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Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality.

Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality. Research Abstract Details 

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  • Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality. Abstract Text:

    bernice c linBernice C Lin,ruth sullivanRuth Sullivan,youngsook leeYoungsook Lee,susan moranSusan Moran,edward gloverEdward Glover,christopher a bradfieldChristopher A Bradfield,bernice c linBernice C Lin,ruth sullivanRuth Sullivan,youngsook leeYoungsook Lee,susan moranSusan Moran,edward gloverEdward Glover,christopher a bradfieldChristopher A Bradfield,bernice c linBernice C Lin,ruth sullivanRuth Sullivan,youngsook leeYoungsook Lee,susan moranSusan Moran,edward gloverEdward Glover,christopher a bradfieldChristopher A Bradfield,

    The aryl hydrocarbon receptor-associated protein 9, ARA9 (also known as XAP2 or AIP1), is a chaperone that is found in complexes with certain xenobiotic receptors, such as the aryl hydrocarbon receptor (AHR) and the peroxisome proliferator-activated receptor alpha (PPARalpha). In an effort to better understand the physiological role of ARA9 outside of its role in xenobiotic signal transduction, we generated a null allele at the Ara9 locus in mice. Mice with a homozygous deletion of this gene die at various time points throughout embryonic development. Embryonic lethality is accompanied by decreased blood flow to head and limbs, as well as a range of heart deformations, including double outlet right ventricle, ventricular-septal defects, and pericardial edema. The early cardiovascular defects observed in Ara9-null mice suggest an essential role for the ARA9 protein in cardiac development. The observation that the developmental aberrations in Ara9-null mice are distinct from those observed for disrupted alleles at Ahr or Pparalpha indicates that the role of ARA9 in cardiac development is independent of its interactions with its known xenobiotic receptor partners.

    Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality. Publishing Authors By Initials

    bc linBC Lin,r sullivanR Sullivan,y leeY Lee,s moranS Moran,e gloverE Glover,ca bradfieldCA Bradfield,bc linBC Lin,r sullivanR Sullivan,y leeY Lee,s moranS Moran,e gloverE Glover,ca bradfieldCA Bradfield,bc linBC Lin,r sullivanR Sullivan,y leeY Lee,s moranS Moran,e gloverE Glover,ca bradfieldCA Bradfield,

    For similar abstracts research abstracts see: abstracts research

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    Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: The Journal of biological chemistry

    VOLUME: 282

    Page Numbers: 35924-32

    Journal Abbreviation: J. Biol. Chem.

    ISSN: 0021-9258

    DAY: 4

    MONTH: 10

    YEAR: 2007

    Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality. Information

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    LANGUAGE: eng

    NlmUniqueID: 2985121

    Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality. Keywords Mesh Terms:

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    Grant and Affiliation Information for Deletion of the aryl hydrocarbon receptor-associated protein 9 leads to cardiac malformation and embryonic lethality.

    AFFILIATION: McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, Wisconsin 53706, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: T32-CA009135

    ACRONYM: CA

    MEDLINETA: J Biol Chem

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