>226</fpage>
<lpage>233</lpage>
<abstract><p id="P1">Genetic factors play a critical role in the pathogenesis of vascular anomalies. Significant advances have been made in recent years in identifying the genetic and molecular determinants of a variety of vascular anomalies using a molecular genetic approach. Several genes for vascular anomalies have been identified. These genes include <italic>AGGF1</italic>
 for Klippel-Trenaunay syndrome, <italic>RASA1</italic>
 for capillary malformations, <italic>KRIT1</italic>
, <italic>MGC4607</italic>
, <italic>PDCD10</italic>
 for cerebral cavernous malformations, <italic>glomulin</italic>
 for glomuvenous malformations, <italic>TIE2</italic>
 for multiple cutaneous and mucosal venous malformations, <italic>VEGFR-3</italic>
, <italic>FOXC2</italic>
, <italic>NEMO</italic>
, <italic>SOX18</italic>
 for lymphedema or related syndromes, <italic>ENG</italic>
, <italic>ACVRLK1</italic>
, <italic>MADH4</italic>
 for HHT or related syndromes, NDP for Coats’ disease, <italic>Notch3</italic>
 for CADASIL, and <italic>PTEN</italic>
 for Proteus Syndrome. These findings have made genetic testing possible in some clinical cases, and may lead to the development of therapeutic strategies for vascular anomalies. Furthermore, these studies have identified critical genes involved in vascular morphogenesis, and provided fundamental understanding of the molecular mechanisms underlying vasculogenesis and angiogenesis.</p>
</abstract>
<contract-num rid="HL1">R01 HL065630-04</contract-num>
<contract-num rid="HL1">R01 HL065630-03</contract-num>
<contract-num rid="HL1">R01 HL065630-02</contract-num>
<contract-num rid="HL1">R01 HL065630-01</contract-num>
<contract-sponsor id="HL1">National Heart, Lung, and Blood Institute : NHLBI</contract-sponsor>
</article-meta>
</front>
</pmc>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/Pmc/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003481 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 003481 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Sante
   |area=    LymphedemaV1
   |flux=    Pmc
   |étape=   Corpus
   |type=    RBID
   |clé=     PMC:1579841
   |texte=   Update on the Molecular Genetics of Vascular Anomalies
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/RBID.i   -Sk "pubmed:16379592" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd   \
       | NlmPubMed2Wicri -a LymphedemaV1

This area was generated with Dilib version V0.6.31.
Data generation: Sat Nov 4 17:40:35 2017. Site generation: Tue Feb 13 16:42:16 2024

	Serveur d'exploration sur le lymphœdème
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur le lymphœdème

Update on the Molecular Genetics of Vascular Anomalies

Update on the Molecular Genetics of Vascular Anomalies

Source :

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki