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2. Mechanosignaling in Bone Health, Trauma and Inflammation

Author

Knapik, Derrick M, Perera, Priyangi, Nam, Jin, Blazek, Alisa D, Rath, Björn, Leblebicioglu, Binnaz, Das, Hiranmoy, Wu, Lai Chu, Hewett, Timothy E, Agarwal, Suresh K, Robling, Alexander G, Flanigan, David C, Lee, Beth S, and Agarwal, Sudha

Subjects
Osteoporosis, Bioengineering, Underpinning research, 2.1 Biological and endogenous factors, Aetiology, 1.1 Normal biological development and functioning, Musculoskeletal, Animals, Bone and Bones, Humans, Inflammation, Mechanotransduction, Cellular, NF-kappa B, Wounds and Injuries, Biochemistry and Cell Biology, Medical Biochemistry and Metabolomics, Pharmacology and Pharmaceutical Sciences, Biochemistry & Molecular Biology
Abstract

SignificanceMechanosignaling is vital for maintaining the structural integrity of bone under physiologic conditions. These signals activate and suppress multiple signaling cascades regulating bone formation and resorption. Understanding these pathways is of prime importance to exploit their therapeutic potential in disorders associated with bone loss due to disuse, trauma, or disruption of homeostatic mechanisms.Recent advancesIn the case of cells of the bone, an impressive amount of data has been generated that provides evidence of a complex mechanism by which mechanical signals can maintain or disrupt cellular homeostasis by driving transcriptional regulation of growth factors, matrix proteins and inflammatory mediators in health and inflammation. Mechanical signals act on cells in a magnitude dependent manner to induce bone deposition or resorption. During health, physiological levels of these signals are essential for maintaining bone strength and architecture, whereas during inflammation, similar signals can curb inflammation by suppressing the nuclear factor kappa B (NF-κB) signaling cascade, while upregulating matrix synthesis via mothers against decapentaplegic homolog and/or Wnt signaling cascades. Contrarily, excessive mechanical forces can induce inflammation via activation of the NF-κB signaling cascade.Critical issuesGiven the osteogenic potential of mechanical signals, it is imperative to exploit their therapeutic efficacy for the treatment of bone disorders. Here we review select signaling pathways and mediators stimulated by mechanical signals to modulate the strength and integrity of the bone.Future directionsUnderstanding the mechanisms of mechanotransduction and its effects on bone lay the groundwork for development of nonpharmacologic mechanostimulatory approaches for osteodegenerative diseases and optimal bone health.

Published
2014

6. Lenalidomide-mediated enhanced translation of C/EBPα-p30 protein up-regulates expression of the antileukemic microRNA-181a in acute myeloid leukemia

Author

Hickey, Christopher J., Schwind, Sebastian, Radomska, Hanna S., Dorrance, Adrienne M., Santhanam, Ramasamy, Mishra, Anjali, Wu, Yue-Zhong, Alachkar, Houda, Maharry, Kati, Nicolet, Deedra, Mrózek, Krzysztof, Walker, Alison, Eiring, Anna M., Whitman, Susan P., Becker, Heiko, Perrotti, Danilo, Wu, Lai-Chu, Zhao, Xi, Fehniger, Todd A., Vij, Ravi, Byrd, John C., Blum, William, Lee, L. James, Caligiuri, Michael A., Bloomfield, Clara D., Garzon, Ramiro, and Marcucci, Guido

Published
2013
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7. Aberrant Overexpression of IL-15 Initiates Large Granular Lymphocyte Leukemia through Chromosomal Instability and DNA Hypermethylation

Author

Mishra, Anjali, Liu, Shujun, Sams, Gregory H., Curphey, Douglas P., Santhanam, Ramasamy, Rush, Laura J., Schaefer, Deanna, Falkenberg, Lauren G., Sullivan, Laura, Jaroncyk, Laura, Yang, Xiaojuan, Fisk, Harold, Wu, Lai-Chu, Hickey, Christopher, Chandler, Jason C., Wu, Yue-Zhong, Heerema, Nyla A., Chan, Kenneth K., Perrotti, Danilo, Zhang, Jianying, Porcu, Pierluigi, Racke, Frederick K., Garzon, Ramiro, Lee, Robert J., Marcucci, Guido, and Caligiuri, Michael A.

