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Showing 1 to 12 of 993 entries
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The role of GLI1 for 5-Fu resistance in colorectal cancer.

Cell & bioscience

Zhang L, Song R, Gu D, Zhang X, Yu B, Liu B, Xie J.
PMID: 28413604
Cell Biosci. 2017 Apr 13;7:17. doi: 10.1186/s13578-017-0145-7. eCollection 2017.

Colorectal cancer is a leading cause of cancer-related mortality worldwide, with Fluorouracil (5-FU)-based chemotherapy as the major treatment for advanced disease. Many patients with advanced colorectal cancer eventually succumb to the disease despite some patients responded initially to chemotherapy....

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Zhang L, Song R, Gu D, et al. The role of GLI1 for 5-Fu resistance in colorectal cancer. Cell Biosci. 2017;7:17doi: 10.1186/s13578-017-0145-7.
Zhang, L., Song, R., Gu, D., Zhang, X., Yu, B., Liu, B., & Xie, J. (2017). The role of GLI1 for 5-Fu resistance in colorectal cancer. Cell & bioscience, 717. https://doi.org/10.1186/s13578-017-0145-7
Zhang, Lining, et al. "The role of GLI1 for 5-Fu resistance in colorectal cancer." Cell & bioscience vol. 7 (2017): 17. doi: https://doi.org/10.1186/s13578-017-0145-7
Zhang L, Song R, Gu D, Zhang X, Yu B, Liu B, Xie J. The role of GLI1 for 5-Fu resistance in colorectal cancer. Cell Biosci. 2017 Apr 13;7:17. doi: 10.1186/s13578-017-0145-7. eCollection 2017. PMID: 28413604; PMCID: PMC5390459.
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Brothers in arms: emerging roles of RNA epigenetics in DNA damage repair.

Cell & bioscience

Zhang J.
PMID: 28484591
Cell Biosci. 2017 May 04;7:24. doi: 10.1186/s13578-017-0151-9. eCollection 2017.

N6-methyladenosine (m

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Zhang J. Brothers in arms: emerging roles of RNA epigenetics in DNA damage repair. Cell Biosci. 2017;7:24doi: 10.1186/s13578-017-0151-9.
Zhang, J. (2017). Brothers in arms: emerging roles of RNA epigenetics in DNA damage repair. Cell & bioscience, 724. https://doi.org/10.1186/s13578-017-0151-9
Zhang, Jinwei. "Brothers in arms: emerging roles of RNA epigenetics in DNA damage repair." Cell & bioscience vol. 7 (2017): 24. doi: https://doi.org/10.1186/s13578-017-0151-9
Zhang J. Brothers in arms: emerging roles of RNA epigenetics in DNA damage repair. Cell Biosci. 2017 May 04;7:24. doi: 10.1186/s13578-017-0151-9. eCollection 2017. PMID: 28484591; PMCID: PMC5418772.
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A physical association between the human mutY homolog (hMYH) and DNA topoisomerase II-binding protein 1 (hTopBP1) regulates Chk1-induced cell cycle arrest in HEK293 cells.

Cell & bioscience

Han SH, Hahm SH, Tran AH, Chung JH, Hong MK, Paik HD, Kim KS, Han YS.
PMID: 26312135
Cell Biosci. 2015 Aug 27;5:50. doi: 10.1186/s13578-015-0042-x. eCollection 2015.

BACKGROUND: Human DNA topoisomerase II-binding protein 1 (hTopBP1) plays an important role in DNA replication and the DNA damage checkpoint pathway. The human mutY homolog (hMYH) is a base excision repair DNA glycosylase that excises adenines or 2-hydroxyadenines that...

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Han SH, Hahm SH, Tran AH, et al. A physical association between the human mutY homolog (hMYH) and DNA topoisomerase II-binding protein 1 (hTopBP1) regulates Chk1-induced cell cycle arrest in HEK293 cells. Cell Biosci. 2015;5:50doi: 10.1186/s13578-015-0042-x.
Han, S. H., Hahm, S. H., Tran, A. H., Chung, J. H., Hong, M. K., Paik, H. D., Kim, K. S., & Han, Y. S. (2015). A physical association between the human mutY homolog (hMYH) and DNA topoisomerase II-binding protein 1 (hTopBP1) regulates Chk1-induced cell cycle arrest in HEK293 cells. Cell & bioscience, 550. https://doi.org/10.1186/s13578-015-0042-x
Han, Se Hee, et al. "A physical association between the human mutY homolog (hMYH) and DNA topoisomerase II-binding protein 1 (hTopBP1) regulates Chk1-induced cell cycle arrest in HEK293 cells." Cell & bioscience vol. 5 (2015): 50. doi: https://doi.org/10.1186/s13578-015-0042-x
Han SH, Hahm SH, Tran AH, Chung JH, Hong MK, Paik HD, Kim KS, Han YS. A physical association between the human mutY homolog (hMYH) and DNA topoisomerase II-binding protein 1 (hTopBP1) regulates Chk1-induced cell cycle arrest in HEK293 cells. Cell Biosci. 2015 Aug 27;5:50. doi: 10.1186/s13578-015-0042-x. eCollection 2015. PMID: 26312135; PMCID: PMC4550056.
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Vemurafenib-resistant BRAF selects alternative branch points different from its wild-type BRAF in intron 8 for RNA splicing.

