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Journal articles on the topic 'Runt related transcription factor'

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Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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1

Saikia, Snigdha, Asad Ur Rehman, Prajjalendra Barooah, Preeti Sarmah, Mallika Bhattacharyya, Muktanjalee Deka, Manab Deka, Bhabadev Goswami, Syed Akhtar Husain, and Subhash Medhi. "Alteration in the expression of MGMT and RUNX3 due to non-CpG promoter methylation and their correlation with different risk factors in esophageal cancer patients." Tumor Biology 39, no. 5 (May 2017): 101042831770163. http://dx.doi.org/10.1177/1010428317701630.

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Promoter methylation reflects in the inactivation of different genes like O6-methylguanine-DNA methyltransferase DNA repair gene and runt-related transcription factor 3, a known tumor suppressor gene in various cancers such as esophageal cancer. The promoter methylation was evaluated for O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 in CpG, CHH, and CHG context (where H is A, T, or C) by next-generation sequencing. The methylation status was correlated with quantitative messenger RNA expression. In addition, messenger RNA expression was correlated with different risk factors like tobacco, alcohol, betel nut consumption, and smoking habit. CpG methylation of O6-methylguanine-DNA methyltransferase promoter had a positive association in the development of esophageal cancer (p < 0.05), whereas runt-related transcription factor 3 promoter methylation showed no significant association (p = 1.0) to develop esophageal cancer. However, the non-CpG methylation, CHH, and CHG were significantly correlated with O6-methylguanine-DNA methyltransferase (p < 0.05) and runt-related transcription factor 3 (p < 0.05) promoters in the development of esophageal cancer. The number of cytosine converted to thymine (C→T) in O6-methylguanine-DNA methyltransferase promoter showed a significant correlation between cases and controls (p < 0.05), but in runt-related transcription factor 3 no such significant correlation was observed. Besides, messenger RNA expression was found to be significantly correlated with promoter hypermethylation of O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 in the context of CHG and CHH (p < 0.05). The CpG hypermethylation in O6-methylguanine-DNA methyltransferase showed positive (p < 0.05) association, whereas in runt-related transcription factor 3, it showed contrasting negative association (p = 0.23) with their messenger RNA expression. Tobacco, betel nut consumption, and smoking habits were associated with altered messenger RNA expression of O6-methylguanine-DNA methyltransferase (p < 0.05) and betel nut consumption and smoking habits were associated with runt-related transcription factor 3 (p < 0.05). There was no significant association between messenger RNA expression of O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 with alcohol consumption (p = 0.32 and p = 0.15). In conclusion, our results suggest that an aberrant messenger RNA expression may be the outcome of CpG, CHG, and CHH methylation in O6-methylguanine-DNA methyltransferase, whereas outcome of CHG and CHH methylation in runt-related transcription factor 3 promoters along with risk factors such as consumption of tobacco, betel nut, and smoking habits in esophageal cancer from Northeast India.
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2

Yu, Shibing, Yu Jiang, Deborah L. Galson, Min Luo, Yumei Lai, Yi Lu, Hong-Jiao Ouyang, Jian Zhang, and Guozhi Xiao. "General Transcription Factor IIA-γ Increases Osteoblast-specificOsteocalcinGene Expression via Activating Transcription Factor 4 and Runt-related Transcription Factor 2." Journal of Biological Chemistry 283, no. 9 (January 2, 2008): 5542–53. http://dx.doi.org/10.1074/jbc.m705653200.

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3

Thirunavukkarasu, Kannan, Muktar Mahajan, Keith W. McLarren, Stefano Stifani, and Gerard Karsenty. "Two Domains Unique to Osteoblast-Specific Transcription Factor Osf2/Cbfa1 Contribute to Its Transactivation Function and Its Inability To Heterodimerize with Cbfβ." Molecular and Cellular Biology 18, no. 7 (July 1, 1998): 4197–208. http://dx.doi.org/10.1128/mcb.18.7.4197.

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ABSTRACT Osf2/Cbfa1, hereafter called Osf2, is a member of the Runt-related family of transcription factors that plays a critical role during osteoblast differentiation. Like all Runt-related proteins, it contains a runt domain, which is the DNA-binding domain, and a C-terminal proline-serine-threonine-rich (PST) domain thought to be the transcription activation domain. Additionally, Osf2 has two amino-terminal domains distinct from any other Runt-related protein. To understand the mechanisms of osteoblast gene regulation by Osf2, we performed an extensive structure-function analysis. After defining a short Myc-related nuclear localization signal, a deletion analysis revealed the existence of three transcription activation domains and one repression domain. AD1 (for activation domain 1) comprises the first 19 amino acids of the molecule, which form the first domain unique to Osf2, AD2 is formed by the glutamine-alanine (QA) domain, the second domain unique to Osf2, and AD3 is located in the N-terminal half of the PST domain and also contains sequences unique to Osf2. The transcription repression domain comprises the C-terminal 154 amino acids of Osf2. DNA-binding, domain-swapping, and protein interaction experiments demonstrated that full-length Osf2 does not interact with Cbfβ, a known partner of Runt-related proteins, whereas a deletion mutant of Osf2 containing only the runt and PST domains does. The QA domain appears to be responsible for preventing this heterodimerization. Thus, our results uncover the unique functional organization of Osf2 by identifying functional domains not shared with other Runt-related proteins that largely control its transactivation and heterodimerization abilities.
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4

Coller, Hilary A. "The Runt-related transcription factor 1 in prostate cancer-associated fibroblasts." Proceedings of the National Academy of Sciences 111, no. 46 (November 10, 2014): 16238–39. http://dx.doi.org/10.1073/pnas.1418976111.

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5

Boström, Kristina I. "DNA Damage Response, Runx2 (Runt-Related Transcription Factor 2), and Vascular Calcification." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 4 (April 2021): 1358–59. http://dx.doi.org/10.1161/atvbaha.121.315836.

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6

Chi, Xin-Zi, Jiyeon Kim, Yong-Hee Lee, Jung-Won Lee, Kyeong-Sook Lee, Heejun Wee, Wun-Jae Kim, et al. "Runt-Related Transcription Factor RUNX3 Is a Target of MDM2-Mediated Ubiquitination." Cancer Research 69, no. 20 (October 6, 2009): 8111–19. http://dx.doi.org/10.1158/0008-5472.can-09-1057.

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7

Huang, Shu-Pin, Yu-Hsuan Lan, Te-Ling Lu, Jiunn-Bey Pao, Ta-Yuan Chang, Hong-Zin Lee, Wen-Hui Yang, et al. "Clinical significance of runt-related transcription factor 1 polymorphism in prostate cancer." BJU International 107, no. 3 (August 24, 2010): 486–92. http://dx.doi.org/10.1111/j.1464-410x.2010.09512.x.

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8

DU, FEIYA, HUILING WU, ZHIQIN ZHOU, and YU LIU. "microRNA-375 inhibits osteogenic differentiation by targeting runt-related transcription factor 2." Experimental and Therapeutic Medicine 10, no. 1 (May 7, 2015): 207–12. http://dx.doi.org/10.3892/etm.2015.2477.

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9

Tanaka, Shigetomi, Hidenori Shiraha, Yutaka Nakanishi, Shin-Ichi Nishina, Minoru Matsubara, Shigeru Horiguchi, Nobuyuki Takaoka, et al. "Runt-related transcription factor 3 reverses epithelial-mesenchymal transition in hepatocellular carcinoma." International Journal of Cancer 131, no. 11 (April 24, 2012): 2537–46. http://dx.doi.org/10.1002/ijc.27575.

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10

Gil-Yarom, Naama, Lihi Radomir, Lital Sever, Matthias P. Kramer, Hadas Lewinsky, Chamutal Bornstein, Ronnie Blecher-Gonen, et al. "CD74 is a novel transcription regulator." Proceedings of the National Academy of Sciences 114, no. 3 (December 28, 2016): 562–67. http://dx.doi.org/10.1073/pnas.1612195114.

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CD74 is a cell-surface receptor for the cytokine macrophage migration inhibitory factor. Macrophage migration inhibitory factor binding to CD74 induces its intramembrane cleavage and the release of its cytosolic intracellular domain (CD74–ICD), which regulates cell survival. In the present study, we characterized the transcriptional activity of CD74–ICD in chronic lymphocytic B cells. We show that following CD74 activation, CD74–ICD interacts with the transcription factors RUNX (Runt related transcription factor) and NF-κB and binds to proximal and distal regulatory sites enriched for genes involved in apoptosis, immune response, and cell migration. This process leads to regulation of expression of these genes. Our results suggest that identifying targets of CD74 will help in understanding of essential pathways regulating B-cell survival in health and disease.
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Tang, Jun, Jing Xie, Wei Chen, Chenyi Tang, Jinjin Wu, Yiping Wang, Xue-Dong Zhou, Hou-De Zhou, and Yi-Ping Li. "Runt-related transcription factor 1 is required for murine osteoblast differentiation and bone formation." Journal of Biological Chemistry 295, no. 33 (June 22, 2020): 11669–81. http://dx.doi.org/10.1074/jbc.ra119.007896.

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Despite years of research investigating osteoblast differentiation, the mechanisms by which transcription factors regulate osteoblast maturation, bone formation, and bone homeostasis is still unclear. It has been reported that runt-related transcription factor 1 (Runx1) is expressed in osteoblast progenitors, pre-osteoblasts, and mature osteoblasts; yet, surprisingly, the exact function of RUNX1 in osteoblast maturation and bone formation remains unknown. Here, we generated and characterized a pre-osteoblast and differentiating chondrocyte-specific Runx1 conditional knockout mouse model to study RUNX1's function in bone formation. Runx1 ablation in osteoblast precursors and differentiating chondrocytes via osterix-Cre (Osx-Cre) resulted in an osteoporotic phenotype and decreased bone density in the long bones and skulls of Runx1f/fOsx-Cre mice compared with Runx1f/f and Osx-Cre mice. RUNX1 deficiency reduced the expression of SRY-box transcription factor 9 (SOX9), Indian hedgehog signaling molecule (IHH), Patched (PTC), and cyclin D1 in the growth plate, and also reduced the expression of osteocalcin (OCN), OSX, activating transcription factor 4 (ATF4), and RUNX2 in osteoblasts. ChIP assays and promoter activity mapping revealed that RUNX1 directly associates with the Runx2 gene promoter and up-regulates Runx2 expression. Furthermore, the ChIP data also showed that RUNX1 associates with the Ocn promoter. In conclusion, RUNX1 up-regulates the expression of Runx2 and multiple bone-specific genes, and plays an indispensable role in bone formation and homeostasis in both trabecular and cortical bone. We propose that stimulating Runx1 activity may be useful in therapeutic approaches for managing some bone diseases such as osteoporosis.
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12

Nakazato, Ryota, Takeshi Takarada, Takumi Watanabe, Binh Thanh Nguyen, Shinsuke Ikeno, Eiichi Hinoi, and Yukio Yoneda. "Constitutive and functional expression of runt-related transcription factor-2 by microglial cells." Neurochemistry International 74 (July 2014): 24–35. http://dx.doi.org/10.1016/j.neuint.2014.04.010.

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13

Horiguchi, Shigeru, Hidenori Shiraha, Teruya Nagahara, Jyunnro Kataoka, Masaya Iwamuro, Minoru Matsubara, Shinichi Nishina, et al. "Loss of runt-related transcription factor 3 induces gemcitabine resistance in pancreatic cancer." Molecular Oncology 7, no. 4 (April 23, 2013): 840–49. http://dx.doi.org/10.1016/j.molonc.2013.04.004.

