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Year Number of Results
2006 2
2007 2
2008 2
2009 1
2010 1
2011 3
2012 5
2013 2
2014 5
2015 2
2016 8
2017 5
2018 4
2019 2
2020 9
2021 5
2022 6
2023 4
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59 results

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Page 1
Sec16A, a key protein in COPII vesicle formation, regulates the stability and localization of the novel ubiquitin ligase RNF183.
Wu Y, Guo XP, Kanemoto S, Maeoka Y, Saito A, Asada R, Matsuhisa K, Ohtake Y, Imaizumi K, Kaneko M. Wu Y, et al. PLoS One. 2018 Jan 4;13(1):e0190407. doi: 10.1371/journal.pone.0190407. eCollection 2018. PLoS One. 2018. PMID: 29300766 Free PMC article.
RNF183 colocalized with Sec16A and interacted through the central conserved domain (CCD) of Sec16A. Although Sec16A is not a substrate for RNF183, RNF183 was more rapidly degraded by the ER-associated degradation (ERAD) in the absence of Sec16A. ...
RNF183 colocalized with Sec16A and interacted through the central conserved domain (CCD) of Sec16A. Although Sec16A is …
SEC16A is a RAB10 effector required for insulin-stimulated GLUT4 trafficking in adipocytes.
Bruno J, Brumfield A, Chaudhary N, Iaea D, McGraw TE. Bruno J, et al. J Cell Biol. 2016 Jul 4;214(1):61-76. doi: 10.1083/jcb.201509052. Epub 2016 Jun 27. J Cell Biol. 2016. PMID: 27354378 Free PMC article.
RAB10 is a regulator of insulin-stimulated translocation of the GLUT4 glucose transporter to the plasma membrane (PM) of adipocytes, which is essential for whole-body glucose homeostasis. We establish SEC16A as a novel RAB10 effector in this process. Colocalization of S
RAB10 is a regulator of insulin-stimulated translocation of the GLUT4 glucose transporter to the plasma membrane (PM) of adipocytes, which i …
Sec16A is critical for both conventional and unconventional secretion of CFTR.
Piao H, Kim J, Noh SH, Kweon HS, Kim JY, Lee MG. Piao H, et al. Sci Rep. 2017 Jan 9;7:39887. doi: 10.1038/srep39887. Sci Rep. 2017. PMID: 28067262 Free PMC article.
Notably, during unconventional secretion, Sec16A was redistributed to cell periphery and associated with GRASP55 in mammalian cells. ...These findings highlight a novel function of Sec16A as an essential mediator of ER stress-associated unconventional secretion....
Notably, during unconventional secretion, Sec16A was redistributed to cell periphery and associated with GRASP55 in mammalian cells. …
Nbeal2 interacts with Dock7, Sec16a, and Vac14.
Mayer L, Jasztal M, Pardo M, Aguera de Haro S, Collins J, Bariana TK, Smethurst PA, Grassi L, Petersen R, Nurden P, Favier R, Yu L, Meacham S, Astle WJ, Choudhary J, Yue WW, Ouwehand WH, Guerrero JA. Mayer L, et al. Blood. 2018 Mar 1;131(9):1000-1011. doi: 10.1182/blood-2017-08-800359. Epub 2017 Nov 29. Blood. 2018. PMID: 29187380 Free PMC article.
We present here the interactome of Nbeal2 with additional validation by reverse immunoprecipitation of Dock7, Sec16a, and Vac14 as interactors of Nbeal2. We show that GPS-causing mutations in its BEACH domain have profound and possible effects on the interaction with Dock7 …
We present here the interactome of Nbeal2 with additional validation by reverse immunoprecipitation of Dock7, Sec16a, and Vac14 as in …
The landscape of genetic diseases in Saudi Arabia based on the first 1000 diagnostic panels and exomes.
Monies D, Abouelhoda M, AlSayed M, Alhassnan Z, Alotaibi M, Kayyali H, Al-Owain M, Shah A, Rahbeeni Z, Al-Muhaizea MA, Alzaidan HI, Cupler E, Bohlega S, Faqeih E, Faden M, Alyounes B, Jaroudi D, Goljan E, Elbardisy H, Akilan A, Albar R, Aldhalaan H, Gulab S, Chedrawi A, Al Saud BK, Kurdi W, Makhseed N, Alqasim T, El Khashab HY, Al-Mousa H, Alhashem A, Kanaan I, Algoufi T, Alsaleem K, Basha TA, Al-Murshedi F, Khan S, Al-Kindy A, Alnemer M, Al-Hajjar S, Alyamani S, Aldhekri H, Al-Mehaidib A, Arnaout R, Dabbagh O, Shagrani M, Broering D, Tulbah M, Alqassmi A, Almugbel M, AlQuaiz M, Alsaman A, Al-Thihli K, Sulaiman RA, Al-Dekhail W, Alsaegh A, Bashiri FA, Qari A, Alhomadi S, Alkuraya H, Alsebayel M, Hamad MH, Szonyi L, Abaalkhail F, Al-Mayouf SM, Almojalli H, Alqadi KS, Elsiesy H, Shuaib TM, Seidahmed MZ, Abosoudah I, Akleh H, AlGhonaium A, Alkharfy TM, Al Mutairi F, Eyaid W, Alshanbary A, Sheikh FR, Alsohaibani FI, Alsonbul A, Al Tala S, Balkhy S, Bassiouni R, Alenizi AS, Hussein MH, Hassan S, Khalil M, Tabarki B, Alshahwan S, Oshi A, Sabr Y, Alsaadoun S, Salih MA, Mohamed S, Sultana H, Tamim A, El-Haj M, Alshahrani S, Bubshait DK, Alfadhel M, Faquih T, El-Kalioby M, Subhani S, Shah … See abstract for full author list ➔ Monies D, et al. Hum Genet. 2017 Aug;136(8):921-939. doi: 10.1007/s00439-017-1821-8. Epub 2017 Jun 9. Hum Genet. 2017. PMID: 28600779 Free PMC article.