Published
2012
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8. Sp1/NFκB/HDAC/ miR-29b Regulatory Network in KIT-Driven Myeloid Leukemia

Author

Liu, Shujun, Wu, Lai-Chu, Pang, Jiuxia, Santhanam, Ramasamy, Schwind, Sebastian, Wu, Yue-Zhong, Hickey, Christopher J., Yu, Jianhua, Becker, Heiko, Maharry, Kati, Radmacher, Michael D., Li, Chenglong, Whitman, Susan P., Mishra, Anjali, Stauffer, Nicole, Eiring, Anna M., Briesewitz, Roger, Baiocchi, Robert A., Chan, Kenneth K., Paschka, Peter, Caligiuri, Michael A., Byrd, John C., Croce, Carlo M., Bloomfield, Clara D., Perrotti, Danilo, Garzon, Ramiro, and Marcucci, Guido

Published
2010
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9. MicroRNA-29b induces global DNA hypomethylation and tumor suppressor gene reexpression in acute myeloid leukemia by targeting directly DNMT3A and 3B and indirectly DNMT1

Author

Garzon, Ramiro, Liu, Shujun, Fabbri, Muller, Liu, Zhongfa, Heaphy, Catherine E.A., Callegari, Elisa, Schwind, Sebastian, Pang, Jiuxia, Yu, Jianhua, Muthusamy, Natarajan, Havelange, Violaine, Volinia, Stefano, Blum, William, Rush, Laura J., Perrotti, Danilo, Andreeff, Michael, Bloomfield, Clara D., Byrd, John C., Chan, Kenneth, Wu, Lai-Chu, Croce, Carlo M., and Marcucci, Guido

Published
2009
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10. Bortezomib induces DNA hypomethylation and silenced gene transcription by interfering with Sp1/NF-κB–dependent DNA methyltransferase activity in acute myeloid leukemia

Author

Liu, Shujun, Liu, Zhongfa, Xie, Zhiliang, Pang, Jiuxia, Yu, Jianhua, Lehmann, Esther, Huynh, Lenguyen, Vukosavljevic, Tamara, Takeki, Mitsui, Klisovic, Rebecca B., Baiocchi, Robert A., Blum, William, Porcu, Pierluigi, Garzon, Ramiro, Byrd, John C., Perrotti, Danilo, Caligiuri, Michael A., Chan, Kenneth K., Wu, Lai-Chu, and Marcucci, Guido

Published
2008
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11. Inhibition of NF-[kappa]B by ZAS3, a zinc-finger protein that also binds to the [kappa]B motif

Author

Hong, Joung-Woo, Allen, Carl E., and Wu, Lai-Chu

Subjects
Proteins -- Research, Science and technology
Abstract

The ZAS proteins are large zinc-finger transcriptional proteins implicated in growth, signal transduction, and lymphoid development. Recombinant ZAS fusion proteins containing one of the two DNA-binding domains have been shown to bind specifically to the [kappa]B motif, but the endogenous ZAS proteins or their physiological functions are largely unknown. The [kappa]B motif, GGGACTTTCC, is a gene regulatory element found in promoters and enhancers of genes involved in immunity, inflammation, and growth. The Rel family of NF-[kappa]B, predominantly p65.p50 and p50.p50, are transcription factors well known for inducing gene expression by means of interaction with the [kappa]B motif during acute-phase responses. A functional link between ZAS and NF-[kappa]B, two distinct families of [kappa]B-binding proteins, stems from our previous in vitro studies that show that a representative member, ZAS3, associates with TRAF2, an adaptor molecule in tumor necrosis factor signaling, to inhibit NF-[kappa]B activation. Biochemical and genetic evidence presented herein shows that ZAS3 encodes major [kappa]B-binding proteins in B lymphocytes, and that NF-[kappa]B is constitutively activated in ZAS3-deficient B cells. The data suggest that ZAS3 plays crucial functions in maintaining cellular homeostasis, at least in part by inhibiting NF-[kappa]B by means of three mechanisms: inhibition of nuclear translocation of p65, competition for [kappa]B gene regulatory elements, and repression of target gene transcription.