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14

Mümmler, Carlo, Olivier Burgy, Sarah Hermann, Kathrin Mutze, Andreas Günther, and Melanie Königshoff. "Cell‐specific expression of runt‐related transcription factor 2 contributes to pulmonary fibrosis." FASEB Journal 32, no. 2 (January 4, 2018): 703–16. http://dx.doi.org/10.1096/fj.201700482r.

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15

Sun, Cheng-Cao, Shu-Jun Li, Zhen-Long Chen, Guang Li, Qian Zhang, and De-Jia Li. "Expression and Prognosis Analyses of Runt-Related Transcription Factor Family in Human Leukemia." Molecular Therapy - Oncolytics 12 (March 2019): 103–11. http://dx.doi.org/10.1016/j.omto.2018.12.008.

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16

Park, Eun-Sil, Jiyeon Park, Renny T. Franceschi, and Misung Jo. "The role for runt related transcription factor 2 (RUNX2) as a transcriptional repressor in luteinizing granulosa cells." Molecular and Cellular Endocrinology 362, no. 1-2 (October 2012): 165–75. http://dx.doi.org/10.1016/j.mce.2012.06.005.

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17

Liu, Bitian, Shen Pan, Junlong Liu, and Chuize Kong. "Cancer-associated fibroblasts and the related Runt-related transcription factor 2 (RUNX2) promote bladder cancer progression." Gene 775 (April 2021): 145451. http://dx.doi.org/10.1016/j.gene.2021.145451.

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18

Fukushima-Nakase, Yoko, Yoshinori Naoe, Ichiro Taniuchi, Hajime Hosoi, Tohru Sugimoto, and Tsukasa Okuda. "Shared and distinct roles mediated through C-terminal subdomains of acute myeloid leukemia/Runt-related transcription factor molecules in murine development." Blood 105, no. 11 (June 1, 2005): 4298–307. http://dx.doi.org/10.1182/blood-2004-08-3372.

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Abstract AML1/Runx1 is a frequent target of human leukemia–associated gene aberration and encodes a transcription factor with nonredundant biologic functions in initial development of definitive hematopoiesis, T-cell development, and steady-state platelet production. AML1/Runx1 and 2 closely related family genes, AML2/Runx3 and AML3/Runx2/Cbfa1, present in mammals, comprise the Runt-domain transcription factor family. Although they have similar structural and biochemical properties, gene-targeting experiments have identified distinct biologic roles. To directly determine the presence of functional overlap among runt-related transcription factor (Runx) family molecules, we replaced the C-terminal portion of acute myeloid leukemia 1 (AML1) with that derived from its family members, which are variable in contrast to conserved Runt domain, using the gene knock-in method. We found that C-terminal portions of either AML2 or AML3 could functionally replace that of AML1 for myeloid development in culture and within the entire mouse. However, while AML2 substituted for AML1 could effectively rescue lymphoid lineages, AML3 could not, resulting in a smaller thymus and lymphoid deficiency in peripheral blood. Substitution by the C-terminal portion of AML3 also led to high infantile mortality and growth retardation, suggesting that AML1 has as yet unidentified effects on these phenotypes. Thus, the C-terminal portions of Runx family members have both similar and distinct biologic functions.
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Zhang, Dianhong, Cui Liang, Pengcheng Li, Lulu Yang, Zhengyang Hao, Lingyao Kong, Xiaoxu Tian, et al. "Runt‐related transcription factor 1 (Runx1) aggravates pathological cardiac hypertrophy by promoting p53 expression." Journal of Cellular and Molecular Medicine 25, no. 16 (June 30, 2021): 7867–77. http://dx.doi.org/10.1111/jcmm.16704.

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Park, Kyung-Ran, SooHyun Kim, MyoungLae Cho, Sang Wook Kang, and Hyung-Mun Yun. "Effects of PIN on Osteoblast Differentiation and Matrix Mineralization through Runt-Related Transcription Factor." International Journal of Molecular Sciences 21, no. 24 (December 16, 2020): 9579. http://dx.doi.org/10.3390/ijms21249579.

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Styrax Japonica Sieb. et Zucc. has been used as traditional medicine in inflammatory diseases, and isolated compounds have shown pharmacological activities. Pinoresinol glucoside (PIN) belonging to lignins was isolated from the stem bark of S. Japonica. This study aimed to investigate the biological function and mechanisms of PIN on cell migration, osteoblast differentiation, and matrix mineralization. Herein, we investigated the effects of PIN in MC3T3-E1 pre-osteoblasts, which are widely used for studying osteoblast behavior in in vitro cell systems. At concentrations ranging from 0.1 to 100 μM, PIN had no cell toxicity in pre-osteoblasts. Pre-osteoblasts induced osteoblast differentiation, and the treatment of PIN (10 and 30 μM) promoted the cell migration rate in a dose-dependent manner. At concentrations of 10 and 30 μM, PIN elevated early osteoblast differentiation in a dose-dependent manner, as indicated by increases in alkaline phosphatase (ALP) staining and activity. Subsequently, PIN also increased the formation of mineralized nodules in a dose-dependent manner, as indicated by alizarin red S (ARS) staining, demonstrating positive effects of PIN on late osteoblast differentiation. In addition, PIN induced the mRNA level of BMP2, ALP, and osteocalcin (OCN). PIN also upregulated the protein level of BMP2 and increased canonical BMP2 signaling molecules, the phosphorylation of Smad1/5/8, and the protein level of Runt-related transcription factor 2 (RUNX2). Furthermore, PIN activated non-canonical BMP2 signaling molecules, activated MAP kinases, and increased β-catenin signaling. The findings of this study indicate that PIN has biological roles in osteoblast differentiation and matrix mineralization, and suggest that PIN might have anabolic effects in bone diseases such as osteoporosis and periodontitis.
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WAKITANI, Shoichi, Daigo YOKOI, Yuichi HIDAKA, and Koichiro NISHINO. "The differentially DNA-methylated region responsible for expression of runt-related transcription factor 2." Journal of Veterinary Medical Science 79, no. 2 (2017): 230–37. http://dx.doi.org/10.1292/jvms.16-0321.

