Association of Connexin43 with E3 Ubiquitin Ligase TRIM21 Reveals a Mechanism for Gap Junction Phosphodegron Control-Reference-Cited by-同舟云学术

Association of Connexin43 with E3 Ubiquitin Ligase TRIM21 Reveals a Mechanism for Gap Junction Phosphodegron Control

Published:2012-11-08 Issue:12 Volume:11 Page:6134-6146
ISSN:1535-3893
Container-title:Journal of Proteome Research
language:en
Short-container-title:J. Proteome Res.

Author:

Chen Vincent C.¹,Kristensen Anders R.¹,Foster Leonard J.¹,Naus Christian C.¹

Affiliation:

1. Department of Biochemistry and Molecular Biology, Centre for High-Throughput Biology, ‡Department of Cellular and Physiological Sciences, Life Sciences Institute, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, V6T 1Z3, Canada

Publisher

American Chemical Society (ACS)

Subject

General Chemistry,Biochemistry

Link

https://pubs.acs.org/doi/pdf/10.1021/pr300790h

Reference88 articles.

1. Cardiac Malformation in Neonatal Mice Lacking Connexin43

2. GENETIC DISEASES AND GENE KNOCKOUTS REVEAL DIVERSE CONNEXIN FUNCTIONS

3. Connexin 43 (GJA1) Mutations Cause the Pleiotropic Phenotype of Oculodentodigital Dysplasia

4. A homozygousGJA1 gene mutation causes a Hallermann-Streiff/ODDD spectrum phenotype

5. A 2-bp deletion in theGJA1 gene is associated with oculo-dento-digital dysplasia with palmoplantar keratoderma

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