help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fantin, V. R.
Right arrow Articles by Lienhard, G. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fantin, V. R.
Right arrow Articles by Lienhard, G. E.
Endocrinology Vol. 140, No. 3 1329-1337
Copyright © 1999 by The Endocrine Society


ARTICLES

Cloning, Tissue Expression, and Chromosomal Location of the Mouse Insulin Receptor Substrate 4 Gene1

Valeria R. Fantin, Brian E. Lavan2, Qing Wang3, Nancy A. Jenkins, Debra J. Gilbert, Neal G. Copeland, Susanna R. Keller and Gustav E. Lienhard

Department of Biochemistry, Dartmouth Medical School, Hanover, New Hampshire 03755; and the Mammalian Genetics Laboratory, ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center (N.A.J., D.J.G., N.G.C.), Frederick, Maryland 21702

Address all correspondence and requests for reprints to: Dr. Gustav E. Lienhard, Department of Biochemistry, Vail Building, Dartmouth Medical School, Hanover, New Hampshire 03755. E-mail: gustav.e.lienhard{at}dartmouth.edu

The insulin receptor substrates (IRSs) are key proteins in signal transduction from the insulin receptor. Recently, we discovered a fourth member of this family, designated IRS-4, cloned its complementary DNA from the human embryonic kidney 293 cell line, and characterized its signaling properties in this cell line. As part of an investigation of the physiological role of this IRS, we have now cloned the mouse IRS-4 gene and determined its tissue expression and chromosomal location. The coding region of the mouse IRS-4 gene contains no introns, and in this regard is the same as that of the genes for IRS-1 and -2. The predicted amino acid sequence of mouse IRS-4 is highly homologous with that of human IRS-4; the pleckstrin homology domain, the phosphotyrosine-binding domain, and the tyrosine phosphorylation motifs are especially well conserved. The tissue distribution of IRS-4 in the mouse was determined by analysis for the expression of its messenger RNA by RT-PCR and for the protein itself by immunoprecipitation and immunoblotting. The messenger RNA was detected in skeletal muscle, brain, heart, kidney, and liver, but the protein itself was not detected in any tissue. These results indicate that IRS-4 is a very rare protein. The chromosomal locations of the mouse IRS-4 and IRS-3 genes were determined by interspecific backcross analysis and were found to be on chromosomes X and 5, respectively. As the mouse genes for IRS-1 and -2 are on chromosomes 1 and 8, respectively, each IRS gene resides on a different chromosome.




This article has been cited by other articles:


Home page
EndocrinologyHome page
S. Lee, E. G. Lynn, J.-a Kim, and M. J. Quon
Protein Kinase C-{zeta} Phosphorylates Insulin Receptor Substrate-1, -3, and -4 But Not -2: Isoform Specific Determinants of Specificity in Insulin Signaling
Endocrinology, May 1, 2008; 149(5): 2451 - 2458.
[Abstract] [Full Text] [PDF]