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22

Kayed, H., X. Jiang, S. Keleg, R. Jesnowski, T. Giese, M. R. Berger, I. Esposito, M. Löhr, H. Friess, and J. Kleeff. "Regulation and functional role of the Runt-related transcription factor-2 in pancreatic cancer." British Journal of Cancer 97, no. 8 (September 18, 2007): 1106–15. http://dx.doi.org/10.1038/sj.bjc.6603984.

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23

Lina, Mei, Wu Changan, and Zhao Qing. "Runt-related transcription factor 3 promoter hypermethylation and gastric cancer risk: A meta-analysis." Open Life Sciences 13, no. 1 (April 10, 2018): 64–70. http://dx.doi.org/10.1515/biol-2018-0009.

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AbstractObjectiveThe aim of this study was to investigate the correlation between runt-related transcription factor 3 (RUNX3) gene promoter hypermethylation and gastric cancer risk by meta-analysis.MethodsBy searching Medline, PubMed, Embase, Cochrane, Ovid and CNKI electronic databases, the open published studies about the association between RUNX3 gene promoter hypermethylation and gastric cancer risk were screened. The hypermethylation rate in cancer tissue and autologous control tissue (normal gastric tissue of gastric cancer patients) were extracted from each included study. The odds ratio (OR) and corresponding 95% confidence interval (95% CI) of RUNX3 gene promoter hypermethylation in cancer tissue versus autologous control tissue of gastric cancer patients were pooled with random or fixed effect models. The publication bias was evaluated by Begg’s funnel plot and Egger’s line regression test.ResultsFinally, twenty three relevant studies were included in this meta-analysis. The hypermethylation rate in cancer tissue and autologous control tissue of gastric cancer patients were 0.56±0.16 and 0.18±0.22 respectively, which demonstrated a hypermethylation rate in cancer tissue significantly higher than that of autologous controls (P<0.05). A significant positive correlation of hypermethylation rate between cancer tissue and autologous control existed for the included 23 studies(rpearson=0.62, P<0.05). For significant heterogeneity across the studies, the OR was pooled by random effects model. The combined OR was 8.06 with the 95% CI of 5.73~11.32, which indicated the hypermethylation frequency in cancer tissue was higher than that of autologous controls.ConclusionThe RUNX3 gene promoter hypermethylation rate was much higher in cancer tissue than that of normal gastric tissue in patients with gastric cancer, which indicates a close association between gastric cancer and RUNX3 gene promoter hypermethylation. Furthermore, RUNX3 gene promoter hypermethylation may be a potential biomarker for gastric cancer diagnosis.
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Shiraha, Hidenori, Shin-ichi Nishina, and Kazuhide Yamamoto. "Loss of runt-related transcription factor 3 causes development and progression of hepatocellular carcinoma." Journal of Cellular Biochemistry 112, no. 3 (February 16, 2011): 745–49. http://dx.doi.org/10.1002/jcb.22973.

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Chuang, Linda Shyue Huey, Jian Ming Khor, Soak Kuan Lai, Shubham Garg, Vaidehi Krishnan, Cheng-Gee Koh, Sang Hyun Lee, and Yoshiaki Ito. "Aurora kinase-induced phosphorylation excludes transcription factor RUNX from the chromatin to facilitate proper mitotic progression." Proceedings of the National Academy of Sciences 113, no. 23 (May 23, 2016): 6490–95. http://dx.doi.org/10.1073/pnas.1523157113.

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The Runt-related transcription factors (RUNX) are master regulators of development and major players in tumorigenesis. Interestingly, unlike most transcription factors, RUNX proteins are detected on the mitotic chromatin and apparatus, suggesting that they are functionally active in mitosis. Here, we identify key sites of RUNX phosphorylation in mitosis. We show that the phosphorylation of threonine 173 (T173) residue within the Runt domain of RUNX3 disrupts RUNX DNA binding activity during mitotic entry to facilitate the recruitment of RUNX proteins to mitotic structures. Moreover, knockdown of RUNX3 delays mitotic entry. RUNX3 phosphorylation is therefore a regulatory mechanism for mitotic entry. Cancer-associated mutations of RUNX3 T173 and its equivalent in RUNX1 further corroborate the role of RUNX phosphorylation in regulating proper mitotic progression and genomic integrity.
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Sase, Tomohiko, Takashi Suzuki, Koh Miura, Kenichi Shiiba, Ikuro Sato, Yasuhiro Nakamura, Kiyoshi Takagi, et al. "Runt-related transcription factor 2 in human colon carcinoma: A potent prognostic factor associated with estrogen receptor." International Journal of Cancer 131, no. 10 (April 17, 2012): 2284–93. http://dx.doi.org/10.1002/ijc.27525.

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Dutta, Bibek, and Motomi Osato. "The RUNX Family, a Novel Multifaceted Guardian of the Genome." Cells 12, no. 2 (January 7, 2023): 255. http://dx.doi.org/10.3390/cells12020255.

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The DNA repair machinery exists to protect cells from daily genetic insults by orchestrating multiple intrinsic and extrinsic factors. One such factor recently identified is the Runt-related transcription factor (RUNX) family, a group of proteins that act as a master transcriptional regulator for multiple biological functions such as embryonic development, stem cell behaviors, and oncogenesis. A significant number of studies in the past decades have delineated the involvement of RUNX proteins in DNA repair. Alterations in RUNX genes cause organ failure and predisposition to cancers, as seen in patients carrying mutations in the other well-established DNA repair genes. Herein, we review the currently existing findings and provide new insights into transcriptional and non-transcriptional multifaceted regulation of DNA repair by RUNX family proteins.
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Daiwile, Atul P., Saravanadevi Sivanesan, Alberto Izzotti, Amit Bafana, Pravin K. Naoghare, Patrizio Arrigo, Hemant J. Purohit, Devendra Parmar, and Krishnamurthi Kannan. "Noncoding RNAs: Possible Players in the Development of Fluorosis." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/274852.

