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Type 2 and type 3 inositol 1,4,5-trisphosphate receptors (IP3R2and IP3R3) are intracellular calcium-release channels whosephysiological roles are unknown. We show exocrine dysfunctionin IP3R2 and IP3R3 double knock-out mice, which caused difficultiesin nutrient digestion. Severely impaired calcium signaling inacinar cells of the salivary glands and the pancreas in thedouble mutants ascribed the secretion deficits to a lack ofintracellular calcium release. Despite a normal caloric intake,the double mutants were hypoglycemic and lean. These resultsreveal IP3R2 and IP3R3 as key molecules in exocrine physiologyunderlying energy metabolism and animal growth.
1 Calcium Oscillation, International Cooperative Research Project, Japan Science and Technology Agency, Tokyo 108-0071, Japan. 2 Laboratory for Developmental Neurobiology, Brain Development Research Group, Brain Science Institute, RIKEN, Saitama 351-0198, Japan. 3 Division of Molecular Neurobiology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan. 4 Department of Anatomy, School of Medicine, Hokkaido University, Sapporo 060-8638, Japan. 5 Department of Cell Biology, Japanese Foundation for Cancer Research, Cancer Institute, Tokyo 170-8455, Japan.
* To whom correspondence should be addressed. E-mail: afutatsu{at}brain.riken.jp (A.F.); mikosiba{at}ims.u-tokyo.ac.jp (K.M.)
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M. J. Betzenhauser, L. E. Wagner II, M. Iwai, T. Michikawa, K. Mikoshiba, and D. I. Yule (2008)
J. Biol. Chem.
283, 21579-21587
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Involvement of autophagy in trypsinogen activation within the pancreatic acinar cells.
D. Hashimoto, M. Ohmuraya, M. Hirota, A. Yamamoto, K. Suyama, S. Ida, Y. Okumura, E. Takahashi, H. Kido, K. Araki, et al. (2008)
J. Cell Biol.
181, 1065-1072
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Osteoblasts induce Ca2+ oscillation-independent NFATc1 activation during osteoclastogenesis.
Y. Kuroda, C. Hisatsune, T. Nakamura, K. Matsuo, and K. Mikoshiba (2008)
PNAS
105, 8643-8648
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Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet-Induced Obesity and Diabetes in Mice.
P. D. Cani, R. Bibiloni, C. Knauf, A. Waget, A. M. Neyrinck, N. M. Delzenne, and R. Burcelin (2008)
Diabetes
57, 1470-1481
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Abnormal Taste Perception in Mice Lacking the Type 3 Inositol 1,4,5-Trisphosphate Receptor.
C. Hisatsune, K. Yasumatsu, H. Takahashi-Iwanaga, N. Ogawa, Y. Kuroda, R. Yoshida, Y. Ninomiya, and K. Mikoshiba (2007)
J. Biol. Chem.
282, 37225-37231
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Role of Inositol 1,4,5-Trisphosphate Receptors in Apoptosis in DT40 Lymphocytes.
M. T. Khan, C. D. Bhanumathy, Z. T. Schug, and S. K. Joseph (2007)
J. Biol. Chem.
282, 32983-32990
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Attenuation of store-operated Ca2+ current impairs salivary gland fluid secretion in TRPC1( / ) mice.
X. Liu, K. T. Cheng, B. C. Bandyopadhyay, B. Pani, A. Dietrich, B. C. Paria, W. D. Swaim, D. Beech, E. Yildrim, B. B. Singh, et al. (2007)
PNAS
104, 17542-17547
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J. K. Foskett, C. White, K.-H. Cheung, and D.-O. D. Mak (2007)
Physiol Rev
87, 593-658
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Protein kinase C phosphorylates the inositol 1,4,5-trisphosphate receptor type 2 and decreases the mobilization of Ca2+in pancreatoma AR4-2J cells.
G. Arguin, Y. Regimbald-Dumas, M.-O. Fregeau, A. Z Caron, and G. Guillemette (2007)
J. Endocrinol.
192, 659-668
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Up-Regulated PAR-2-Mediated Salivary Secretion in Mice Deficient in Muscarinic Acetylcholine Receptor Subtypes.
T. Nishiyama, T. Nakamura, K. Obara, H. Inoue, K. Mishima, N. Matsumoto, M. Matsui, T. Manabe, K. Mikoshiba, and I. Saito (2007)
J. Pharmacol. Exp. Ther.
320, 516-524
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Inositol 1,4,5-Trisphosphate Receptor Type 1 in Granule Cells, Not in Purkinje Cells, Regulates the Dendritic Morphology of Purkinje Cells through Brain-Derived Neurotrophic Factor Production..
C. Hisatsune, Y. Kuroda, T. Akagi, T. Torashima, H. Hirai, T. Hashikawa, T. Inoue, and K. Mikoshiba (2006)
J. Neurosci.
26, 10916-10924
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IP3Rs are sufficient for dendritic cell Ca2+ signaling in the absence of RyR1.
M. Stolk, M. Leon-Ponte, M. Merrill, G. P. Ahern, and P. J. O'Connell (2006)
J. Leukoc. Biol.
80, 651-658
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ATP Binding to a Unique Site in the Type-1 S2- Inositol 1,4,5-Trisphosphate Receptor Defines Susceptibility to Phosphorylation by Protein Kinase A.
L. E. Wagner II, M. J. Betzenhauser, and D. I. Yule (2006)
J. Biol. Chem.
281, 17410-17419
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IRBIT, an inositol 1,4,5-trisphosphate receptor-binding protein, specifically binds to and activates pancreas-type Na+/HCO3- cotransporter 1 (pNBC1).
K. Shirakabe, G. Priori, H. Yamada, H. Ando, S. Horita, T. Fujita, I. Fujimoto, A. Mizutani, G. Seki, and K. Mikoshiba (2006)
PNAS
103, 9542-9547
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