Home page
Mol. Endocrinol.Home page
J. Wauman, A.-S. De Smet, D. Catteeuw, D. Belsham, and J. Tavernier
Insulin Receptor Substrate 4 Couples the Leptin Receptor to Multiple Signaling Pathways
Mol. Endocrinol., April 1, 2008; 22(4): 965 - 977.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
Y. Kaburagi, R. Yamashita, Y. Ito, H. Okochi, R. Yamamoto-Honda, K. Yasuda, H. Sekihara, T. Sasazuki, T. Kadowaki, and Y. Yazaki
Insulin-Induced Cell Cycle Progression Is Impaired in Chinese Hamster Ovary Cells Overexpressing Insulin Receptor Substrate-3
Endocrinology, December 1, 2004; 145(12): 5862 - 5874.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
Y.-H. Tseng, K. M. Kriauciunas, E. Kokkotou, and C. R. Kahn
Differential Roles of Insulin Receptor Substrates in Brown Adipocyte Differentiation
Mol. Cell. Biol., March 1, 2004; 24(5): 1918 - 1929.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
E. L. Whiteman, J. J. Chen, and M. J. Birnbaum
Platelet-Derived Growth Factor (PDGF) Stimulates Glucose Transport in 3T3-L1 Adipocytes Overexpressing PDGF Receptor by a Pathway Independent of Insulin Receptor Substrates
Endocrinology, September 1, 2003; 144(9): 3811 - 3820.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
M. Schubert, D. P. Brazil, D. J. Burks, J. A. Kushner, J. Ye, C. L. Flint, J. Farhang-Fallah, P. Dikkes, X. M. Warot, C. Rio, et al.
Insulin Receptor Substrate-2 Deficiency Impairs Brain Growth and Promotes Tau Phosphorylation
J. Neurosci., August 6, 2003; 23(18): 7084 - 7092.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
S. Schreyer, D. Ledwig, I. Rakatzi, I. Kloting, and J. Eckel
Insulin Receptor Substrate-4 Is Expressed in Muscle Tissue without Acting as a Substrate for the Insulin Receptor
Endocrinology, April 1, 2003; 144(4): 1211 - 1218.
[Abstract] [Full Text] [PDF]


Home page
Genes Dev.Home page
P. G. Laustsen, M. D. Michael, B. E. Crute, S. E. Cohen, K. Ueki, R. N. Kulkarni, S. R. Keller, G. E. Lienhard, and C. R. Kahn
Lipoatrophic diabetes in Irs1-/-/Irs3-/- double knockout mice
Genes & Dev., December 15, 2002; 16(24): 3213 - 3222.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
P. Vollenweider, B. Menard, and P. Nicod
Insulin Resistance, Defective Insulin Receptor Substrate 2--Associated Phosphatidylinositol-3' Kinase Activation, and Impaired Atypical Protein Kinase C ({zeta}/{lambda}) Activation in Myotubes From Obese Patients With Impaired Glucose Tolerance
Diabetes, April 1, 2002; 51(4): 1052 - 1059.
[Abstract] [Full Text] [PDF]


Home page
FASEB J.Home page
G. SESTI, M. FEDERICI, M. L. HRIBAL, D. LAURO, P. SBRACCIA, and R. LAURO
Defects of the insulin receptor substrate (IRS) system in human metabolic disorders
FASEB J, October 1, 2001; 15(12): 2099 - 2111.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
K. Tsuruzoe, R. Emkey, K. M. Kriauciunas, K. Ueki, and C. R. Kahn
Insulin Receptor Substrate 3 (IRS-3) and IRS-4 Impair IRS-1- and IRS-2-Mediated Signaling
Mol. Cell. Biol., January 1, 2001; 21(1): 26 - 38.
[Abstract] [Full Text]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
V. R. Fantin, Q. Wang, G. E. Lienhard, and S. R. Keller
Mice lacking insulin receptor substrate 4 exhibit mild defects in growth, reproduction, and glucose homeostasis
Am J Physiol Endocrinol Metab, January 1, 2000; 278(1): E127 - E133.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
B.-H. Qu, M. Karas, A. Koval, and D. LeRoith
Insulin Receptor Substrate-4 Enhances Insulin-like Growth Factor-I-induced Cell Proliferation
J. Biol. Chem., October 29, 1999; 274(44): 31179 - 31184.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
S. C. H. Liu, Q. Wang, G. E. Lienhard, and S. R. Keller
Insulin Receptor Substrate 3 Is Not Essential for Growth or Glucose Homeostasis
J. Biol. Chem., June 18, 1999; 274(25): 18093 - 18099.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
H. Zhang, H. Hoff, and C. Sell
Insulin-like Growth Factor I-mediated Degradation of Insulin Receptor Substrate-1 Is Inhibited by Epidermal Growth Factor in Prostate Epithelial Cells
J. Biol. Chem., July 14, 2000; 275(29): 22558 - 22562.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1999 by The Endocrine Society