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Fluorosis is caused by excess of fluoride intake over a long period of time. Aberrant change in the Runt-related transcription factor 2 (RUNX2) mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Up to date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling of short noncoding RNAs, in particular miRNAs and snoRNAs, was carried out in sodium fluoride (NaF) treated human osteosarcoma (HOS) cells to understand their possible role in the development of fluorosis. qPCR and in silico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of Runt-related transcription factor 2 (RUNX2) and receptor activator of nuclear factorκ-B ligand (RANKL) genes. Compared to control, C/D box analysis revealed marked elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We show that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure.
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Giuliani, Nicola, Gina Lisignoli, Marina Magnani, Costantina Racano, Marina Bolzoni, Benedetta Dalla Palma, Angelica Spolzino, et al. "New Insights into Osteogenic and Chondrogenic Differentiation of Human Bone Marrow Mesenchymal Stem Cells and Their Potential Clinical Applications for Bone Regeneration in Pediatric Orthopaedics." Stem Cells International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/312501.

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Human mesenchymal stem cells (hMSCs) are pluripotent adult stem cells capable of being differentiated into osteoblasts, adipocytes, and chondrocytes. The osteogenic differentiation of hMSCs is regulated either by systemic hormones or by local growth factors able to induce specific intracellular signal pathways that modify the expression and activity of several transcription factors. Runt-related transcription factor 2 (Runx2) and Wnt signaling-related molecules are the major factors critically involved in the osteogenic differentiation process by hMSCs, and SRY-related high-mobility-group (HMG) box transcription factor 9 (SOX9) is involved in the chondrogenic one. hMSCs have generated a great interest in the field of regenerative medicine, particularly in bone regeneration. In this paper, we focused our attention on the molecular mechanisms involved in osteogenic and chondrogenic differentiation of hMSC, and the potential clinical use of hMSCs in osteoarticular pediatric disease characterized by fracture nonunion and pseudarthrosis.
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Park, Kyung-Ran, SooHyun Kim, MyoungLae Cho, and Hyung-Mun Yun. "Limonoid Triterpene, Obacunone Increases Runt-Related Transcription Factor 2 to Promote Osteoblast Differentiation and Function." International Journal of Molecular Sciences 22, no. 5 (March 2, 2021): 2483. http://dx.doi.org/10.3390/ijms22052483.

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Root bark of Dictamnus dasycarpus Turcz. has been widely used as a traditional medicine and is a well-known anti-inflammatory agent. We isolated limonoid triterpene, obacunone (Obac) from the dried root bark of D. dasycarpus. Obac has been reported to exhibit varieties of biological activities including anti-inflammatory, anti-cancer, and anti-oxidant effects. This study aimed to investigate the beneficial effects and biological mechanisms of Obac in osteoblast differentiation and bone matrix mineralization. In the present study, Obac at concentrations ranging from 1 to 100 μM showed no proliferation effects in MC3T3-E1. The treatment of Obac (1 and 10 μM) increased wound healing and migration rates in a dose-dependent manner. Alkaline phosphatase (ALP) staining and activity showed that Obac (1 and 10 μM) enhanced early osteoblast differentiation in a dose-dependent manner. Obac also increased late osteoblast differentiation in a dose-dependent manner, as indicated by the mineralized nodule formation of ARS staining. The effects of Obac on osteoblast differentiation was validated by the levels of mRNAs encoding the bone differentiation markers, including Alp, bone sialoprotein (Bsp), osteopontin (Opn), and osteocalcin (Ocn). Obac increased the expression of bone morphogenetic protein (BMP), and the phosphorylation of smad1/5/8, and the expression of runt-related transcription factor 2 (RUNX2); Obac also inhibited GSK3β and upregulated the protein level of β-catenin in a dose-dependent manner during osteoblast differentiation. Obac-mediated osteoblast differentiation was attenuated by a BMP2 inhibitor, Noggin and a Wnt/β-catenin inhibitor, Dickkopf-1 (Dkk1) with the abolishment of RUNX2 expression and nuclear accumulation by Obac. Taken together, the findings of this study demonstrate that Obac has pharmacological and biological activates to promote osteoblast differentiation and bone mineralization through BMP2, β-catenin, and RUNX2 pathways, and suggest that Obac might be a therapeutic effect for the treatment and prevention of bone diseases such as osteoporosis and periodontitis.
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Jeong, Pildu, Yun-Sok Ha, Ji Sang Kim, In-Chang Cho, Won Tae Kim, Yong-June Kim, Isaac Yi Kim, et al. "Runt-related transcription factor 3 methylation as a possible prognosticator in muscle-invasive bladder cancer." Cancer Biomarkers 10, no. 5 (June 8, 2012): 205–11. http://dx.doi.org/10.3233/cbm-2012-0248.

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Tang, Xiaoju, Ling Sun, Xiaodong Jin, Yifan Chen, Hui Zhu, Yasha Liang, Qingbo Wu, et al. "Runt-Related Transcription Factor 1 Regulates LPS-Induced Acute Lung Injury via NF-κB Signaling." American Journal of Respiratory Cell and Molecular Biology 57, no. 2 (August 2017): 174–83. http://dx.doi.org/10.1165/rcmb.2016-0319oc.

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Monteiro, Nelson, Diana Ribeiro, Albino Martins, Susana Faria, Nuno A. Fonseca, João N. Moreira, Rui L. Reis, and Nuno M. Neves. "Instructive Nanofibrous Scaffold Comprising Runt-Related Transcription Factor 2 Gene Delivery for Bone Tissue Engineering." ACS Nano 8, no. 8 (July 30, 2014): 8082–94. http://dx.doi.org/10.1021/nn5021049.

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Gu, Liugen, Juan Zhao, Shiqing Zhang, Weisong Xu, Runzhou Ni, and Xiaojuan Liu. "Runt-related transcription factor 2 (RUNX2) inhibits apoptosis of intestinal epithelial cells in Crohn’s disease." Pathology - Research and Practice 214, no. 2 (February 2018): 245–52. http://dx.doi.org/10.1016/j.prp.2017.11.004.

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Matsuda, Miyuki, Kouichi Tamura, Hiromichi Wakui, Toru Dejima, Akinobu Maeda, Masato Ohsawa, Tomohiko Kanaoka, et al. "Involvement of Runx3 in the basal transcriptional activation of the mouse angiotensin II type 1 receptor-associated protein gene." Physiological Genomics 43, no. 14 (July 2011): 884–94. http://dx.doi.org/10.1152/physiolgenomics.00005.2011.

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We previously cloned a molecule that interacts with angiotensin II type 1 (AT1) receptor to exert an inhibitory function on AT1 receptor signaling that we named ATRAP/ Agtrap (for AT1 receptor-associated protein). In the present study we examined the regulation of basal ATRAP gene expression using renal distal convoluted tubule cells. We found that serum starvation upregulated basal expression of ATRAP gene, a response that required de novo mRNA and protein synthesis. Luciferase assay revealed that the proximal promoter region directs transcription and that a putative binding site of runt-related transcription factors (RBE) is important for transcriptional activation. The results of RBE-decoy transfection and endogenous knockdown by small interference RNA showed that the runt-related transcription factor Runx3 is involved in ATRAP gene expression. Chromatin immunoprecipitation assay also supported the binding of Runx3 to the ATRAP promoter in renal distal convoluted tubule cells. Immunohistochemistry demonstrated the expression of Runx3 and ATRAP proteins in the distal convoluted and connecting tubules of the kidney in consecutive sections. Furthermore, the Runx3 immunostaining was decreased together with a concomitant suppression of ATRAP expression in the affected kidney after 7 days of unilateral ureteral obstruction. These findings indicate that Runx3 plays a role in ATRAP gene expression in renal distal tubular cells both in vitro and in vivo.
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Riddell, Alexandra, Martin McBride, Thomas Braun, Stuart A. Nicklin, Ewan Cameron, Christopher M. Loughrey, and Tamara P. Martin. "RUNX1: an emerging therapeutic target for cardiovascular disease." Cardiovascular Research 116, no. 8 (March 10, 2020): 1410–23. http://dx.doi.org/10.1093/cvr/cvaa034.

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Abstract Runt-related transcription factor-1 (RUNX1), also known as acute myeloid leukaemia 1 protein (AML1), is a member of the core-binding factor family of transcription factors which modulate cell proliferation, differentiation, and survival in multiple systems. It is a master-regulator transcription factor, which has been implicated in diverse signalling pathways and cellular mechanisms during normal development and disease. RUNX1 is best characterized for its indispensable role for definitive haematopoiesis and its involvement in haematological malignancies. However, more recently RUNX1 has been identified as a key regulator of adverse cardiac remodelling following myocardial infarction. This review discusses the role RUNX1 plays in the heart and highlights its therapeutic potential as a target to limit the progression of adverse cardiac remodelling and heart failure.
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ter Elst, Arja, Bin Ma, Frank J. G. Scherpen, Hendrik J. M. de Jonge, Jenny Douwes, Albertus T. J. Wierenga, Jan Jacob Schuringa, Willem A. Kamps, and Eveline S. J. M. de Bont. "Repression of Vascular Endothelial Growth Factor Expression by the Runt-Related Transcription Factor 1 in Acute Myeloid Leukemia." Cancer Research 71, no. 7 (March 31, 2011): 2761–71. http://dx.doi.org/10.1158/0008-5472.can-10-0402.

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Susperregui, Antonio R. G., Cristina Gamell, Edgardo Rodríguez-Carballo, Maria José Ortuño, Ramon Bartrons, José Luis Rosa, and Francesc Ventura. "Noncanonical BMP Signaling Regulates Cyclooxygenase-2 Transcription." Molecular Endocrinology 25, no. 6 (June 1, 2011): 1006–17. http://dx.doi.org/10.1210/me.2010-0515.

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Abstract Activation of p38 MAPK has been shown to be relevant for a number of bone morphogenetic protein (BMP) physiological effects. We report here the involvement of noncanonical phosphorylated mothers against decapentaplegic (Smad) signaling in the transcriptional induction of Cox2 (Ptgs2) by BMP-2 in mesenchymal cells and organotypic calvarial cultures. We demonstrate that different regulatory elements are required for regulation of Cox2 expression by BMP-2: Runt-related transcription factor-2 and cAMP response element sites are essential, whereas a GC-rich Smad binding element is important for full responsiveness. Efficient transcriptional activation requires cooperation between transcription factors because mutation of any element results in a strong decrease of BMP-2 responsiveness. BMP-2 activation of p38 leads to increased recruitment of activating transcription factor-2, Runx2, Smad, and coactivators such as p300 at the responsive sites in the Cox2 proximal promoter. We demonstrate, by either pharmacological or genetic analysis, that maximal BMP-2 effects on Cox2 and JunB expression require the function of p38 and its downstream effector mitogen/stress-activated kinase 1. Altogether our results strongly suggest that cooperative effects between canonical and noncanonical BMP signaling allow the fine-tuning of BMP transcriptional responses on specific target genes.
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Kim, Kabsun, Jung Ha Kim, Inyoung Kim, Semun Seong, Jeong Eun Han, Keun-Bae Lee, Jeong-Tae Koh, and Nacksung Kim. "Transcription Factor Lmx1b Negatively Regulates Osteoblast Differentiation and Bone Formation." International Journal of Molecular Sciences 23, no. 9 (May 7, 2022): 5225. http://dx.doi.org/10.3390/ijms23095225.

