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32 results on '"Yuen, Tony"'

1. First-in-class humanized FSH blocking antibody targets bone and fat

Author

Gera, Sakshi, Sant, Damini, Haider, Shozeb, Korkmaz, Funda, Kuo, Tan-Chun, Mathew, Mehr, Perez-Pena, Helena, Xie, Honglin, Chend, Hao, Batista, Rogerio, Ma, Kejun, Cheng, Zhen, Hadelia, Elina, Robinson, Cemre, Macdonald, Anne, Miyashita, Sari, Williams, Anthony, Jebian, Gregory, Miyashita, Hirotaka, Gumerova, Anisa, Ievleva, Kseniia, Smith, Pinar, He, Jiahuan, Ryu, Vitaly, DeMambro, Victoria, Quinn, Matthew A., Meseck, Marcia, Kim, Se-Min, Kumar, T. Rajendra, Iqbal, Jameel, New, Maria I., Lizneva, Daria, Rosen, Clifford J., Hsueh, Aaron J., Yuen, Tony, and Zaidi, Mone

Published
2020

2. Repurposing erectile dysfunction drugs tadalafil and vardenafil to increase bone mass

Author

Kim, Se-Min, Taneja, Charit, Perez-Pena, Helena, Ryu, Vitaly, Gumerova, Anisa, Li, Wenliang, Ahmad, Naseer, Zhu, Ling-Ling, Liu, Peng, Mathew, Mehr, Korkmaz, Funda, Gera, Sakshi, Sant, Damini, Hadelia, Elina, Ievleva, Kseniia, Kuo, Tan-Chun, Miyashita, Hirotaka, Liu, Li, Tourkova, Irina, Stanley, Sarah, Lizneva, Daria, Iqbal, Jameel, Sun, Li, Tamler, Ronald, Blair, Harry C., New, Maria I., Haider, Shozeb, Yuen, Tony, and Zaidi, Mone

Published
2020

3. Oxytocin regulates body composition

Author

Sun, Li, Lizneva, Daria, Ji, Yaoting, Colaianni, Graziana, Hadelia, Elina, Gumerova, Anisa, Ievleva, Kseniia, Kuo, Tan-Chun, Korkmaz, Funda, Ryu, Vitaly, Rahimova, Alina, Gera, Sakshi, Taneja, Charit, Khan, Ayesha, Ahmad, Naseer, Tamma, Roberto, Bian, Zhuan, Zallone, Alberta, Kim, Se-Min, New, Maria I., Iqbal, Jameel, Yuen, Tony, and Zaidi, Mone

Published
2019

6. FSIP1 regulates autophagy in breast cancer

Author

Liu, Caigang, Sun, Lisha, Yang, Jie, Liu, Tong, Yang, Yongliang, Kim, Se-Min, Ou, Xunyan, Wang, Yining, Sun, Li, Zaidi, Mone, New, Maria I., Yuen, Tony, and Guo, Qiyong

Published
2018

7. Epitope-specific monoclonal antibodies to FSHβ increase bone mass

Author

Ji, Yaoting, Liu, Peng, Yuen, Tony, Haider, Shozeb, He, Jiahuan, Romero, Raquel, Chen, Hao, Bloch, Madison, Kim, Se-Min, Lizneva, Daria, Munshi, Lubna, Zhou, Chunxue, Lu, Ping, Iqbal, Jameel, Cheng, Zhen, New, Maria I., Hsueh, Aaron J., Bian, Zhuan, Rosen, Clifford J., Sun, Li, and Zaidi, Mone

Published
2018

8. Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11β-hydroxysteroid dehydrogenase type 2 deficiency

Author

Yau, Mabel, Haider, Shozeb, Khattab, Ahmed, Ling, Chen, Mathew, Mehr, Zaidi, Samir, Bloch, Madison, Patel, Monica, Ewert, Sinead, Abdullah, Wafa, Toygar, Aysenur, Mudryi, Vitalii, Badi, Maryam Al, Alzubdi, Mouch, Wilson, Robert C., Azkawi, Hanan Said Al, Ozdemir, Hatice Nur, Abu-Amer, Wahid, Hertecant, Jozef, Razzaghy-Azar, Maryam, Funder, John W., Senani, Aisha Al, Sun, Li, Kim, Se-Min, Yuen, Tony, Zaidi, Mone, and New, Maria I.

Published
2017

10. Clinical, genetic, and structural basis of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency

Author

Khattab, Ahmed, Haider, Shozeb, Kumar, Ameet, Dhawan, Samarth, Alam, Dauood, Romero, Raquel, Burns, James, Li, Di, Estatico, Jessica, Rahi, Simran, Fatima, Saleel, Alzahrani, Ali, Hafez, Mona, Musa, Noha, Azar, Maryam Razzghy, Khaloul, Najoua, Gribaa, Moez, Saad, Ali, Charfeddine, Ilhem Ben, de Mendonça, Berenice Bilharinho, Belgorosky, Alicia, Dumic, Katja, Dumic, Miroslav, Aisenberg, Javier, Kandemir, Nurgun, Alikasifoglu, Ayfer, Ozon, Alev, Gonc, Nazli, Cheng, Tina, Kuhnle-Krahl, Ursula, Cappa, Marco, Holterhus, Paul-Martin, Nour, Munier A., Pacaud, Daniele, Holtzman, Assaf, Li, Sun, Zaidi, Mone, Yuen, Tony, and New, Maria I.

Published
2017

11. Anabolic actions of Notch on mature bone

Author

Liu, Peng, Ping, Yilin, Ma, Meng, Zhang, Demao, Liu, Connie, Zaidi, Samir, Gao, Song, Ji, Yaoting, Lou, Feng, Yu, Fanyuan, Lu, Ping, Stachnik, Agnes, Bai, Mingru, Wei, Chengguo, Zhang, Liaoran, Wang, Ke, Chen, Rong, New, Maria I., Rowe, David W., Yuen, Tony, Sun, Li, and Zaidi, Mone

Published
2016

12. Functions of vasopressin and oxytocin in bone mass regulation

Author

Sun, Li, Tamma, Roberto, Yuen, Tony, Colaianni, Graziana, Ji, Yaoting, Cuscito, Concetta, Bailey, Jack, Dhawan, Samarth, Lu, Ping, Calvano, Cosima D., Zhu, Ling-Ling, Zambonin, Carlo G., Di Benedetto, Adriana, Stachnik, Agnes, Liu, Peng, Grano, Maria, Colucci, Silvia, Davies, Terry F., New, Maria I., Zallone, Alberta, and Zaidi, Mone

Published
2016

13. The myokine irisin increases cortical bone mass

Author

Colaianni, Graziana, Cuscito, Concetta, Mongelli, Teresa, Pignataro, Paolo, Buccoliero, Cinzia, Liu, Peng, Lu, Ping, Sartini, Loris, Di Comite, Mariasevera, Mori, Giorgio, Di Benedetto, Adriana, Brunetti, Giacomina, Yuen, Tony, Sun, Li, Reseland, Janne E., Colucci, Silvia, New, Maria I., Zaidi, Mone, Cinti, Saverio, and Grano, Maria

Published
2015

14. Bisphosphonates inactivate human EGFRs to exert antitumor actions

Author

Yuen, Tony, Stachnik, Agnes, Iqbal, Jameel, Sgobba, Miriam, Gupta, Yogesh, Lu, Ping, Colaianni, Graziana, Ji, Yaoting, Zhu, Ling-Ling, Kim, Se-Min, Li, Jianhua, Liu, Peng, Izadmehr, Sudeh, Sangodkar, Jaya, Bailey, Jack, Latif, Yathin, Mujtaba, Shiraz, Epstein, Solomon, Davies, Terry F., Bian, Zhuan, Zallone, Alberta, Aggarwal, Aneel K., Haider, Shozeb, New, Maria I., Sun, Li, Narla, Goutham, and Zaidi, Mone

Published
2014

15. Repurposing of bisphosphonates for the prevention and therapy of nonsmall cell lung and breast cancer

Author

Stachnik, Agnes, Yuen, Tony, Iqbal, Jameel, Sgobba, Miriam, Gupta, Yogesh, Lu, Ping, Colaianni, Graziana, Ji, Yaoting, Zhu, Ling-Ling, Kim, Se-Min, Li, Jianhua, Liu, Peng, Izadmehr, Sudeh, Sangodkar, Jaya, Scherer, Thomas, Mujtaba, Shiraz, Galsky, Matthew, Gomez, Jorge, Epstein, Solomon, Buettner, Christoph, Bian, Zhuan, Zallone, Alberta, Aggarwal, Aneel K., Haider, Shozeb, New, Maria I., Sun, Li, Narla, Goutham, and Zaidi, Mone

Published
2014

17. Glucocerebrosidase 2 gene deletion rescues type 1 Gaucher disease

Author

Mistry, Pramod K., Liu, Jun, Li Sun, Chuang, Wei-Lien, Yuen, Tony, Yang, Ruhua, Lu, Ping, Zhang, Kate, Li, Jianhua, Keutzer, Joan, Stachnik, Agnes, Mennone, Albert, Boyer, James L., Jain, Dhanpat, Brady, Roscoe O., New, Maria I., and Zaidi, Mone

Published
2014

26. FSIP1 regulates autophagy in breast cancer.

Author

Caigang Liu, Lisha Sun, Jie Yang, Tong Liu, Yongliang Yang, Se-Min Kim, Xunyan Ou, Yining Wang, Li Sun, Zaidi, Mone, New, Maria I., Yuen, Tony, and Qiyong Guo

Subjects
BREAST cancer, CANCER chemotherapy, IMMUNOPRECIPITATION, PROTEIN kinases, RAPAMYCIN
Abstract

Fibrous sheath interacting protein 1 (FSIP1) is a cancer antigen expressed in the majority of breast cancer tissues and is associatedwith poor prognosis. However, the role of FSIP1 in the progression and drug sensitivity of triple-negative breast cancer (TNBC) has not been explored. Here, we show that FSIP1 deficiency by shRNA-mediated knockdown or CRISPR-Cas9-mediated knockout significantly inhibits the proliferation and invasion of TNBC cells and impairs chemotherapyinduced growth inhibition in vivo. Computational modeling predicted that FSIP1 binds to ULK1, and this was established by coimmunoprecipitation. FSIP1 deficiency promoted autophagy, enhanced AMP-activated protein kinase (AMPK) signaling, and decreased mechanistic target of rapamycin (mTOR) and Wnt/β-catenin activity. In contrast, knockdown of AMPK or inhibition of autophagy restored the sensitivity to chemotherapy drugs in TNBC cells. Our findings uncover a role of FSIP1 as well as mechanisms underlying FSIP1 action in drug sensitivity andmay, therefore, aid in design of TNBC therapies. [ABSTRACT FROM AUTHOR]

Published
2018
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27. Epitope-specific monoclonal antibodies to FSHβ increase bone mass.

Author

Yaoting Ji, Peng Liu, Yuen, Tony, Haider, Shozeb, Jiahuan He, Romero, Raquel, Hao Chen, Bloch, Madison, Se-Min Kim, Lizneva, Daria, Munshi, Lubna, Chunxue Zhou, Ping Lu, Iqbal, Jameel, Zhen Cheng, New, Maria I., Hsueh, Aaron J., Zhuan Bian, Rosen, Clifford J., and Li Sun

Subjects
FOLLICLE-stimulating hormone, BONE density, EPITOPES, MONOCLONAL antibodies, OSTEOPOROSIS treatment, OBESITY treatment, BONE resorption
Abstract

Pituitary hormones have long been thought solely to regulate single targets. Challenging this paradigm, we discovered that both anterior and posterior pituitary hormones, including FSH, had other functions in physiology. We have shown that FSH regulates skeletal integrity, and, more recently, find that FSH inhibition reduces body fat and induces thermogenic adipose tissue. A polyclonal antibody raised against a short, receptor-binding epitope of FSHß was found not only to rescue bone loss postovariectomy, but also to display marked antiobesity and probeiging actions. Questioning whether a single agent could be used to treat two medical conditions of public health importance--osteoporosis and obesity--we developed two further monoclonal antibodies, Hf2 and Mf4, against computationally defined receptor-binding epitopes of FSHß. Hf2 has already been shown to reduce body weight and fat mass and cause beiging in mice on a high-fat diet. Here, we show that Hf2, which binds mouse Fsh in immunoprecipitation assays, also increases cortical thickness and trabecular bone volume, and microstructural parameters, in sham-operated and ovariectomized mice, noted on microcomputed tomography. This effect was largely recapitulated with Mf4, which inhibited bone resorption by osteoclasts and stimulated new bone formation by osteoblasts. These effects were exerted in the absence of alterations in serum estrogen in wild-type mice. We also reconfirm the existence of Fshrs in bone by documenting the specific binding of fluorescently labeled FSH, FSH-CH, in vivo. Our study provides the framework for the future development of an FSH-based therapeutic that could potentially target both bone and fat. [ABSTRACT FROM AUTHOR]

Published
2018
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28. Anabolic actions of Notch on mature bone.

