NEMO/IKKγ: linking NF-κB to human disease
Identifieur interne : 006983 ( Istex/Corpus ); précédent : 006982; suivant : 006984NEMO/IKKγ: linking NF-κB to human disease
Auteurs : Gilles Courtois ; Asma Smahi ; Alain IsraëlSource :
- Trends in Molecular Medicine [ 1471-4914 ] ; 2001.
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Abstract
Until recently, no genetic disease caused by NF-κB dysfunction was known. This changed with the identification of the X-linked gene encoding a molecule of the NF-κB signaling pathway, NEMO/IKKγ. Two distinct X-linked human diseases, incontinentia pigmenti (IP) and anhidrotic ectodermal dysplasia associated with immunodeficiency (EDA-ID), have been linked to NEMO/IKKγ dysfunction, providing a unique view of the role that NF-κB plays in human development, skin homeostasis and innate and acquired immunity.
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DOI: 10.1016/S1471-4914(01)02154-2
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Location of NEMO mutations resulting in incontinentia pigmenti or anhidrotic ectodermal dysplasia associated with immunodeficiency are shown above and below the NEMO protein, respectively. Black arrows indicate missense mutations, red arrows indicate nonsense mutations and red brackets indicate frameshift/deletion mutations. In the case of frameshift mutations the number of extra amino acids is indicated. The truncated NEMO molecule that is produced in 85% of IP patients, as a result of an identical DNA rearrangement, is indicated with a blue bracket. Major structural domains of NEMO [coiled coils (CC) 1 and 2, leucine zipper (LZ) and zinc finger (ZF)] are shown together with the binding domain to IKK (blue line) and the regulatory domain (purple line) that connects the molecule to various upstream activators.</note><note type="content">Fig. 2: Participation of nuclear factor (NF)-κB in a new developmental pathway. The morphogenesis of skin appendages (hair follicles, sweat glands and teeth) is triggered by EDA-A1–EDAR interaction and requires NF-κB activation via NEMO. EDA-A1 is a member of the tumour necrosis factor (TNF) family that is released as a trimer in the extracellular medium by furin-dependent cleavage. Its binding to EDAR, a member of the TNF-R family, induces NF-κB activation through a signaling pathway that remains incompletely defined. Indicated in red are molecules that have a genetic involvement in anhidrotic ectodermal dysplasia. Mutations in crinkled also produces an EDA phenotype in mice. The identity of the affected gene, as well as the level at which it acts in the EDA-A1/EDAR pathway, remains unknown.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">NEMO/IKKγ: linking NF-κB to human disease</title><author xml:id="author-0000"><persName><forename type="first">Gilles</forename><surname>Courtois</surname></persName><email>gmcourt@pasteur.fr</email><affiliation>Unité de Biologie Moléculaire de l'Expression Génique, URA CNRS 1773, Institut Pasteur, Paris, France</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Asma</forename><surname>Smahi</surname></persName><affiliation>Unité de Recherches sur les Handicaps Génétiques de l'Enfant, INSERM U-393, Hopital Necker-Enfants Malades, Paris, France</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Alain</forename><surname>Israël</surname></persName><affiliation>Unité de Biologie Moléculaire de l'Expression Génique, URA CNRS 1773, Institut Pasteur, Paris, France</affiliation></author><idno type="istex">E1C1B012843F5F5A2CC26151D74727E46666F6CC</idno><idno type="DOI">10.1016/S1471-4914(01)02154-2</idno><idno type="PII">S1471-4914(01)02154-2</idno></analytic><monogr><title level="j">Trends in Molecular Medicine</title><title level="j" type="abbrev">TRMOME</title><idno type="pISSN">1471-4914</idno><idno type="PII">S1471-4914(00)X0009-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">7</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="427">427</biblScope><biblScope unit="page" to="430">430</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Until recently, no genetic disease caused by NF-κB dysfunction was known. This changed with the identification of the X-linked gene encoding a molecule of the NF-κB signaling pathway, NEMO/IKKγ. Two distinct X-linked human diseases, incontinentia pigmenti (IP) and anhidrotic ectodermal dysplasia associated with immunodeficiency (EDA-ID), have been linked to NEMO/IKKγ dysfunction, providing a unique view of the role that NF-κB plays in human development, skin homeostasis and innate and acquired immunity.</p></abstract><textClass><keywords scheme="keyword"><list><head>article-category</head><item><term>Research news</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>NK-kappaB</term></item><item><term>incontinenita pigmenti</term></item><item><term>anhidrotic ectodermal dysplasia</term></item><item><term>NEMO</term></item><item><term>IKKgamma</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Molecular Medicine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/E1C1B012843F5F5A2CC26151D74727E46666F6CC/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="rev" xml:lang="en"><item-info><jid>TRMOME</jid><aid>00002154</aid><ce:pii>S1471-4914(01)02154-2</ce:pii><ce:doi>10.1016/S1471-4914(01)02154-2</ce:doi><ce:copyright type="full-transfer" year="2001">Elsevier Science Ltd</ce:copyright><ce:doctopics><ce:doctopic><ce:text>Research news</ce:text></ce:doctopic></ce:doctopics></item-info><head><ce:dochead><ce:textfn>Research update</ce:textfn></ce:dochead><ce:title>NEMO/IKKγ: linking NF-κB to human disease</ce:title><ce:author-group><ce:author><ce:given-name>Gilles</ce:given-name><ce:surname>Courtois</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:e-address type="email">gmcourt@pasteur.fr</ce:e-address></ce:author><ce:author><ce:given-name>Asma</ce:given-name><ce:surname>Smahi</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Alain</ce:given-name><ce:surname>Israël</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Unité de Biologie Moléculaire de l'Expression Génique, URA CNRS 1773, Institut Pasteur, Paris, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Unité de Recherches sur les Handicaps Génétiques de l'Enfant, INSERM U-393, Hopital Necker-Enfants Malades, Paris, France</ce:textfn></ce:affiliation></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Until recently, no genetic disease caused by NF-κB dysfunction was known. This changed with the identification of the X-linked gene encoding a molecule of the NF-κB signaling pathway, NEMO/IKKγ. Two distinct X-linked human diseases, incontinentia pigmenti (IP) and anhidrotic ectodermal dysplasia associated with immunodeficiency (EDA-ID), have been linked to NEMO/IKKγ dysfunction, providing a unique view of the role that NF-κB plays in human development, skin homeostasis and innate and acquired immunity.