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105. Control of PTH secretion by the TRPC1 ion channel

Author

Onopiuk, Marta, primary, Eby, Bonnie, additional, Nesin, Vasyl, additional, Ngo, Peter, additional, Lerner, Megan, additional, Gorvin, Caroline M., additional, Stokes, Victoria J., additional, Thakker, Rajesh V., additional, Brandi, Maria Luisa, additional, Chang, Wenhan, additional, Humphrey, Mary Beth, additional, Tsiokas, Leonidas, additional, and Lau, Kai, additional

Published
2020
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108. List of contributors

Author

Adams, John S., Amrein, Karin, Anderson, Paul H., Arnold, Leggy A., Arora, Juhi, Artusa, Patricio, Ascherio, Alberto, Asmussen, Niels C., Astier, Anne L., Bak, Min Ji, Bauerle, Kevin T., Belorusova, Anna Y., Benkusky, Nancy A., Bernal-Mizrachi, Carlos, Bhattoa, Harjit P., Bikle, Daniel D., Bilezikian, John P., Binkley, Neil C., Bischoff-Ferrari, Heike A., Bishop, Charles W., Blomberg Jensen, Martin, Boisen, Ida Marie, Boucher, Barbara J., Bouillon, Roger, Boyan, Barbara D., Bradford, Dana, Brancatella, Alessandro, Buburuzan, Laura, Burne, Thomas H.J., Buschittari, Damien, Calkins, Hannah, Calvo, Mona S., Camargo, Carlos A., Jr., Campbell, Moray J., Cantorna, Margherita T., Cappellani, Daniele, Carlberg, Carsten, Carmeliet, Geert, Cashman, Kevin D., Ceglia, Lisa, Cetani, Filomena, Chang, Wenhan, Cheadle, Charlotte, Chou, Sharon H., Christakos, Sylvia, Christopher, Kenneth B., Chu, Emily Y., Chun, Rene F., Cleal, Jane K., Cobice, Diego F., Cooper, Cyrus, Coort, Susan L.M., Cui, Xiaoying, Curtis, Elizabeth M., Danilenko, Michael, Darling, Andrea L., David Roodman, G., Dawson-Hughes, Bess, de Jongh, Renate, Demay, Marie B., Dennison, Elaine M., Dixon, Katie M., Dong, Bingning, Doroudi, Maryam, Dusso, Adriana, Dvorzhinskiy, Aleksey, Ebeling, Peter R., Erben, Reinhold G., Evelo, Chris T.A., Eyles, Darryl, Feldman, David, Ferrer-Mayorga, Gemma, Fleet, James C., Forcellati, Marianela, Foster, Brian L., Gafni, Rachel I., Gayan-Ramirez, Ghislaine, Giovannucci, Edward, Girgis, Christian M., Glencross, Drew A., Glorieux, Francis H., Gocek, Elzbieta, Goldfarb, David S., Goltzman, David, González-Sancho, José Manuel, Grant, William B., Groves, Natalie J., Gysemans, Conny, Harrison, Stephanie, Harvey, Nicholas C., Haseltine, Katherine, Hawrylowicz, Catherine M., Hayes, Colleen E., Heckel, John E., Hershberger, Pamela A., Hewison, Martin, Högler, Wolfgang, Holick, Michael F., Hollis, Bruce W., Holt, Rune, Hujoel, Philippe P., Hyppönen, Elina, Ismailova, Aiten, Jablonski, Nina G., Jakobsen, Jette, Janssens, Wim, Jeffery, Louisa, Jenkinson, Carl, Jensen, Marie Bagge, Jetten, Anton M., Jiang, Heng, Johnson, Candace S., Jones, Glenville, Jones, Kerry S., Jüppner, Harald, Kalia, Vandana, Kallay, Enikö, Karapalis, Andrew C., Kaufmann, Martin, Kiely, Mairead, Kim, Hanseul, Kim, Tiffany Y., Kojima, Hiroyuki, Kooij, Ireen, Kovacs, Christopher S., Kremer, Richard, Krieger, Kirsten, Kritmetapak, Kittrawee, Krueger, Diane C., Kumar, Rajiv, Kurihara, Noriyoshi, Lane, Joseph M., Lanham-New, Susan A., Latic, Nejla, LeBoff, Meryl S., Lee, Maija B., Lee, Seong Min, Levine, Michael A., Lewis, Richard, Lewis, Rohan M., Li, Wei, Li, Yan Chun, Lincoln, Matthew R., Lips, Paul, Lisse, Thomas S., Liu, Eva S., López de Maturana, Evangelina, Lugg, Sebastian T., Machado, Christopher J., Maes, Karen, Maestro, Miguel A., Malats, Núria, Malloy, Peter J., Manousaki, Despoina, Marcinkowska, Ewa, Marcocci, Claudio, Martens, Pieter-Jan, Martineau, Adrian R., Mason, Rebecca S., Mathieu, Chantal, Mayne, Phoebe, McGrath, John J., Mehta, Mansi, Mellanby, Richard John, Merchant, Nadia, Meyer, Mark B., Miao, Dengshun, Moon, Rebecca J., Mortensen, Li Juel, Motlaghzadeh, Yasaman, Munger, Kassandra L., Muñoz, Alberto, Nakamichi, Yuko, Narvaez, Carmen J., Nikiphorou, Elena, Nonn, Larisa, Pal, Lubna, Parekh, Dhruv, Pettifor, John M., Pike, J. Wesley, Pilz, Stefan, Pittas, Anastassios G., Pludowski, Pawel, Prosser, David E., Pullagura, Sri Ramulu N., Raphael, Joseph, Rauz, Saaeha, Raza, Karim, Real, Francisco X., Reichrath, Jörg, Richards, J. Brent, Rivadeneira, Fernando, Rochel, Natacha, Roizen, Jeffrey D., Ryan, Brittany A., Sarkar, Surojit, Sarmadi, Fatemeh, Schafer, Anne L., Schepelmann, Martin, Schoenmakers, Inez, Schuit, Frans, Schwartz, Zvi, Scott, Kayla M., Sellmeyer, Deborah E., Sempos, Christopher T., Sepiashvili, Lusia, Seshadri, Mukund, Shane, Elizabeth, Shaurova, Tatiana, Shieh, Albert, Shui, Irene, Singh, Ravinder J., Slominski, Andrzej T., Smith, Karl W., St-Arnaud, René, Stein, Emily M., Studzinski, George P., Suda, Tatsuo, Takahashi, Naoyuki, Taylor, Hugh S., Tebben, Peter J., Thacher, Tom D., Thandrayen, Kebashni, Thickett, David R., Tiosano, Dov, Trajanoska, Katerina, Tu, Chia-Ling, Tuckey, Robert C., Tutaworn, Teerapat, Udagawa, Nobuyuki, Uday, Suma, Unnanuntana, Aasis, van Driel, Marjolein, van Leeuwen, Johannes P.T.M., van Schoor, Natasja, Verlinden, Lieve, Vieth, Reinhold, Vimaleswaran, Karina S., Wagner, Carol L., Wallace, Graham R., Weaver, Connie M., Webb, Daniel A., Welsh, JoEllen, White, John H., Whiting, Susan J., Williams, Emma L., Yahyavi, Sam Kafai, Yamamoto, Keiko, Yates, Clayton, Zagorac, Sladjana, Zhang, Rong Mei, Zhao, Hengguang, Zhou, Ang, and Zittermann, Armin

Published
2023
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117. Regulation of Ca2+-conducting currents in parathyroid cells by extracellular Ca2+ and channel blockers

Author

Chang, Wenhan, Chen, Tsui-Hua, Gardner, Phyllis, and Shoback, Dolores

Subjects
Parathyroid hormone -- Physiological aspects, Calcium channels -- Physiological aspects, Nifedipine -- Physiological aspects, Parathyroid glands -- Physiological aspects, Biological sciences
Abstract

Whole cell patch-clamp techniques have identified two types of Ca2+-conducting currents in parathyroid cells in response to changes in Ca2+ concentrations and to blockade by nifedipine and Cd2+. Type 1 currents were enhanced by Ca2+ concentrations and by the presence of nifedine and Cd2+, while type 2 currents were resistant to blockade by these agents. Cell perfusion experiments showed that both types are cation selective, independent over a broad range of membrane potentials and exhibit similar responses to a number of blockade agents.

Published
1995

119. Prevention of Injury-Induced Osteoarthritis in Rodent Temporomandibular Joint by Targeting Chondrocyte CaSR

Author

Zhang, Mian, Yang, Hongxu, Wan, Xianghong, Lu, Lei, Zhang, Jing, Zhang, Hongyun, Ye, Tao, Liu, Qian, Xie, Mianjiao, Liu, Xiaodong, Yu, Shibin, Guo, Shaoxiong, Chang, Wenhan, and Wang, Meiqing

Subjects
Male, Mice, Knockout, Temporomandibular Joint, Naphthalenes, Temporomandibular Joint Disorders, Article, Rats, Rats, Sprague-Dawley, Mice, Chondrocytes, Osteoarthritis, Animals, Female, Receptors, Calcium-Sensing
Abstract

Traumatic joint injuries produce osteoarthritic cartilage manifesting accelerated chondrocyte terminal differentiation and matrix degradation via unknown cellular and molecular mechanisms. Here we report the ability of biomechanical stress to increase expression of the calcium-sensing receptor (CaSR), a pivotal driver of chondrocyte terminal differentiation, in cultured chondrogenic cells subjected to fluid flow shear stress (FFSS) and in chondrocytes of rodent temporomandibular joint (TMJ) cartilage subjected to unilateral anterior cross-bite (UAC). In cultured ATDC5 cells or TMJ chondrocytes, FFSS induced Ca(2+)-loading and CaSR localization in endoplasmic reticulum (ER), casually accelerating cell differentiation that could be abrogated by emptying ER Ca(2+) stores or CaSR knockdown. Likewise, acute chondrocyte-specific Casr knockout (KO) prevented the UAC-induced acceleration of chondrocyte terminal differentiation and matrix degradation in TMJ cartilage in mice. More importantly, local injections of CaSR antagonist, NPS2143, replicated the effects of Casr KO in preventing the development of osteoarthritic phenotypes in TMJ cartilage of the UAC-treated rats. Our study revealed a novel pathological action of CaSR in development of osteoarthritic cartilage due to aberrant mechanical stimuli and supports a therapeutic potential of calcilytics in preventing osteoarthritis in temporomandibular Joints by targeting the CaSR.

Published
2019

123. Calcium-sensing receptor (CaSR) drives lung ECM remodelling and fibrosis in murine asthma models and in ageing mice

Author

Bruce, Richard, primary, Huang, Ping, additional, Yarova, Polina, additional, Schepelmann, Martin, additional, Wolffs, Kasope, additional, Mansfield, Bethan, additional, Ford, William, additional, Kidd, Emma, additional, Chang, Wenhan, additional, Ecker, Rupert, additional, Nica, Robert, additional, Ying, Sun, additional, Kemp, Paul, additional, and Riccardi, Daniela, additional

Published
2019
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125. Calcium-Sensing Receptors in Chondrocytes and Osteoblasts Are Required for Callus Maturation and Fracture Healing in Mice

Author

Cheng, Zhiqiang, primary, Li, Alfred, additional, Tu, Chia-Ling, additional, Maria, Christian Santa, additional, Szeto, Nicholas, additional, Herberger, Amanda, additional, Chen, Tsui-Hua, additional, Song, Fuqing, additional, Wang, Jiali, additional, Liu, Xiaodong, additional, Shoback, Dolores M, additional, and Chang, Wenhan, additional

Published
2019
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138. Prevention of Injury-Induced Osteoarthritis in Rodent Temporomandibular Joint by Targeting Chondrocyte CaSR

Author

Zhang, Mian, primary, Yang, Hongxu, additional, Wan, Xianghong, additional, Lu, Lei, additional, Zhang, Jing, additional, Zhang, Hongyun, additional, Ye, Tao, additional, Liu, Qian, additional, Xie, Mianjiao, additional, Liu, Xiaodong, additional, Yu, Shibin, additional, Guo, Shaoxiong, additional, Chang, Wenhan, additional, and Wang, Meiqing, additional

Published
2018
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143. Linoleic acid blunts early osteoblast differentiation and impairs oxidative phosphorylation in vitro.

Author

Nesbeth, Paula-Dene C., Ziegler, Thomas R., Tripathi, Ashish Kumar, Dabeer, Sadaf, Weiss, Daiana, Hao, Li, Smith, Matthew R., Jones, Dean P., Maner-Smith, Kristal M., Tu, Chia-Ling, Chang, Wenhan, Weitzmann, M. Neale, and Alvarez, Jessica A.