Author

Peng Liu, Yilin Ping, Meng Ma, Demao Zhang, Liu, Connie, Zaidi, Samir, Song Gao, Yaoting Ji, Feng Lou, Fanyuan Yu, Ping Lu, Stachnik, Agnes, Mingru Bai, Chengguo Wei, Liaoran Zhang, Ke Wang, Rong Chen, New, Maria I., Rowe, David W., and Yuen, Tony

Subjects
NOTCH signaling pathway, OSTEOCYTES, BONES, OSTEOPOROSIS, OSTEOBLASTS, CELL differentiation
Abstract

Notch controls skeletogenesis, but its role in the remodeling of adult bone remains conflicting. In mature mice, the skeleton can become osteopenic or osteosclerotic depending on the time point at which Notch is activated or inactivated. Using adult EGFP reporter mice, we find that Notch expression is localized to osteocytes embedded within bone matrix. Conditional activation of Notch signaling in osteocytes triggers profound bone formation, mainly due to increased mineralization, which rescues both age-associated and ovariectomy-induced bone loss and promotes bone healing following osteotomy. In parallel, mice rendered haploinsufficient in γ-secretase presenilin-1 (Psen1), which inhibits downstream Notch activation, display almost-absent terminal osteoblast differentiation. Consistent with this finding, pharmacologic or genetic disruption of Notch or its ligand Jagged1 inhibits mineralization. We suggest that stimulation of Notch signaling in osteocytes initiates a profound, therapeutically relevant, anabolic response. [ABSTRACT FROM AUTHOR]

Published
2016
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29. Functions of vasopressin and oxytocin in bone mass regulation.

Author

Li Sun, Tamma, Roberto, Yuen, Tony, Colaianni, Graziana, Yaoting Ji, Cuscito, Concetta, Bailey, Jack, Dhawan, Samarth, Ping Lu, Calvano, Cosima D., Ling-Ling Zhu, Zambonin, Carlo G., Di Benedetto, Adriana, Stachnik, Agnes, Peng Liu, Grano, Maria, Colucci, Silvia, Davies, Terry F., New, Maria I., and Zallone, Alberta

Subjects
VASOPRESSIN, OXYTOCIN, G protein coupled receptors, BONE growth, OSTEOBLASTS, LABORATORY mice, WESTERN immunoblotting
Abstract

Prior studies show that oxytocin (Oxt) and vasopressin (Avp) have opposing actions on the skeleton exerted through high-affinity G protein-coupled receptors. We explored whether Avp and Oxtr can share their receptors in the regulation of bone formation by osteoblasts. We show that the Avp receptor 1α (Avpr1α) and the Oxt receptor (Oxtr) have opposing effects on bone mass: Oxtr-/- mice have osteopenia, and Avpr1α-/- mice display a high bone mass phenotype. More notably, this high bone mass phenotype is reversed by the deletion of Oxtr in Oxtr-/-:Avpr1α-/- doublemutant mice. However, although Oxtr is not indispensable for Avp action in inhibiting osteoblastogenesis and gene expression, Avpstimulated gene expression is inhibited when the Oxtr is deleted in Avpr1α-/- cells. In contrast, Oxt does not interact with Avprs in vivo in a model of lactation-induced bone loss in which Oxt levels are high. Immunofluorescence microscopy of isolated nucleoplasts and Western blotting and MALDI-TOF of nuclear extracts show that Avp triggers Avpr1α localization to the nucleus. Finally, a specific Avpr2 inhibitor, tolvaptan, does not affect bone formation or bone mass, suggesting that Avpr2, which primarily functions in the kidney, does not have a significant role in bone remodeling. [ABSTRACT FROM AUTHOR]

Published
2016
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30. Smoke carcinogens cause bone loss through the aryl hydrocarbon receptor and induction of Cyp1 enzymes.