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>NK-kappaB</ce:text></ce:keyword><ce:keyword><ce:text>incontinenita pigmenti</ce:text></ce:keyword><ce:keyword><ce:text>anhidrotic ectodermal dysplasia</ce:text></ce:keyword><ce:keyword><ce:text>NEMO</ce:text></ce:keyword><ce:keyword><ce:text>IKKgamma</ce:text></ce:keyword></ce:keywords><ce:keywords class="idt"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Molecular Medicine</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>NEMO/IKKγ: linking NF-κB to human disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>NEMO/IKKγ: linking NF-κB to human disease</title></titleInfo><name type="personal"><namePart type="given">Gilles</namePart><namePart type="family">Courtois</namePart><affiliation>Unité de Biologie Moléculaire de l'Expression Génique, URA CNRS 1773, Institut Pasteur, Paris, France</affiliation><affiliation>E-mail: gmcourt@pasteur.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Asma</namePart><namePart type="family">Smahi</namePart><affiliation>Unité de Recherches sur les Handicaps Génétiques de l'Enfant, INSERM U-393, Hopital Necker-Enfants Malades, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alain</namePart><namePart type="family">Israël</namePart><affiliation>Unité de Biologie Moléculaire de l'Expression Génique, URA CNRS 1773, Institut Pasteur, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="Review article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Until recently, no genetic disease caused by NF-κB dysfunction was known. This changed with the identification of the X-linked gene encoding a molecule of the NF-κB signaling pathway, NEMO/IKKγ. Two distinct X-linked human diseases, incontinentia pigmenti (IP) and anhidrotic ectodermal dysplasia associated with immunodeficiency (EDA-ID), have been linked to NEMO/IKKγ dysfunction, providing a unique view of the role that NF-κB plays in human development, skin homeostasis and innate and acquired immunity.</abstract><note type="content">Section title: Research update</note><note type="content">Fig. 1: NEMO mutations in human pathology. Location of NEMO mutations resulting in incontinentia pigmenti or anhidrotic ectodermal dysplasia associated with immunodeficiency are shown above and below the NEMO protein, respectively. Black arrows indicate missense mutations, red arrows indicate nonsense mutations and red brackets indicate frameshift/deletion mutations. In the case of frameshift mutations the number of extra amino acids is indicated. The truncated NEMO molecule that is produced in 85% of IP patients, as a result of an identical DNA rearrangement, is indicated with a blue bracket. Major structural domains of NEMO [coiled coils (CC) 1 and 2, leucine zipper (LZ) and zinc finger (ZF)] are shown together with the binding domain to IKK (blue line) and the regulatory domain (purple line) that connects the molecule to various upstream activators.</note><note type="content">Fig. 2: Participation of nuclear factor (NF)-κB in a new developmental pathway. The morphogenesis of skin appendages (hair follicles, sweat glands and teeth) is triggered by EDA-A1–EDAR interaction and requires NF-κB activation via NEMO. EDA-A1 is a member of the tumour necrosis factor (TNF) family that is released as a trimer in the extracellular medium by furin-dependent cleavage. Its binding to EDAR, a member of the TNF-R family, induces NF-κB activation through a signaling pathway that remains incompletely defined. Indicated in red are molecules that have a genetic involvement in anhidrotic ectodermal dysplasia. Mutations in crinkled also produces an EDA phenotype in mice. The identity of the affected gene, as well as the level at which it acts in the EDA-A1/EDAR pathway, remains unknown.</note><subject><genre>article-category</genre><topic>Research news</topic></subject><subject lang="en"><genre>Keywords</genre><topic>NK-kappaB</topic><topic>incontinenita pigmenti</topic><topic>anhidrotic ectodermal dysplasia</topic><topic>NEMO</topic><topic>IKKgamma</topic></subject><subject lang="en"><genre>Keywords</genre><topic>Molecular Medicine</topic></subject><relatedItem type="host"><titleInfo><title>Trends in Molecular Medicine</title></titleInfo><titleInfo type="abbreviated"><title>TRMOME</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">20011001</dateIssued></originInfo><identifier type="ISSN">1471-4914</identifier><identifier type="PII">S1471-4914(00)X0009-3</identifier><part><date>20011001</date><detail type="volume"><number>7</number><caption>vol.</caption></detail><detail type="issue"><number>10</number><caption>no.</caption></detail><extent unit="issue pages"><start>427</start><end>476</end></extent><extent unit="pages"><start>427</start><end>430</end></extent></part></relatedItem><identifier type="istex">E1C1B012843F5F5A2CC26151D74727E46666F6CC</identifier><identifier type="DOI">10.1016/S1471-4914(01)02154-2</identifier><identifier type="PII">S1471-4914(01)02154-2</identifier><accessCondition type="use and reproduction" contentType="copyright">©2001 Elsevier Science Ltd</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science Ltd, ©2001</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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