| We demonstrate through human and Drosophila genetic and in vitro molecular studies, that a severe neurological syndrome is caused by a null mutation in SEC31A, reducing cell viability through enhanced ER-stress response, in line with SEC31A's role in the COP-II complex. | SEC31A mutation affects ER homeostasis, causing a neurological syndrome.
Halperin D, Kadir R, Perez Y, Drabkin M, Yogev Y, Wormser O, Berman EM, Eremenko E, Rotblat B, Shorer Z, Gradstein L, Shelef I, Birk R, Abdu U, Flusser H, Birk OS. | 05/16/2020 |
| USP8 deubiquitinates Sec31A and inhibits the formation of large COPII carriers, thereby suppressing collagen IV secretion. | Ubiquitin-specific protease 8 deubiquitinates Sec31A and decreases large COPII carriers and collagen IV secretion.
Kawaguchi K, Endo A, Fukushima T, Madoka Y, Tanaka T, Komada M. | 10/13/2018 |
| Results show the crystal structure of the complex between ALG-2 and a peptide of Sec31A and found that the peptide binds to the third hydrophobic pocket (Pocket 3) and that ALG-2 recognizing 2 types of motifs at different hydrophobic surfaces of Sec31A. | Structural analysis of the complex between penta-EF-hand ALG-2 protein and Sec31A peptide reveals a novel target recognition mechanism of ALG-2.
Takahashi T, Kojima K, Zhang W, Sasaki K, Ito M, Suzuki H, Kawasaki M, Wakatsuki S, Takahara T, Shibata H, Maki M., Free PMC Article | 10/3/2015 |
| findings suggest that AnxA11 maintains architectural and functional features of the ERES by coordinating with ALG-2 to stabilize Sec31A at the ERES. | A new role for annexin A11 in the early secretory pathway via stabilizing Sec31A protein at the endoplasmic reticulum exit sites (ERES).
Shibata H, Kanadome T, Sugiura H, Yokoyama T, Yamamuro M, Moss SE, Maki M., Free PMC Article | 05/9/2015 |
| ALG-2/Sec31A interactions were not required for the localization of Sec31A to ER exit sites per se but appeared to acutely regulate the stability and trafficking of the cargo receptor p24 and the distribution of the vesicle tether protein p115 | Apoptosis-linked gene-2 (ALG-2)/Sec31 interactions regulate endoplasmic reticulum (ER)-to-Golgi transport: a potential effector pathway for luminal calcium.
Helm JR, Bentley M, Thorsen KD, Wang T, Foltz L, Oorschot V, Klumperman J, Hay JC., Free PMC Article | 12/20/2014 |
| ALG-2 attenuates COPII budding in vitro and stabilizes the Sec23/Sec31A complex. | ALG-2 attenuates COPII budding in vitro and stabilizes the Sec23/Sec31A complex.
la Cour JM, Schindler AJ, Berchtold MW, Schekman R., Free PMC Article | 06/21/2014 |
| These results suggest that Sec31 phosphorylation by CK2 controls the duration of COPII vesicle formation, which regulates ER-to-Golgi trafficking. | CK2 phosphorylates Sec31 and regulates ER-To-Golgi trafficking.
Koreishi M, Yu S, Oda M, Honjo Y, Satoh A., Free PMC Article | 07/20/2013 |
| efficient COPII-dependent secretion, notably assembly of Sec13-Sec31, is required to drive epithelial morphogenesis in both two- and three-dimensional cultures | Epithelial organization and cyst lumen expansion require efficient Sec13-Sec31-driven secretion.
Townley AK, Schmidt K, Hodgson L, Stephens DJ., Free PMC Article | 09/8/2012 |
| SEC31A-ALK fusions are recurrent in ALK-positive large B-cell lymphomas. | Cytogenetically complex SEC31A-ALK fusions are recurrent in ALK-positive large B-cell lymphomas.
Bedwell C, Rowe D, Moulton D, Jones G, Bown N, Bacon CM., Free PMC Article | 10/1/2011 |
| t(4;9)(q21;p24) leads to a novel SEC31A-JAK2 fusion in Hodgkin lymphoma | JAK2 rearrangements, including the novel SEC31A-JAK2 fusion, are recurrent in classical Hodgkin lymphoma.
Van Roosbroeck K, Cox L, Tousseyn T, Lahortiga I, Gielen O, Cauwelier B, De Paepe P, Verhoef G, Marynen P, Vandenberghe P, De Wolf-Peeters C, Cools J, Wlodarska I. | 06/25/2011 |
| the alg2 binding site is one of the key determinants of the retention kinetics of Sec31A at endoplasmic reticulum exit sites | The ALG-2 binding site in Sec31A influences the retention kinetics of Sec31A at the endoplasmic reticulum exit sites as revealed by live-cell time-lapse imaging.
Shibata H, Inuzuka T, Yoshida H, Sugiura H, Wada I, Maki M. | 02/26/2011 |
| Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator) | Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score.
Rose JE, Behm FM, Drgon T, Johnson C, Uhl GR., Free PMC Article | 06/30/2010 |
| Data show that coupling of the Sec23/24 and Sec13/31 layers of the COPII coat is required to drive export of collagen from the endoplasmic reticulum, and that efficient COPII assembly is essential for normal craniofacial development during embryogenesis. | Efficient coupling of Sec23-Sec24 to Sec13-Sec31 drives COPII-dependent collagen secretion and is essential for normal craniofacial development.
Townley AK, Feng Y, Schmidt K, Carter DA, Porter R, Verkade P, Stephens DJ. | 01/21/2010 |
| The Sec31 active fragment is accommodated in a binding groove supported in part by Sec23 residue Phe380. | Insights into COPII coat nucleation from the structure of Sec23.Sar1 complexed with the active fragment of Sec31.
Bi X, Mancias JD, Goldberg J., Free PMC Article | 01/21/2010 |
| Genomic PCR and subsequent sequencing showed that the breakpoints were located in intron 23 of SEC31L1 and intron 20 of anaplastic lymphoma kinase | Fusion of the SEC31L1 and ALK genes in an inflammatory myofibroblastic tumor.
Panagopoulos I, Nilsson T, Domanski HA, Isaksson M, Lindblom P, Mertens F, Mandahl N. | 01/21/2010 |
| three-dimensional reconstruction of Sec13/31 cages at 30 A resolution using cryo-electron microscopy and single particle analysis | Structure of the Sec13/31 COPII coat cage.
Stagg SM, Gürkan C, Fowler DM, LaPointe P, Foss TR, Potter CS, Carragher B, Balch WE. | 01/21/2010 |
| ALG-2 is recruited to endoplasmic reticulum exit sites via Ca(2+)-dependent interaction with Sec31A and in turn stabilizes the localization of Sec31A at these sites. | The Ca2+-binding protein ALG-2 is recruited to endoplasmic reticulum exit sites by Sec31A and stabilizes the localization of Sec31A.
Yamasaki A, Tani K, Yamamoto A, Kitamura N, Komada M., Free PMC Article | 01/21/2010 |
| In vitro GST pull down analysis demonstrated that ALG-2 and its alternatively spliced isoform interact with the COPII component Sec31A in a Ca2+-dependent manner, and a biotin-labeled ALG-2 overlay assay revealed direct binding of ALG-2 to Sec31A. | ALG-2 directly binds Sec31A and localizes at endoplasmic reticulum exit sites in a Ca2+-dependent manner.
Shibata H, Suzuki H, Yoshida H, Maki M. | 01/21/2010 |