研究者詳細 - 齋藤　康太

Abstract

Insulin is an essential peptide hormone that maintains blood glucose levels. Although the mechanisms underlying insulin exocytosis have been investigated, the mechanism of proinsulin export from the endoplasmic reticulum (ER) remains unclear. Here, we demonstrated that Surf4, a cargo receptor homolog, regulates the ER export of proinsulin via its recruitment to ER exit sites (ERES). Under high-glucose conditions, Surf4 expression was upregulated, and Surf4 proteins mainly localized to the ER at a steady state and accumulated in the ERES, along with proinsulin in rat insulinoma INS-1 cells. Surf4-knockdown resulted in proinsulin retention in the ER and decreased the levels of mature insulin in secretory granules, thereby significantly reducing insulin secretion. Surf4 forms an oligomer and can physically interact with proinsulin and Sec12, essential for COPII vesicle formation. Our findings suggest that Surf4 interacts with proinsulin and delivers it into COPII vesicles for ER export in co-operation with Sec12 and COPII.

DOI

Mitotic ER exit site dynamics: insights into blockade of secretion from the ER during mitosis

Maeda M.

Molecular and Cellular Oncology ( Molecular and Cellular Oncology ) 7 ( 6 ) 2020年11月 [査読有り]

研究論文（学術雑誌）

DOI

Mitotic ER Exit Site Disassembly and Reassembly Are Regulated by the Phosphorylation Status of TANGO1

Kota Saito

Developmental Cell 2020年08月

研究論文（学術雑誌）

DOI

Not just a cargo receptor for large cargoes; an emerging role of TANGO1 as an organizer of ER exit sites.

Saito, K. and Maeda, M.

J. Biochem. 166 ( 2 ) 115 - 119 2019年08月 [査読有り] [招待有り]

研究論文（学術雑誌）国内共著

LTK is an ER-resident receptor tyrosine kinase that regulates secretion

Federica G. Centonze, Veronika Reiterer, Karsten Nalbach, Kota Saito, Krzysztof Pawlowski, Christian Behrends, Hesso Farhan

Journal of Cell Biology ( Rockefeller University Press ) 218 ( 8 ) 2470 - 2480 2019年06月

研究論文（学術雑誌）

<jats:p>The endoplasmic reticulum (ER) is a key regulator of cellular proteostasis because it controls folding, sorting, and degradation of secretory proteins. Much has been learned about how environmentally triggered signaling pathways regulate ER function, but only little is known about local signaling at the ER. The identification of ER-resident signaling molecules will help gain a deeper understanding of the regulation of ER function and thus of proteostasis. Here, we show that leukocyte tyrosine kinase (LTK) is an ER-resident receptor tyrosine kinase. Depletion of LTK as well as its pharmacologic inhibition reduces the number of ER exit sites and slows ER-to-Golgi transport. Furthermore, we show that LTK interacts with and phosphorylates Sec12. Expression of a phosphoablating mutant of Sec12 reduces the efficiency of ER export. Thus, LTK-to-Sec12 signaling represents the first example of an ER-resident signaling module with the potential to regulate proteostasis.</jats:p>

DOI CiNii Research

COPII proteins exhibit distinct subdomains within each ER exit site for executing their functions.

Maeda, M., Kurokawa, K., Katada, T., Nakano, A. and Saito, K.

Sci. Rep. 9 7346 2019年05月

研究論文（学術雑誌）国内共著

Not just a cargo receptor for large cargoes; an emerging role of TANGO1 as an organizer of ER exit sites

Kota Saito, Miharu Maeda

The Journal of Biochemistry ( Oxford University Press (OUP) ) 166 ( 2 ) 115 - 119 2019年05月

研究論文（学術雑誌）

<jats:title>Abstract</jats:title>
<jats:p>Proteins synthesized within the endoplasmic reticulum (ER) are exported from ER exit sites via coat protein complex II (COPII)-coated vesicles. Although the mechanisms of COPII-vesicle formation at the ER exit sites are highly conserved among species, vertebrate cells secrete a wide range of materials, including collagens and chylomicrons, which form bulky structures within the ER that are too large to fit into conventional carriers. Transport ANd Golgi Organization 1 (TANGO1) was initially identified as a cargo receptor for collagens but has been recently rediscovered as an organizer of ER exit sites. We would like to review recent advances in the mechanism of large cargo secretion and organization of ER exit sites through the function of TANGO1.</jats:p>

DOI CiNii Research

The binding of TBK1 to STING requires exocytic membrane traffic from the ER.

Ogawa, E., Mukai, K., Saito, K., Arai, H. and Taguchi, T.

Biochem. Biophys. Res. Commun. 503 ( 1 ) 138 - 145 2018年09月 [査読有り]

研究論文（学術雑誌）国内共著

Remodeling of ER-exit sites initiates a membrane supply pathway for autophagosome biogenesis.

Ge, L., Zhang, M., Kenny, S., Liu, D., Maeda, M., Saito, K., Mathur, A., Xu, K. and Schekman, R.

EMBO Rep. 18 1586 - 1603 2017年09月 [査読有り]

研究論文（学術雑誌）国際共著

Regulation of the Sar1 GTPase Cycle Is Necessary for Large Cargo Secretion from the Endoplasmic Reticulum.

Saito, K. Maeda, M. and Katada, T.

Front. Cell Dev. Biol. 5 ( 75 ) 2017年08月

研究論文（学術雑誌）国内共著

CREB3L2-mediated expression of Sec23A/Sec24D is involved in hepatic stellate cell activation through ER-Golgi transport.

Tomoishi, S., Fukushima, S., Shinohara, K., Katada, T. and Saito, K.

Sci. Rep. 7 ( 7992 ) 2017年08月 [査読有り]

研究論文（学術雑誌）単著

TANGO1 recruits Sec16 to coordinately organize ER exit sites for efficient secretion.

Maeda, M., Katada, T. and Saito, K.

J. Cell Biol. 216 ( 6 ) 1731 - 1743 2017年06月 [査読有り]

研究論文（学術雑誌）国内共著

Distinct isoform-specific complexes of TANGO1 cooperatively facilitate collagen secretion from the endoplasmic reticulum.

Maeda, M., Saito, K, and Katada, T.

Mol. Biol. Cell 27 2688 - 2696 2016年09月 [査読有り]

研究論文（学術雑誌）国内共著

Dual function of cTAGE5 in collagen export from the endoplasmic reticulum.

Tanabe, T., Maeda, M., Saito, K., and Katada, T.

Mol. Biol. Cell 27 2008 - 2013 2016年07月 [査読有り]

研究論文（学術雑誌）国内共著

Mechanisms for exporting large-sized cargoes from the endoplasmic reticulum.

Saito, K. and Katada, T.

Cell. Mol. Life Sci. 72 ( 19 ) 3709 - 3720 2015年10月 [査読有り] [招待有り]

研究論文（学術雑誌）国内共著

Concentration of Sec12 at ER exit sites via interaction with cTAGE5 is required for collagen export.

Saito, K., Yamashiro, K., Shimazu, N., Tanabe, T., Kontani, K. and Katada, T.

J. Cell. Biol. 206 ( 6 ) 751 - 762 2014年09月 [査読有り]

研究論文（学術雑誌）国内共著

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研究等業績 - 原著論文 - 齋藤　康太