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The atypical kinase Cdk5 is activated by insulin, regulates the association between GLUT4 and E-Syt1, and modulates glucose transport in 3T3-L1 adipocytes

Vasiliki Lalioti, Gemma Muruais, Ana Dinarina, Jozef Van Damme UGent, Joël Vandekerckhove UGent and Ignacio V. Sandoval (2009) PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 106(11). p.4249-4253
abstract
Here, we report that Cdk5 activation is stimulated by insulin and plays a key role in the regulation of GLUT4-mediated glucose uptake in 3T3-L1 adipocytes. Insulin activation of Cdk5 requires PI3K signaling. Insulin-activated Cdk5 phosphorylates E-Syt1, a 5 C2-domain protein-related to the synaptotagmins that is induced during adipocyte differentiation. Phosphorylated E-Syt1 associates with GLUT4, an event inhibited by the Cdks inhibitor roscovitine. Cdk5 silencing inhibits glucose uptake by 3T3-L1 adipocytes. These studies elucidate a previously unknown activity of Cdk5 and demonstrate the involvement of this kinase in the regulation of insulin-dependent glucose uptake in adipocytes.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
P35, CYCLIN-DEPENDENT KINASE-5, CDKAL1, PROTEIN-KINASE, INHIBITOR, FAMILY, ROLES, CELLS, TRANSLOCATION
journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Proc. Natl. Acad. Sci. U. S. A.
volume
106
issue
11
pages
4249 - 4253
publisher
NATL ACAD SCIENCES
place of publication
WASHINGTON, DC 20418 USA
Web of Science type
Article
Web of Science id
000264278800037
JCR category
MULTIDISCIPLINARY SCIENCES
JCR impact factor
9.432 (2009)
JCR rank
3/48 (2009)
JCR quartile
1 (2009)
ISSN
0027-8424
DOI
10.1073/pnas.0900218106
language
English
UGent publication?
yes
classification
A1
id
539248
handle
http://hdl.handle.net/1854/LU-539248
date created
2009-04-07 14:22:45
date last changed
2013-01-30 09:41:46
@article{539248,
  abstract     = {Here, we report that Cdk5 activation is stimulated by insulin and plays a key role in the regulation of GLUT4-mediated glucose uptake in 3T3-L1 adipocytes. Insulin activation of Cdk5 requires PI3K signaling. Insulin-activated Cdk5 phosphorylates E-Syt1, a 5 C2-domain protein-related to the synaptotagmins that is induced during adipocyte differentiation. Phosphorylated E-Syt1 associates with GLUT4, an event inhibited by the Cdks inhibitor roscovitine. Cdk5 silencing inhibits glucose uptake by 3T3-L1 adipocytes. These studies elucidate a previously unknown activity of Cdk5 and demonstrate the involvement of this kinase in the regulation of insulin-dependent glucose uptake in adipocytes.},
  author       = {Lalioti, Vasiliki and Muruais, Gemma and Dinarina, Ana and Van Damme, Jozef and Vandekerckhove, Jo{\"e}l and Sandoval, Ignacio V.},
  issn         = {0027-8424},
  journal      = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA},
  keyword      = {P35,CYCLIN-DEPENDENT KINASE-5,CDKAL1,PROTEIN-KINASE,INHIBITOR,FAMILY,ROLES,CELLS,TRANSLOCATION},
  language     = {eng},
  number       = {11},
  pages        = {4249--4253},
  publisher    = {NATL ACAD SCIENCES},
  title        = {The atypical kinase Cdk5 is activated by insulin, regulates the association between GLUT4 and E-Syt1, and modulates glucose transport in 3T3-L1 adipocytes},
  url          = {http://dx.doi.org/10.1073/pnas.0900218106},
  volume       = {106},
  year         = {2009},
}

Chicago
Lalioti, Vasiliki, Gemma Muruais, Ana Dinarina, Jozef Van Damme, Joël Vandekerckhove, and Ignacio V. Sandoval. 2009. “The Atypical Kinase Cdk5 Is Activated by Insulin, Regulates the Association Between GLUT4 and E-Syt1, and Modulates Glucose Transport in 3T3-L1 Adipocytes.” Proceedings of the National Academy of Sciences of the United States of America 106 (11): 4249–4253.
APA
Lalioti, V., Muruais, G., Dinarina, A., Van Damme, J., Vandekerckhove, J., & Sandoval, I. V. (2009). The atypical kinase Cdk5 is activated by insulin, regulates the association between GLUT4 and E-Syt1, and modulates glucose transport in 3T3-L1 adipocytes. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 106(11), 4249–4253.
Vancouver
1.
Lalioti V, Muruais G, Dinarina A, Van Damme J, Vandekerckhove J, Sandoval IV. The atypical kinase Cdk5 is activated by insulin, regulates the association between GLUT4 and E-Syt1, and modulates glucose transport in 3T3-L1 adipocytes. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. WASHINGTON, DC 20418 USA: NATL ACAD SCIENCES; 2009;106(11):4249–53.
MLA
Lalioti, Vasiliki, Gemma Muruais, Ana Dinarina, et al. “The Atypical Kinase Cdk5 Is Activated by Insulin, Regulates the Association Between GLUT4 and E-Syt1, and Modulates Glucose Transport in 3T3-L1 Adipocytes.” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 106.11 (2009): 4249–4253. Print.