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The LIM-homeodomain transcription factor Lmx1b plays a key role in body pattern formation during development. Although Lmx1b is essential for the normal development of multiple tissues, its regulatory mechanism in bone cells remains unclear. Here, we demonstrated that Lmx1b negatively regulates bone morphogenic protein 2 (BMP2)-induced osteoblast differentiation. Overexpressed Lmx1b in the osteoblast precursor cells inhibited alkaline phosphatase (ALP) activity and nodule formation, as well as the expression of osteoblast maker genes, including runt-related transcription factor 2 (Runx2), alkaline phosphatase (Alpl), bone sialoprotein (Ibsp), and osteocalcin (Bglap). Conversely, the knockdown of Lmx1b in the osteoblast precursors enhanced the osteoblast differentiation and function. Lmx1b physically interacted with and repressed the transcriptional activity of Runx2 by reducing the recruitment of Runx2 to the promoter region of its target genes. In vivo analysis of BMP2-induced ectopic bone formation revealed that the knockdown of Lmx1b promoted osteogenic differentiation and bone regeneration. Our data demonstrate that Lmx1b negatively regulates osteoblast differentiation and function through regulation of Runx2 and provides a molecular basis for therapeutic targets for bone diseases.
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Kundu, Mondira, Sheila Compton, Lisa Garrett-Beal, Terryl Stacy, Matthew F. Starost, Michael Eckhaus, Nancy A. Speck, and P. Paul Liu. "Runx1 deficiency predisposes mice to T-lymphoblastic lymphoma." Blood 106, no. 10 (November 15, 2005): 3621–24. http://dx.doi.org/10.1182/blood-2005-04-1447.

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Abstract Chromosomal rearrangements affecting RUNX1 and CBFB are common in acute leukemias. These mutations result in the expression of fusion proteins that act dominant-negatively to suppress the normal function of the Runt-related transcription factor 1 (RUNX)/core binding factor β (CBFβ) complexes. In addition, loss-of-function mutations in Runt-related transcription factor 1 (RUNX1) have been identified in sporadic cases of acute myeloid leukemia (AML) and in association with the familial platelet disorder with propensity to develop AML (FPD/AML). In order to examine the hypothesis that decreased gene dosage of RUNX1 may be a critical event in the development of leukemia, we treated chimeric mice generated from Runx1lacZ/lacZ embryonic stem (ES) cells that have homozygous disruption of the Runx1 gene with N-ethyl-N-nitrosourea (ENU). We observed an increased incidence of T-lymphoblastic lymphoma in Runx1lacZ/lacZ compared with wild-type chimeras and confirmed that the tumors were of ES-cell origin. Our results therefore suggest that deficiency of Runx1 can indeed predispose mice to hematopoietic malignancies.
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41

Liu, Jing, Eun-Sil Park, and Misung Jo. "Runt-Related Transcription Factor 1 Regulates Luteinized Hormone-Induced Prostaglandin-Endoperoxide Synthase 2 Expression in Rat Periovulatory Granulosa Cells." Endocrinology 150, no. 7 (April 2, 2009): 3291–300. http://dx.doi.org/10.1210/en.2008-1527.

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Runt-related transcription factor 1 (RUNX1), a transcription factor, is transiently induced by the LH surge and regulates gene expression in periovulatory granulosa cells. Potential binding sites for RUNX are present in the 5′-flanking region of the Ptgs2 (prostaglandin-endoperoxide synthase 2) gene. Periovulatory Ptgs2 expression is essential for ovulation. In the present study, we investigated the role of RUNX1 in mediating the LH-induced expression of Ptgs2 in periovulatory granulosa cells. We first determined whether the suppression of Runx1 expression or activity affects Ptgs2 expression using cultured preovulatory granulosa cells isolated from immature rat ovaries primed with pregnant mare serum gonadotropin for 48 h. Knockdown of human chorionic gonadotropin-induced Runx1 expression by small interfering RNA or inhibition of endogenous RUNX activities by dominant-negative RUNX decreased human chorionic gonadotropin or agonist-stimulated Ptgs2 expression and transcriptional activity of Ptgs2 promoter reporter constructs. Results from chromatin immunoprecipitation assays revealed in vivo binding of endogenous RUNX1 to the Ptgs2 promoter region in rat periovulatory granulosa cells. Direct binding of RUNX1 to two RUNX-binding motifs in the Ptgs2 promoter region was confirmed by EMSA. The mutation of these two binding motifs resulted in decreased transcriptional activity of Ptgs2 promoter reporter constructs in preovulatory granulosa cells. Taken together, these findings provide experimental evidence that the LH-dependent induction of Ptgs2 expression results, in part, from RUNX1-mediated transactivation of the Ptgs2 promoter. The results of the present study assign potential significance for LH-induced RUNX1 in the ovulatory process via regulating Ptgs2 gene expression.
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42

Costa, Max, Yusha Zhu, and Angelica Ortiz. "Wrong place, wrong time: Runt-related transcription factor 2/SATB2 pathway in bone development and carcinogenesis." Journal of Carcinogenesis 20, no. 1 (2021): 2. http://dx.doi.org/10.4103/jcar.jcar_22_20.

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43

Kaptan, E., S. Sancar Bas, A. Sancakli, H. Gumushan Aktas, and S. Bolkent. "Runt-related transcription factor 2 (Runx2) is responsible for galectin-3 overexpression in human thyroid carcinoma." European Journal of Cancer 61 (July 2016): S87. http://dx.doi.org/10.1016/s0959-8049(16)61305-9.

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Sun, Shan-Shan, Lun Zhang, Jingxuan Yang, and Xuan Zhou. "Role of runt-related transcription factor 2 in signal network of tumors as an inter-mediator." Cancer Letters 361, no. 1 (May 2015): 1–7. http://dx.doi.org/10.1016/j.canlet.2015.02.042.

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Kaptan, Engin, Serap Sancar Bas, Aylin Sancakli, Hatice Gumushan Aktas, Bertan Boran Bayrak, Refiye Yanardag, and Sehnaz Bolkent. "Runt‐Related Transcription Factor 2 (Runx2) Is Responsible for Galectin‐3 Overexpression in Human Thyroid Carcinoma." Journal of Cellular Biochemistry 118, no. 11 (May 23, 2017): 3911–19. http://dx.doi.org/10.1002/jcb.26043.