Abstract

• Linoleic acid (LNA) suppressed expression of key genes involved in osteoblast differentiation and function. • LNA impaired mitochondrial ATP production in MC3T3-E1 osteoblast precursors. • LNA induced production of oxidized LNA metabolites known to be associated with mitochondrial dysfunction in other tissues. Linoleic acid (LNA), an essential polyunsaturated fatty acid (PUFA), plays a crucial role in cellular functions. However, excessive intake of LNA, characteristic of Western diets, can have detrimental effects on cells and organs. Human observational studies have shown an inverse relationship between plasma LNA concentrations and bone mineral density. The mechanism by which LNA impairs the skeleton is unclear, and there is a paucity of research on the effects of LNA on bone-forming osteoblasts. The effect of LNA on osteoblast differentiation, cellular bioenergetics, and production of oxidized PUFA metabolites in vitro , was studied using primary mouse bone marrow stromal cells (BMSC) and MC3T3-E1 osteoblast precursors. LNA treatment decreased alkaline phosphatase activity, an early marker of osteoblast differentiation, but had no effect on committed osteoblasts or on mineralization by differentiated osteoblasts. LNA suppressed osteoblast commitment by blunting the expression of Runx2 and Osterix , key transcription factors involved in osteoblast differentiation, and other key osteoblast-related factors involved in bone formation. LNA treatment was associated with increased production of oxidized LNA- and arachidonic acid-derived metabolites and blunted oxidative phosphorylation, resulting in decreased ATP production. Our results show that LNA inhibited early differentiation of osteoblasts and this inhibitory effect was associated with increased production of oxidized PUFA metabolites that likely impaired energy production via oxidative phosphorylation. [ABSTRACT FROM AUTHOR]

Published
2024
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144. Parathyroid cells express dihydropyridine-sensitive cation currents and L-type calcium channel subunits

Author

CHANG, WENHAN, PRATT, STACY A., CHEN, TSUI-HUA, TU, CHIA-LING, MIKALA, GABOR, SCHWARTZ, ARNOLD, and SHOBACK, DOLORES

Subjects
Parathyroid glands -- Physiological aspects, Calcium channels -- Research, Dihydropyridine -- Physiological aspects, Biological sciences
Abstract

Parathyroid cells express dihydropyridine-sensitive cation currents and L-type calcium channel subunits. Am J Physiol Endocrinol Metab 281: E180-E189, 2001.--Parathyroid cells express [Ca.sup.2+]-conducting currents that are activated by raising the extracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.o]). We investigated the sensitivity of these currents to dihydropyridines, the expression of voltage-dependent [Ca.sup.2+] channel (VDCC) subunits, and the effects of dihydropyridines on the intracellular free [[Ca.sup.2+]] ([[[Ca.sup.2+]].sub.i]) and secretion in these cells. Dihydropyridine channel antagonists dose dependently suppressed [Ca.sup.2+]-conducting currents, and agonists partially reversed the inhibitory effects of the antagonists in these cells. From a bovine parathyroid cDNA library, we isolated cDNA fragments encoding parts of an [[Alpha].sub.1S]- and a [[Beta].sub.3]-subunit of L-type [Ca.sup.2+] channels. The [[Alpha].sub.1S]-subunit cDNA from the parathyroid represents an alternatively spliced variant lacking exon 29 of the corresponding gene. Northern blot analysis and immunocytochemistry confirmed the presence of transcripts and proteins for [[Alpha].sub.1-] and [[Beta].sub.3]-subunits in the parathyroid gland. The addition of dihydropyridines had no significant effects on high [[[Ca.sup.2+]].sub.o]-induced changes in [[[Ca.sup.2+]].sub.i] and parathyroid hormone (PTH) release. Thus our studies indicate that parathyroid cells express alternatively spliced L-type [Ca.sup.2+] channel subunits, which do not modulate acute intracellular [Ca.sup.2+] responses or changes in PTH release. intracellular [Ca.sup.2+] mobilization; [Ca.sup.2+] receptor; [Ca.sup.2+] sensing

Published
2001

145. Calcium-sensing receptor (CaSR) as a novel target for ischemic neuroprotection

Author

Kim, Jong Youl, Ho, Hanson, Kim, Nuri, Liu, Jialing, Tu, Chia-Ling, Yenari, Midori A, and Chang, Wenhan

Subjects
Stroke, Neurological, Clinical Sciences, Genetics, Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Brain Disorders
Abstract

ObjectIschemic brain injury is the leading cause for death and long-term disability in patients who suffer cardiac arrest and embolic stroke. Excitotoxicity and subsequent Ca(2+)-overload lead to ischemic neuron death. We explore a novel mechanism concerning the role of the excitatory extracellular calcium-sensing receptor (CaSR) in the induction of ischemic brain injury.MethodMice were exposed to forebrain ischemia and the actions of CaSR were determined after its genes were ablated specifically in hippocampal neurons or its activities were inhibited pharmacologically. Since the CaSR forms a heteromeric complex with the inhibitory type B γ-aminobutyric acid receptor 1 (GABABR1), we compared neuronal responses to ischemia in mice deficient in CaSR, GABABR1, or both, and in mice injected locally or systemically with a specific CaSR antagonist (or calcilytic) in the presence or absence of a GABABR1 agonist (baclofen).ResultsBoth global and focal brain ischemia led to CaSR overexpression and GABABR1 downregulation in injured neurons. Genetic ablation of Casr genes or blocking CaSR activities by calcilytics rendered robust neuroprotection and preserved learning and memory functions in ischemic mice, partly by restoring GABABR1 expression. Concurrent ablation of Gabbr1 gene blocked the neuroprotection caused by the Casr gene knockout. Coinjection of calcilytics with baclofen synergistically enhanced neuroprotection. This combined therapy remained robust when given 6 h after ischemia.InterpretationOur study demonstrates a novel receptor interaction, which contributes to ischemic neuron death through CaSR upregulation and GABABR1 downregulation, and feasibility of neuroprotection by concurrently targeting these two receptors.

Published
2014
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146. Ephrin B2/EphB4 mediates the actions of IGF-I signaling in regulating endochondral bone formation

Author

Wang, Yongmei, Menendez, Alicia, Fong, Chak, ElAlieh, Hashem Z., Chang, Wenhan, and Bikle, Daniel D.

Subjects
endocrine system, animal structures, Knockout, Blotting, Western, Receptor, EphB4, Ephrin-B2, Cell Communication, Medical and Health Sciences, Article, Mice, Engineering, Osteogenesis, EPHRIN B2, Animals, 2.1 Biological and endogenous factors, Developmental, EPHB4, Insulin-Like Growth Factor I, Aetiology, Mice, Knockout, Osteoblasts, Blotting, CELL-CELL COMMUNICATION, Gene Expression Regulation, Developmental, Cell Differentiation, Biological Sciences, Anatomy & Morphology, Immunohistochemistry, IGF-I, Gene Expression Regulation, embryonic structures, sense organs, CHONDROCYTE, Western, hormones, hormone substitutes, and hormone antagonists, Receptor, Signal Transduction
Abstract

Ephrin B2/EphB4 mediates interactions among osteoblasts (OBs), osteoclasts (OCLs), and chondrocytes to regulate their differentiation. We investigated the role of ephrin B2/EphB4 signaling in mediating the anabolic effects of insulin-like growth factor-I (IGF-I) and parathyroid hormone (PTH) on those cells and overall endochondral bone formation. Immunohistochemistry demonstrated that the expression of ephrin B2 in OBs, OCLs, and osteocytes, and the expression of EphB4 in OBs and osteocytes was dramatically decreased in global IGF-I knockout mice. Inactivation of EphB4 by EphB4 small, interfering RNA (siRNA) in cultured bone marrow stromal cells significantly decreased the mRNA levels of OB differentiation markers and abolished the stimulatory effects of IGF-I on these markers. Blocking the interaction of EphB4 and ephrin B2 in the OB-OCL cocultures with the EphB4 specific peptide TNYL-RAW or deletion of ephrin B2 in OCL prior to coculture led to fewer and smaller tartrate-resistant acid phosphatase (TRAP)-positive cells, decreased expression of OB differentiation markers, and blunted response to IGF-I for both OCL and OB differentiation. In the growth plate, both ephrin B2 and EphB4 are expressed in late stage proliferating and prehypertrophic chondrocytes, and their expression was decreased in mice lacking the IGF-I receptor specifically in chondrocytes. In vitro, blocking the interaction of EphB4 and ephrin B2 in chondrogenic ATDC5 cells with TNYL-RAW significantly decreased both basal and IGF1-induced expression of type II and type X collagen. In the cocultures of ATDC5 cells and spleen cells (osteoclast precursors), TNYL-RAW decreased the numbers of TRAP-positive cells and the expression of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) and receptor activator of NF-κB (RANK), and blocked their stimulation by IGF-I. Our data indicate that IGF-I/IGF-IR signaling promotes OB, OCL, and chondrocyte differentiation via ephrin B2/EphB4 mediated cell-cell communication.