Author

Iqbal, Jameel, Li Sun, Cao, Jay, Yuen, Tony, Ping Lu, Bab, Itai, Leu, N. Adrian, Srinivasan, Satish, Wagage, Sagie, Hunter, Christopher A., Nebert, Daniel W., Zaidi, Mone, and Avadhani, Narayan G.

Subjects
CARCINOGENS, BONE resorption, BONE diseases, ARYL hydrocarbon receptors, TETRACHLORODIBENZODIOXIN
Abstract

Smoking is a major risk factor for osteoporosis and fracture, but the mechanism through which smoke causes bone loss remains unclear. Here, we show that the smoke toxins benzo(a)pyrene (BaP) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interact with the aryl hydrocarbon receptor (Ahr) to induce osteoclastic bone resorption through the activation of cytochrome P450 1a/1b (Cyp1) enzymes. BaP and TCDD enhanced osteoclast formation in bone marrow cell cultures and gavage with BaP stimulated bone resorption and osteoclastogenesis in vivo. The osteoclastogenesis triggered by BaP or RANK-L was reduced in Ahr cells, consistent with the high bone mass noted in Ahr-/- male mice. The receptor activator of NF-κB ligand (RANK-L) also failed to induce the expression of Cyp1 enzymes in Ahr-/- cells. Furthermore, the osteoclastogenesis induced by TCDD was lower in Cyp1a1/1a2-/- and Cyp1a1/1a2f1b1-/- cultures, indicating that Ahr was upstream of the Cyp enzymes. Likewise, the pharmacological inhibition of the Cyp1 enzymes with tetramethylsilane or proadifen reduced osteoclastogenesis. Finally, deletion of the Cyp1a1, Cypla2, and Cyp1b1 in triple knockout mice resulted in reduced bone resorption and recapitulated the high bone mass phenotype of Ahr-/- mice. Overall, the data identify the Ahr and Cyp1 enzymes not only in the pathophysiology of smoke-induced osteoporosis, but also as potential targets for selective modulation by new therapeutics. [ABSTRACT FROM AUTHOR]

Published
2013
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31. Gaucher disease gene GBA functions in immune regulation.

Author

Jun Liu, Halene, Stephanie, Mei Yang, Iqbal, Jameel, Ruhua Yang, Mehal, Wajahat Z., Wei-Lien Chuang, Jain, Dhanpat, Yuen, Tony, Li Sun, Zaidi, Mone, and Mistry, Pramod K.

Subjects
GAUCHER'S disease, IMMUNOREGULATION, GLUCOSIDASES, GENETIC mutation, CLINICAL trials, THYMOCYTES, CELL proliferation, CYTOKINES
Abstract

Inherited deficiency of acid β-glucosidase (GCase) due to biallelic mutations ¡n the GBA (glucosidase, β, acid) gene causes the classic manifestations of Gaucher disease (GD) involving the viscera, the skeleton, and the lungs. Clinical observations point to immune defects in GD beyond the accumulation of activated macrophages engorged with lysosomal glucosylceramide. Here, we show a plethora of immune cell aberrations in mice in which the GBA gene is deleted conditionally in hematopoietic stem cells (HSCs). The thymus exhibited the earliest and most striking alterations reminiscent of impaired T-cell maturation, aberrant B-cell recruitment, enhanced antigen presentation, and impaired egress of mature thymocytes. These changes correlated strongly with disease severity. In contrast to the profound defects in the thymus, there were only limited cellular defects in peripheral lymphoid organs, mainly restricted to mice with severe disease. The cellular changes in GCase deficiency were accompanied by elevated T-helper (Th)1 and Th2 cytokines that also tracked with disease severity. Finally, the proliferation of GCase-deficient HSCs was inhibited significantly by both GL1 and Lyso-GL1, suggesting that the "supply" of early thymic progenitors from bone marrow may, in fact, be reduced in GBA deficiency. The results not only point to a fundamental role for GBA in immune regulation but also suggest that GBA mutations in GD may cause widespread immune dysregulation through the accumulation of substrates. [ABSTRACT FROM AUTHOR]

Published
2012
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