Finally, we have encountered candidate variants in 75 genes (ABHD6, ACY3, ADGRB2, ADGRG7, AGTPBP1, AHNAK2, AKAP6, ASB3, ATXN1L, C17orf62, CABP1, CCDC186, CCP110, CLSTN2, CNTN3, CNTN5, CTNNA2, CWC22, DMAP1, DMKN, DMXL1, DSCAM, DVL2, ECI1, EP400, EPB41L5, FBXL22, GAP43, GEMIN7, GIT …
Finally, we have encountered candidate variants in 75 genes (ABHD6, ACY3, ADGRB2, ADGRG7, AGTPBP1, AHNAK2, AKAP6, ASB3, ATXN1L, C17orf62, CA …
KMT2A-MLLT1 and the Novel SEC16A-KMT2A in a Cryptic 3-Way Translocation t(9;11;19) Present in an Infant With Acute Lymphoblastic Leukemia.
de Matos RRC, Ferreira GM, Meyer C, Marschalek R, Larghero P, Ribeiro RC, Liehr T, Othman M, Bizarro MTSM, Sobral da Costa E, Land MGP, Abdelhay E, Binato R, Silva MLM. de Matos RRC, et al. J Pediatr Hematol Oncol. 2022 Apr 1;44(3):e719-e722. doi: 10.1097/MPH.0000000000002386. J Pediatr Hematol Oncol. 2022. PMID: 34966090
Interestingly, long-distance inverse polymerase chain reaction sequencing revealed a KMT2A-MLLT1 and the yet unreported out-of-frame SEC16A-KMT2A fusion, associated with low SEC16A expression and KMT2A overexpression, in an infant with B-acute lymphoblastic leukemia …
Interestingly, long-distance inverse polymerase chain reaction sequencing revealed a KMT2A-MLLT1 and the yet unreported out-of-frame SEC1
Sec16A defines the site for vesicle budding from the endoplasmic reticulum on exit from mitosis.
Hughes H, Stephens DJ. Hughes H, et al. J Cell Sci. 2010 Dec 1;123(Pt 23):4032-8. doi: 10.1242/jcs.076000. Epub 2010 Nov 2. J Cell Sci. 2010. PMID: 21045114 Free PMC article.
Here, we show that unlike all other COPII components, which are cytosolic during metaphase, Sec16A remains associated with ER exit sites throughout mitosis, and thereby could provide a template for the rapid assembly of functional export domains in anaphase. ...
Here, we show that unlike all other COPII components, which are cytosolic during metaphase, Sec16A remains associated with ER exit si …
[Clinical value of plasma scaffold protein SEC16A in evaluating hepatitis B-related liver cirrhosis and hepatocellular carcinoma].
Dong C, Chang CD, Zhao DD, Zhang XX, Guo PL, Dou Y, Zhao SX, Nan YM. Dong C, et al. Zhonghua Gan Zang Bing Za Zhi. 2023 Jun 20;31(6):621-626. doi: 10.3760/cma.j.cn501113-20230220-00067. Zhonghua Gan Zang Bing Za Zhi. 2023. PMID: 37400387 Chinese.
SEC16A, age, and AFP were independent risk factors for the occurrence of HBV-LC and HCC. ...Conclusion: Plasma SEC16A can be used as a diagnostic marker for hepatitis B-related liver cirrhosis and hepatocellular carcinoma. ...
SEC16A, age, and AFP were independent risk factors for the occurrence of HBV-LC and HCC. ...Conclusion: Plasma SEC16A can be u
Leucine-rich repeat kinase 2 regulates Sec16A at ER exit sites to allow ER-Golgi export.
Cho HJ, Yu J, Xie C, Rudrabhatla P, Chen X, Wu J, Parisiadou L, Liu G, Sun L, Ma B, Ding J, Liu Z, Cai H. Cho HJ, et al. EMBO J. 2014 Oct 16;33(20):2314-31. doi: 10.15252/embj.201487807. Epub 2014 Sep 8. EMBO J. 2014. PMID: 25201882 Free PMC article.
Here we show that LRRK2 regulates the anterograde ER-Golgi transport through anchoring Sec16A at the endoplasmic reticulum exit sites (ERES). LRRK2 interacted and co-localized with Sec16A, a key protein in the formation of ERES. Lrrk2 depletion caused a dispersion o …
Here we show that LRRK2 regulates the anterograde ER-Golgi transport through anchoring Sec16A at the endoplasmic reticulum exit sites …
Regulation of Sec16 levels and dynamics links proliferation and secretion.
Tillmann KD, Reiterer V, Baschieri F, Hoffmann J, Millarte V, Hauser MA, Mazza A, Atias N, Legler DF, Sharan R, Weiss M, Farhan H. Tillmann KD, et al. J Cell Sci. 2015 Feb 15;128(4):670-82. doi: 10.1242/jcs.157115. Epub 2014 Dec 19. J Cell Sci. 2015. PMID: 25526736
Consistent with this notion, Sec16A is also regulated by short-term growth factor treatment that leads to increased turnover of Sec16A at ERES. Finally, we demonstrate that Sec16A depletion reduces proliferation, whereas its overexpression increases prolifera …
Consistent with this notion, Sec16A is also regulated by short-term growth factor treatment that leads to increased turnover of Se
59 results