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46

Songdej, Natthapol, and A. Koneti Rao. "Hematopoietic transcription factor mutations: important players in inherited platelet defects." Blood 129, no. 21 (May 25, 2017): 2873–81. http://dx.doi.org/10.1182/blood-2016-11-709881.

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Abstract Transcription factors (TFs) are proteins that bind to specific DNA sequences and regulate expression of genes. The molecular and genetic mechanisms in most patients with inherited platelet defects are unknown. There is now increasing evidence that mutations in hematopoietic TFs are an important underlying cause for defects in platelet production, morphology, and function. The hematopoietic TFs implicated in patients with impaired platelet function and number include runt-related transcription factor 1, Fli-1 proto-oncogene, E-twenty-six (ETS) transcription factor (friend leukemia integration 1), GATA-binding protein 1, growth factor independent 1B transcriptional repressor, ETS variant 6, ecotropic viral integration site 1, and homeobox A11. These TFs act in a combinatorial manner to bind sequence-specific DNA within promoter regions to regulate lineage-specific gene expression, either as activators or repressors. TF mutations induce rippling downstream effects by simultaneously altering the expression of multiple genes. Mutations involving these TFs affect diverse aspects of megakaryocyte biology, and platelet production and function, culminating in thrombocytopenia and platelet dysfunction. Some are associated with predisposition to hematologic malignancies. These TF variants may occur more frequently in patients with inherited platelet defects than generally appreciated. This review focuses on alterations in hematopoietic TFs in the pathobiology of inherited platelet defects.
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Amarasekara, Dulshara Sachini, Sumi Kim, and Jaerang Rho. "Regulation of Osteoblast Differentiation by Cytokine Networks." International Journal of Molecular Sciences 22, no. 6 (March 11, 2021): 2851. http://dx.doi.org/10.3390/ijms22062851.

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Osteoblasts, which are bone-forming cells, play pivotal roles in bone modeling and remodeling. Osteoblast differentiation, also known as osteoblastogenesis, is orchestrated by transcription factors, such as runt-related transcription factor 1/2, osterix, activating transcription factor 4, special AT-rich sequence-binding protein 2 and activator protein-1. Osteoblastogenesis is regulated by a network of cytokines under physiological and pathophysiological conditions. Osteoblastogenic cytokines, such as interleukin-10 (IL-10), IL-11, IL-18, interferon-γ (IFN-γ), cardiotrophin-1 and oncostatin M, promote osteoblastogenesis, whereas anti-osteoblastogenic cytokines, such as tumor necrosis factor-α (TNF-α), TNF-β, IL-1α, IL-4, IL-7, IL-12, IL-13, IL-23, IFN-α, IFN-β, leukemia inhibitory factor, cardiotrophin-like cytokine, and ciliary neurotrophic factor, downregulate osteoblastogenesis. Although there are gaps in the body of knowledge regarding the interplay of cytokine networks in osteoblastogenesis, cytokines appear to be potential therapeutic targets in bone-related diseases. Thus, in this study, we review and discuss our osteoblast, osteoblast differentiation, osteoblastogenesis, cytokines, signaling pathway of cytokine networks in osteoblastogenesis.
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Nakao, Mitsushige, Shigeo Horiike, Yoko Fukushima-Nakase, Motohiro Nishimura, Yasuko Fujita, Masafumi Taniwaki, and Tsukasa Okuda. "Novel loss-of-function mutations of the haematopoiesis-related transcription factor, acute myeloid leukaemia 1/runt-related transcription factor 1, detected in acute myeloblastic leukaemia and myelodysplastic syndrome." British Journal of Haematology 125, no. 6 (April 27, 2004): 709–19. http://dx.doi.org/10.1111/j.1365-2141.2004.04966.x.

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Hirai, Hideyo, Igor M. Samokhvalov, Tetsuhiro Fujimoto, Satomi Nishikawa, Jiro Imanishi, and Shin-Ichi Nishikawa. "Involvement of Runx1 in the down-regulation of fetal liver kinase-1 expression during transition of endothelial cells to hematopoietic cells." Blood 106, no. 6 (September 15, 2005): 1948–55. http://dx.doi.org/10.1182/blood-2004-12-4872.

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Abstract During early mouse embryogenesis, fetal liver kinase-1 (Flk-1), a receptor for vascular endothelial growth factor, and Runx1, a runt domain transcription factor, have prerequisite roles in the generation of hematopoietic lineages. Flk-1 expression is maintained in successive stages from mesodermal to endothelial cells and is down-regulated in nascent hematopoietic cells, whereas Runx1 (Runt-related transcription factor 1) is expressed in embryonic sites of hematopoietic cell de novo generation and in practically all hematopoietic organs. Here we show that Runx1 represses Flk-1 during the development of hemogenic endothelial cells into hematopoietic cells. We established embryonic stem cell clones carrying the Venus gene, a modified version of yellow fluorescence protein, in the Runx1 locus and cultured them on OP9 cells. Flk-1+ cells appeared on day 3.5, and Runx1+ cells first appeared from the Flk-1+ fraction on day 4.5. The Flk-1+Runx1+ cells rapidly stopped expressing Flk-1 with further incubation and eventually gave rise to CD45+ or TER119+ cells. Runx1 repressed Flk-1 promoter transcriptional activity in an endothelial cell line, and this repression required intact DNA-binding and transactivating domains of Runx1 protein. The repressor activity of Runx1 endogenous Flk-1 was also confirmed overexpressing Runx1 in embryonic stem cell differentiation cultures. These results provide novel insight into the role Runx1 during the development of hematopoietic cell lineages.
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Yao, Fuli, Licheng Yin, shiyu Feng, Xinyan Wang, Anying Zhang, and Hong Zhou. "Functional characterization of grass carp runt-related transcription factor 3: Involvement in TGF-β1-mediated c-Myc transcription in fish cells." Fish & Shellfish Immunology 82 (November 2018): 130–35. http://dx.doi.org/10.1016/j.fsi.2018.08.018.

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