Published
2003

16. Reciprocal regulation of nuclear factor kappa B and its inhibitor ZAS3 after peripheral nerve injury

Author

Madiai Francesca, Goettl Virginia M, Wu Lai-Chu, Hackshaw Kevin V, and Hussain Syed-Rehan A

Subjects
Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Neurophysiology and neuropsychology, QP351-495
Abstract

Abstract Background NF-κB binds to the κB motif to regulate transcription of genes involved in growth, immunity and inflammation, and plays a pivotal role in the production of pro-inflammatory cytokines after nerve injuries. The zinc finger protein ZAS3 also binds to the κB or similar motif. In addition to competition for common DNA sites, in vitro experiments have shown that ZAS3 can inhibit NF-κB via the association with TRAF2 to inhibit the nuclear translocation of NF-κB. However, the physiological significance of the ZAS3-mediated inhibition of NF-κB has not been demonstrated. The purpose of this study is to characterize ZAS3 proteins in nervous tissues and to use spinal nerve ligation, a neuropathic pain model, to demonstrate a functional relationship between ZAS3 and NF-κB. Results Immunohistochemical experiments show that ZAS3 is expressed in specific regions of the central and peripheral nervous system. Abundant ZAS3 expression is found in the trigeminal ganglion, hippocampal formation, dorsal root ganglia, and motoneurons. Low levels of ZAS3 expressions are also found in the cerebral cortex and in the grey matter of the spinal cord. In those nervous tissues, ZAS3 is expressed mainly in the cell bodies of neurons and astrocytes. Together with results of Western blot analyses, the data suggest that ZAS3 protein isoforms with differential cellular distribution are produced in a cell-specific manner. Further, neuropathic pain confirmed by persistent mechanical allodynia was manifested in rats seven days after L5 and L6 lumbar spinal nerve ligation. Changes in gene expression, including a decrease in ZAS3 and an increase in the p65 subunit of NF-κB were observed in dorsal root ganglion ipsilateral to the ligation when compared to the contralateral side. Conclusion ZAS3 is expressed in nervous tissues involved in cognitive function and pain modulation. The down-regulation of ZAS3 after peripheral nerve injury may lead to activation of NF-κB, allowing Wallerian regeneration and induction of NF-κB-dependent gene expression, including pro-inflammatory cytokines. We propose that reciprocal changes in the expression of ZAS3 and NF-κB might generate neuropathic pain after peripheral nerve injury.

Published
2006
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17. Interleukin-18 drives ILC3 proliferation and promotes interleukin-22 production via NF-κB1

Author

Victor, Aaron R., Nalin, Ansel P., Dong, Wenjuan, McClory, Susan, Wei, Min, Mao, Charlene, Kladney, Raleigh D., Youssef, Youssef, Chan, Wing Keung, Briercheck, Edward L., Hughes, Tiffany, Scoville, Steven D., Pitarresi, Jason R., Chen, Charlie, Manz, Sarah, Wu, Lai-Chu, Zhang, Jianying, Ostrowski, Michael C., Freud, Aharon G., Leone, Gustavo W., Caligiuri, Michael A., and Yu, Jianhua

Subjects
Interleukin-15, Interleukins, Palatine Tonsil, Interleukin-18, NF-kappa B, Transcription Factor RelA, Dendritic Cells, Article, Immunity, Innate, Humans, Lymphocytes, Promoter Regions, Genetic, Cell Proliferation, Signal Transduction
Abstract

Group 3 innate lymphoid cells (ILC3s) are important regulators of the immune system, maintaining homeostasis in the presence of commensal bacteria, but activating immune defenses in response to microbial pathogens. ILC3s are a robust source of IL-22, a cytokine critical for stimulating the anti-microbial response. We sought to identify cytokines that can promote proliferation and induce or maintain IL-22 production by ILC3s and determine a molecular mechanism for this process. We identified IL-18 as a cytokine that cooperates with an ILC3 survival factor, IL-15, to induce proliferation of human ILC3s, as well as induce and maintain IL-22 production. To determine a mechanism of action, we examined the NF-κB pathway, which is activated by IL-18 signaling. We found that the NF-κB complex signaling component, p65, binds to the proximal region of the IL22 promoter and promotes transcriptional activity. Finally, we observed that CD11c+ dendritic cells expressing IL-18 are found in close proximity to ILC3s in human tonsils in situ. Therefore, we identify a new mechanism by which human ILC3s proliferate and produce IL-22, and identify NF-κB as a potential therapeutic target to be considered in pathologic states characterized by overproduction of IL-18 and/or IL-22.

Published
2017

18. The κB transcriptional enhancer motif and signal sequences of V(D)J recombination are targets for the zinc finger protein HIVEP3/KRC: a site selection amplification binding study

Author

Wu Lai-Chu, Mak Chi-ho, and Allen Carl E

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background The ZAS family is composed of proteins that regulate transcription via specific gene regulatory elements. The amino-DNA binding domain (ZAS-N) and the carboxyl-DNA binding domain (ZAS-C) of a representative family member, named κB DNA binding and recognition component (KRC), were expressed as fusion proteins and their target DNA sequences were elucidated by site selection amplification binding assays, followed by cloning and DNA sequencing. The fusion proteins-selected DNA sequences were analyzed by the MEME and MAST computer programs to obtain consensus motifs and DNA elements bound by the ZAS domains. Results Both fusion proteins selected sequences that were similar to the κB motif or the canonical elements of the V(D)J recombination signal sequences (RSS) from a pool of degenerate oligonucleotides. Specifically, the ZAS-N domain selected sequences similar to the canonical RSS nonamer, while ZAS-C domain selected sequences similar to the canonical RSS heptamer. In addition, both KRC fusion proteins selected oligonucleoties with sequences identical to heptamer and nonamer sequences within endogenous RSS. Conclusions The RSS are cis-acting DNA motifs which are essential for V(D)J recombination of antigen receptor genes. Due to its specific binding affinity for RSS and κB-like transcription enhancer motifs, we hypothesize that KRC may be involved in the regulation of V(D)J recombination.

Published
2002
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19. SMAD4 promotes TGF-β–independent NK cell homeostasis and maturation and antitumor immunity

Author

Wang, Youwei, primary, Chu, Jianhong, additional, Yi, Ping, additional, Dong, Wejuan, additional, Saultz, Jennifer, additional, Wang, Yufeng, additional, Wang, Hongwei, additional, Scoville, Steven, additional, Zhang, Jianying, additional, Wu, Lai-Chu, additional, Deng, Youcai, additional, He, Xiaoming, additional, Mundy-Bosse, Bethany, additional, Freud, Aharon G., additional, Wang, Li-Shu, additional, Caligiuri, Michael A., additional, and Yu, Jianhua, additional

Published
2018
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20. The proinflammatory protein HMGB1 is a substrate of transglutaminase-2 and forms high-molecular weight complexes with autoantigens

Author

Willis, William L., primary, Wang, Linan, additional, Wada, Takuma Tsuzuki, additional, Gardner, Mark, additional, Abdouni, Omar, additional, Hampton, Jeffrey, additional, Valiente, Giancarlo, additional, Young, Nicholas, additional, Ardoin, Stacy, additional, Agarwal, Sudha, additional, Freitas, Michael A., additional, Wu, Lai-Chu, additional, and Jarjour, Wael N., additional

Published
2018
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21. Daily Moderate Exercise Is Beneficial and Social Stress Is Detrimental to Disease Pathology in Murine Lupus Nephritis

Author

Aqel, Saba I., primary, Hampton, Jeffrey M., additional, Bruss, Michael, additional, Jones, Kendra T., additional, Valiente, Giancarlo R., additional, Wu, Lai-Chu, additional, Young, Matthew C., additional, Willis, William L., additional, Ardoin, Stacy, additional, Agarwal, Sudha, additional, Bolon, Brad, additional, Powell, Nicole, additional, Sheridan, John, additional, Schlesinger, Naomi, additional, Jarjour, Wael N., additional, and Young, Nicholas A., additional

Published
2017
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22. Thymoquinone exerts potent growth-suppressive activity on leukemia through DNA hypermethylation reversal in leukemia cells

Author

Pang, Jiuxia, primary, Shen, Na, additional, Yan, Fei, additional, Zhao, Na, additional, Dou, Liping, additional, Wu, Lai-Chu, additional, Seiler, Christopher L., additional, Yu, Li, additional, Yang, Ke, additional, Bachanova, Veronika, additional, Weaver, Eric, additional, Tretyakova, Natalia Y., additional, and Liu, Shujun, additional

Published
2017
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24. Hematopoietic stem cells improve dopaminergic neuron in the MPTP-mice

Author

Lu, Jingwei, Kanji, Suman, Aggarwal, Reeva, Das, Manjusri, Joseph, Matthew, Wu, Lai-Chu, Mao, Hai-Quan, Pompili, Vincent J., Hadjiconstantinou, Maria, and Das, Hiranmoy

Subjects
Neurons, Disease Models, Animal, Mice, Base Sequence, Parkinsonian Disorders, Dopamine, Animals, Hematopoietic Stem Cells, Polymerase Chain Reaction, Article, DNA Primers
Abstract

Because of their ability for self-renewal and neural differentiation, stem cells are believed to be ideal for cell replacement therapy in Parkinson’s disease (PD). Nanofiber-expanded human umbilical cord hematopoietic stem cells (HUHSCs) are advantageous to other stem cells as they provide a source of unlimited stem cell production for clinical application. In this study, we investigated whether 1. nanofiber-expanded HUHSCs are capable of neural differentiation in vitro, and 2. they could improve dopaminergic neuron morphology in the caudate/putamen (CPu) and substantia nigra pars compacta (SNc) of the MPTP-mouse model of PD. When cultured under neural differentiation conditions, nanofiber-expanded HUHSCs were able to undergo neural differentiation in vitro, as determined by gene and protein expression of neural markers such as MAP2, NeuN, HuC, GFAP and Oligo2. Thirty days after a single intracardioventricular injection of HUHSCs to MPTP-mice there was a significant recovery of tyrosine hydroxylase (TH) immunostaining in CPu. There was an increase in the size and staining density of TH(+) cells in SNc, while their number was unchanged.

Published
2013

25. Targeting Activation Induced Cytidine Deaminase Overcome Tumor Evasion of Immunotherapy by Cytotoxic T Lymphocytes

Author

Liu, Jin-Qing, Joshi, Pramod S., Wang, Chuansong, El-Omrani, Hani Y., Xiao, Yi, Liu, Xiuping, Hagan, John P., Liu, Chang-Gong, Wu, Lai-Chu, and Bai, Xue-Feng

Subjects
Cytotoxicity, Immunologic, Mice, Inbred BALB C, Mice, Transgenic, Immunotherapy, Adoptive, Article, Mice, Mice, Inbred DBA, Cell Line, Tumor, Cytidine Deaminase, Gene Targeting, Mutagenesis, Site-Directed, Animals, Tumor Escape, RNA, Small Interfering, Plasmacytoma, T-Lymphocytes, Cytotoxic
Abstract

Activation induced cytidine deaminase (AID) is an enzyme essential for the generation of antibody diversity in B cells and is considered to be a general gene mutator. In addition, AID expression was also implicated in the pathogenesis of human B cell malignancies and associated with poor prognosis. Here we report that siRNA silencing of AID in plasmacytoma dramatically increased its susceptibility to immunotherapy by cytotoxic T lymphocytes. AID silencing did not decrease the mutation frequencies of tumor antigen gene P1A. Gene-array analysis showed dramatically altered expression of a number of genes in AID-silenced plasmacytoma cells and upregulation of CD200 was shown to be in favor of tumor eradication by CTL. Taken together, we demonstrate a novel function of AID in tumor evasion of CTL therapy and that targeting AID should be beneficial in the immunotherapy of AID positive tumors.

Published
2010

31. Curcumin Down-Regulates DNA Methyltransferase 1 and Plays an Anti-Leukemic Role in Acute Myeloid Leukemia

Author

Yu, Jianhua, primary, Peng, Yong, additional, Wu, Lai-Chu, additional, Xie, Zhiliang, additional, Deng, Youcai, additional, Hughes, Tiffany, additional, He, Shun, additional, Mo, XiaoKui, additional, Chiu, Ming, additional, Wang, Qi-En, additional, He, Xiaoming, additional, Liu, Shujun, additional, Grever, Michael R., additional, Chan, Kenneth K., additional, and Liu, Zhongfa, additional

Published
2013
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32. Micrornas Promote Activation and Maturation of Natural Killer Cells Through Toll-Like Receptor Signaling.

Author

Yu, Jianhua, primary, He, Shun, additional, Wu, Lai-Chu, additional, Mao, Hsiaoyin, additional, Vasu, Sumithira, additional, Jaglowski, Samantha M., additional, Peng, Yong, additional, Alvarez-Breckenridge, Christopher, additional, Yuan, Shunzong, additional, Wei, Min, additional, Zhang, Jianying, additional, Hughes, Tiffany L, additional, Ghoshal, Kalpana, additional, Devine, Steven M., additional, and Caligiuri, Michael A., additional

Published
2012
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36. Abstract 2014: Modulation of DNA methyltransferases in leukemia cells by curcumin and its associated anti-leukemia activities

Author

Liu, Zhongfa, primary, Wang, Hongyan, additional, Wu, Lai-chu, additional, Xie, Zhiliang, additional, Du, Liping, additional, Mo, Xiaokui, additional, Chiu, Ming, additional, Perrotti, Danilo, additional, Grever, Michael, additional, Byrd, John C., additional, Liu, Shujun, additional, Marcucci, Guido, additional, and Chan, Kenneth K., additional