Published
2014

148. Sprouty2 regulates endochondral bone formation by modulation of RTK and BMP signaling.

Author

Joo, Adriane, Joo, Adriane, Long, Roger, Cheng, Zhiqiang, Alexander, Courtney, Chang, Wenhan, Klein, Ophir D, Joo, Adriane, Joo, Adriane, Long, Roger, Cheng, Zhiqiang, Alexander, Courtney, Chang, Wenhan, and Klein, Ophir D

Abstract

Skeletal development is regulated by the coordinated activity of signaling molecules that are both produced locally by cartilage and bone cells and also circulate systemically. During embryonic development and postnatal bone remodeling, receptor tyrosine kinase (RTK) superfamily members play critical roles in the proliferation, survival, and differentiation of chondrocytes, osteoblasts, osteoclasts, and other bone cells. Recently, several molecules that regulate RTK signaling have been identified, including the four members of the Sprouty (Spry) family (Spry1-4). We report that Spry2 plays an important role in regulation of endochondral bone formation. Mice in which the Spry2 gene has been deleted have defective chondrogenesis and endochondral bone formation, with a postnatal decrease in skeletal size and trabecular bone mass. In these constitutive Spry2 mutants, both chondrocytes and osteoblasts undergo increased cell proliferation and impaired terminal differentiation. Tissue-specific Spry2 deletion by either osteoblast- (Col1-Cre) or chondrocyte- (Col2-Cre) specific drivers led to decreased relative bone mass, demonstrating the critical role of Spry2 in both cell types. Molecular analyses of signaling pathways in Spry2(-/-) mice revealed an unexpected upregulation of BMP signaling and decrease in RTK signaling. These results identify Spry2 as a critical regulator of endochondral bone formation that modulates signaling in both osteoblast and chondrocyte lineages.

Published
2016

149. Interplay between CaSR and PTH1R signaling in skeletal development and osteoanabolism.

Author

Santa Maria, Christian, Santa Maria, Christian, Cheng, Zhiqiang, Li, Alfred, Wang, Jiali, Shoback, Dolores, Tu, Chia-Ling, Chang, Wenhan, Santa Maria, Christian, Santa Maria, Christian, Cheng, Zhiqiang, Li, Alfred, Wang, Jiali, Shoback, Dolores, Tu, Chia-Ling, and Chang, Wenhan

Abstract

Parathyroid hormone (PTH)-related peptide (PTHrP) controls the pace of pre- and post-natal growth plate development by activating the PTH1R in chondrocytes, while PTH maintains mineral and skeletal homeostasis by modulating calciotropic activities in kidneys, gut, and bone. The extracellular calcium-sensing receptor (CaSR) is a member of family C, G protein-coupled receptor, which regulates mineral and skeletal homeostasis by controlling PTH secretion in parathyroid glands and Ca(2+) excretion in kidneys. Recent studies showed the expression of CaSR in chondrocytes, osteoblasts, and osteoclasts and confirmed its non-redundant roles in modulating the recruitment, proliferation, survival, and differentiation of the cells. This review emphasizes the actions of CaSR and PTH1R signaling responses in cartilage and bone and discusses how these two signaling cascades interact to control growth plate development and maintain skeletal metabolism in physiological and pathological conditions. Lastly, novel therapeutic regimens that exploit interrelationship between the CaSR and PTH1R are proposed to produce more robust osteoanabolism.

Published
2016

150. Calcium-Sensing Receptor Promotes Breast Cancer by Stimulating Intracrine Actions of Parathyroid Hormone–Related Protein

Author

Kim, Wonnam, primary, Takyar, Farzin M., additional, Swan, Karena, additional, Jeong, Jaekwang, additional, VanHouten, Joshua, additional, Sullivan, Catherine, additional, Dann, Pamela, additional, Yu, Herbert, additional, Fiaschi-Taesch, Nathalie, additional, Chang, Wenhan, additional, and Wysolmerski, John, additional

Published
2016
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