|
|
|
|||||||
|
|||||||||
J Biol Chem, Vol. 273, Issue 43, 28461-28469, October 23, 1998
From the Two cytoplasmic regions of the
prolactin (PRL) receptor are well documented for their participation in
PRL signal transduction, the membrane proximal box 1 and the
COOH-terminal region. In order to study the role of these regions in
PRL-induced Ca2+ increase, we use Chinese hamster
ovary (CHO) cells stably transfected with mutated PRL receptor
cDNA. These cells express the long form of PRL receptor deleted
from box 1 (CHO We conclude from these findings that box 1 and COOH-terminal regions
are both needed for PRL-induced Ca2+ changes.
Distinct Cytoplasmic Regions of the Prolactin Receptor Are
Required for Prolactin-induced Calcium Entry
,,
Laboratoire de Neurophysiologie, Centre
National de la Recherche Scientifique UMR 5543, Université de
Bordeaux 2, 33076 Bordeaux Cédex, France and the
¶ Unité d'Endocrinologie Moléculaire, Institut
National de la Recherche Agronomique,
78352 Jouy en Josas Cédex, France
1 cells) or the 141 amino acids of the COOH-terminal
region (CHO H3 cells). The patch-clamp technique in "whole-cell"
configuration and microfluorimetric techniques were used singly or in
combination. Data obtained for these cells were compared with those we
have recently published using CHO cells expressing the wild-type long
form of the PRL receptor (CHO TSE32). In contrast to CHO TSE32 cells,
exposure of CHO 1 or H3 cells to PRL (0.05-50 nM) did
not modify [Ca2+]i. We have previously shown that
the PRL-induced calcium influx via voltage-insensitive,
Ca2+ channels was due to the activation of tyrosine
kinase-dependent K+ channels that hyperpolarize
the CHO TSE32 cell membrane (hyperpolarization-driven Ca2+
influx). Therefore, two events are involved in PRL-induced
Ca2+ changes (i) JAK2-activation of K+ channels and (ii)
intracellular messenger-opening of Ca2+ channels. In CHO
1 cells, PRL (0.05-50 nM) neither hyperpolarized the
membrane potential nor stimulated the JAK2-dependent
K+ current, confirming the pivotal role played by box
1/JAK2 in the PRL-induced activation of K+ channels.
However, when these cells were voltage-clamped below the resting
membrane potential, application of 5 nM PRL resulted in an
increase in Ca2+ influx. Therefore, box 1/JAK2 was not
involved in the opening of these Ca2+ channels. In CHO H3
cells, 5 nM PRL activated the K+ current and
hyperpolarized the membrane potential without any effect on
[Ca2+]i. Moreover, PRL was also ineffective on
CHO H3 cells voltage-clamped below the resting membrane potential.
Therefore, the COOH-terminal region is involved in the production of
the intracellular messenger that opens voltage-independent
Ca2+ channels.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  R. Shao, M. Nutu, B. Weijdegard, E. Egecioglu, J. Fernandez-Rodriguez, E. Tallet, V. Goffin, C. Ling, and H. Billig Differences in Prolactin Receptor (PRLR) in Mouse and Human Fallopian Tubes: Evidence for Multiple Regulatory Mechanisms Controlling PRLR Isoform Expression in Mice Biol Reprod, October 1, 2008; 79(4): 748 - 757. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. R. Grattan, C. L. Jasoni, X. Liu, G. M. Anderson, and A. E. Herbison Prolactin Regulation of Gonadotropin-Releasing Hormone Neurons to Suppress Luteinizing Hormone Secretion in Mice Endocrinology, September 1, 2007; 148(9): 4344 - 4351. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. C. Kokay, P. M. Bull, R. L. Davis, M. Ludwig, and D. R. Grattan Expression of the long form of the prolactin receptor in magnocellular oxytocin neurons is associated with specific prolactin regulation of oxytocin neurons Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2006; 290(5): R1216 - R1225. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Lajus, P. Vacher, D. Huber, M. Dubois, M.-N. Benassy, Y. Ushkaryov, and J. Lang {alpha}-Latrotoxin Induces Exocytosis by Inhibition of Voltage-dependent K+ Channels and by Stimulation of L-type Ca2+ Channels via Latrophilin in beta-Cells J. Biol. Chem., March 3, 2006; 281(9): 5522 - 5531. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Zhang, M. Kohler, S.-N. Yang, F. Zhang, O. Larsson, and P.-O. Berggren Growth Hormone Promotes Ca2+-Induced Ca2+ Release in Insulin-Secreting Cells by Ryanodine Receptor Tyrosine Phosphorylation Mol. Endocrinol., July 1, 2004; 18(7): 1658 - 1669. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ducret, A.-M. Vacher, and P. Vacher Effects of Prolactin on Ionic Membrane Conductances in the Human Malignant Astrocytoma Cell Line U87-MG J Neurophysiol, March 1, 2004; 91(3): 1203 - 1216. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. P. Tam, P. Lau, J. Djiane, D. J. Hilton, and M. J. Waters Tissue-Specific Induction of SOCS Gene Expression by PRL Endocrinology, November 1, 2001; 142(11): 5015 - 5026. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Freeman, B. Kanyicska, A. Lerant, and G. Nagy Prolactin: Structure, Function, and Regulation of Secretion Physiol Rev, October 1, 2000; 80(4): 1523 - 1631. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Bowen and P. L. Keyes Repeated Exposure to Prolactin Is Required to Induce Luteal Regression in the Hypophysectomized Rat Biol Reprod, April 1, 2000; 63(4): 1179 - 1184. [Abstract] [Full Text]
|
|
|
|
|
|
V. Kansra, C. Groves, J. C. Gutierrez-Ramos, and R. D. Polakiewicz Phosphatidylinositol 3-Kinase-dependent Extracellular Calcium Influx Is Essential for CX3CR1-mediated Activation of the Mitogen-activated Protein Kinase Cascade J. Biol. Chem., August 17, 2001; 276(34): 31831 - 31838. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |