Literature DB >> 22028074

Kazrin, and its binding partners ARVCF- and delta-catenin, are required for Xenopus laevis craniofacial development.

Kyucheol Cho1, Moonsup Lee, Dongmin Gu, William A Munoz, Hong Ji, Malgorzata Kloc, Pierre D McCrea.   

Abstract

The novel adaptor protein Kazrin associates with multifunctional entities including p120-subfamily members (ARVCF-, delta-, and p0071-catenin). Critical contributions of Kazrin to development or homeostasis are indicated with respect to ectoderm formation, integrity and keratinocyte differentiation, whereas its presence in varied tissues suggests broader roles. We find that Kazrin is maternally loaded, is expressed across development and becomes enriched in the forming head. Kazrin's potential contributions to craniofacial development were probed by means of knockdown in the prospective anterior neural region. Cartilaginous head structures as well as eyes on injected sides were reduced in size, with molecular markers suggesting an impact upon neural crest cell establishment and migration. Similar effects followed the depletion of ARVCF (or delta-catenin), with Kazrin:ARVCF functional interplay supported upon ARVCF partial rescue of Kazrin knockdown phenotypes. Thus, Kazrin and its associating ARVCF- and delta-catenins, are required to form craniofacial tissues originating from cranial neural crest and precordal plate.
Copyright © 2011 Wiley Periodicals, Inc.

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Year:  2011        PMID: 22028074      PMCID: PMC3408392          DOI: 10.1002/dvdy.22721

Source DB:  PubMed          Journal:  Dev Dyn        ISSN: 1058-8388            Impact factor:   3.780


  40 in total

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6.  Xenopus Kazrin interacts with ARVCF-catenin, spectrin and p190B RhoGAP, and modulates RhoA activity and epithelial integrity.

Authors:  Kyucheol Cho; Travis G Vaught; Hong Ji; Dongmin Gu; Catherine Papasakelariou-Yared; Nicola Horstmann; Jean Marie Jennings; Moonsup Lee; Lisa M Sevilla; Malgorzata Kloc; Albert B Reynolds; Fiona M Watt; Richard G Brennan; Andrew P Kowalczyk; Pierre D McCrea
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6.  Novel truncating mutations in CTNND1 cause a dominant craniofacial and cardiac syndrome.

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  6 in total

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