Published
2011
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37. The Large Zinc Finger Protein ZAS3 Is a Critical Modulator of Osteoclastogenesis

Author

Liu, Shujun, primary, Madiai, Francesca, additional, Hackshaw, Kevin V., additional, Allen, Carl E., additional, Carl, Joseph, additional, Huschart, Emily, additional, Karanfilov, Chris, additional, Litsky, Alan, additional, Hickey, Christopher J., additional, Marcucci, Guido, additional, Huja, Sarandeep, additional, Agarwal, Sudha, additional, Yu, Jianhua, additional, Caligiuri, Michael A., additional, and Wu, Lai-Chu, additional

Published
2011
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39. Interleukin-15 Is a Proto-Oncogene In Acute Large Granular Lymphocyte Leukemia

Author

Mishra, Anjali, primary, Liu, Shujun, additional, Sams, Gregory H, additional, Curphey, Douglas P, additional, Santhanam, Ramasamy, additional, Rush, Laura J, additional, Schaefer, Deanna, additional, Falkenberg, Lauren G, additional, Sullivan, Laura, additional, Jaroncyk, Laura, additional, Zou, Xunchang, additional, Fisk, Harold, additional, Labanowska, Jadwiga, additional, Caserta, Enrico, additional, Wu, Lai-Chu, additional, Becker, Heiko, additional, Schwind, Sebastian, additional, Chandler, Jason C., additional, Wu, Yue-Zhong, additional, Heerema, Nyla A., additional, Porcu, Pierluigi, additional, Garzon, Ramiro, additional, Marcucci, Guido, additional, and Caligiuri, Michael A., additional

Published
2010
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40. Abstract 3558: The natural product silvestrol decreases oncogenic FLT3 and miR-155 levels in FLT3-ITD positive Acute Myeloid Leukemia (AML) cells

Author

Alachkar, Houda, primary, Liu, Shujun, additional, Schwind, Sebastian, additional, Becker, Heiko, additional, Metzeler, Klaus H., additional, Hickey, Christopher, additional, Pang, Jiuxia, additional, Whitman, Susan P., additional, Chan, Kenneth K., additional, Garzon, Ramiro, additional, Lucas, David M., additional, Perrotti, Danilo, additional, Wu, Lai-Chu, additional, Grever, Michael R., additional, Kinghorn, A D., additional, and Marcucci, Guido, additional

Published
2010
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41. Sp1/NFκB/HDAC/miR-29b Regulatory Network in KIT-Driven Myeloid Leukemia

Author

Liu, Shujun, primary, Wu, Lai-Chu, additional, Pang, Jiuxia, additional, Santhanam, Ramasamy, additional, Schwind, Sebastian, additional, Wu, Yue-Zhong, additional, Hickey, Christopher J., additional, Yu, Jianhua, additional, Becker, Heiko, additional, Maharry, Kati, additional, Radmacher, Michael D., additional, Li, Chenglong, additional, Whitman, Susan P., additional, Mishra, Anjali, additional, Stauffer, Nicole, additional, Eiring, Anna M., additional, Briesewitz, Roger, additional, Baiocchi, Robert A., additional, Chan, Kenneth K., additional, Paschka, Peter, additional, Caligiuri, Michael A., additional, Byrd, John C., additional, Croce, Carlo M., additional, Bloomfield, Clara D., additional, Perrotti, Danilo, additional, Garzon, Ramiro, additional, and Marcucci, Guido, additional

Published
2010
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42. Evidence of MicroRNA-29b and Sp1/NFκB-HDAC Regulatory Network for KIT Expression in KIT-Driven Acute Myeloid Leukemia (AML): Biologic and Therapeutic Implications.

Author

Liu, Shujun, primary, Wu, Lai Chu, additional, Pang, Jiuxia, additional, Santhanam, Ramasamy, additional, Schwind, Sebastian, additional, Wu, Yue-Zhong, additional, Hickey, Christopher, additional, Yu, Jianhua, additional, Mishra, Anjali, additional, Becker, Heiko, additional, Li, Chenglong, additional, Briesewitz, Roger, additional, Baiocchi, Robert A., additional, Chan, Kenneth K., additional, Caligiuri, Michael A., additional, Byrd, John C., additional, Perrotti, Danilo, additional, Garzon, Ramiro, additional, and Marcucci, Guido, additional

Published
2009
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