Cell & bioscience

Ajiro M, Zheng ZM.
PMID: 26697165
Cell Biosci. 2015 Dec 21;5:70. doi: 10.1186/s13578-015-0061-7. eCollection 2015.

One mechanism of resistance of the melanoma-associated BRAF kinase to its small molecule inhibitor vemurafenib is by point mutations in its intron 8 resulting in exons 4-8 skipping. In this report, we carried out in vitro BRAF RNA splicing...

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Ajiro M, Zheng ZM. Vemurafenib-resistant BRAF selects alternative branch points different from its wild-type BRAF in intron 8 for RNA splicing. Cell Biosci. 2015;5:70doi: 10.1186/s13578-015-0061-7.
Ajiro, M., & Zheng, Z. M. (2015). Vemurafenib-resistant BRAF selects alternative branch points different from its wild-type BRAF in intron 8 for RNA splicing. Cell & bioscience, 570. https://doi.org/10.1186/s13578-015-0061-7
Ajiro, Masahiko, and Zheng, Zhi-Ming. "Vemurafenib-resistant BRAF selects alternative branch points different from its wild-type BRAF in intron 8 for RNA splicing." Cell & bioscience vol. 5 (2015): 70. doi: https://doi.org/10.1186/s13578-015-0061-7
Ajiro M, Zheng ZM. Vemurafenib-resistant BRAF selects alternative branch points different from its wild-type BRAF in intron 8 for RNA splicing. Cell Biosci. 2015 Dec 21;5:70. doi: 10.1186/s13578-015-0061-7. eCollection 2015. PMID: 26697165; PMCID: PMC4687071.
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Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences.

Cell & bioscience

Park O, Ki SH, Xu M, Wang H, Feng D, Tam J, Osei-Hyiaman D, Kunos G, Gao B.
PMID: 26064446
Cell Biosci. 2015 May 30;5:25. doi: 10.1186/s13578-015-0015-0. eCollection 2015.

BACKGROUND: Interleukin-22 (IL-22), a cytokine with important functions in anti-microbial defense and tissue repair, has been recently suggested to have beneficial effects in obesity and metabolic syndrome in some but not in other studies. Here, we re-examined the effects...

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Park O, Ki SH, Xu M, et al. Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences. Cell Biosci. 2015;5:25doi: 10.1186/s13578-015-0015-0.
Park, O., Ki, S. H., Xu, M., Wang, H., Feng, D., Tam, J., Osei-Hyiaman, D., Kunos, G., & Gao, B. (2015). Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences. Cell & bioscience, 525. https://doi.org/10.1186/s13578-015-0015-0
Park, Ogyi, et al. "Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences." Cell & bioscience vol. 5 (2015): 25. doi: https://doi.org/10.1186/s13578-015-0015-0
Park O, Ki SH, Xu M, Wang H, Feng D, Tam J, Osei-Hyiaman D, Kunos G, Gao B. Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences. Cell Biosci. 2015 May 30;5:25. doi: 10.1186/s13578-015-0015-0. eCollection 2015. PMID: 26064446; PMCID: PMC4462081.
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Studies of genetic variability of the hepatocyte nuclear factor-1α gene in an Indian maturity-onset diabetes of the young family.

Cell & bioscience

Yang J, Jiang F, Guo H, Soniya T, Yan CX, Tian ZF, Shi BY.
PMID: 27148439
Cell Biosci. 2016 May 04;6:29. doi: 10.1186/s13578-016-0095-5. eCollection 2016.

Maturity-onset diabetes of the young (MODY), one of the specific types of diabetes mellitus, is a monogenetic disorder characterized by an autosomal dominant (AD) inheritance and β-cell dysfunction. To study an Indian family with clinical diagnosis of MODY and...

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Yang J, Jiang F, Guo H, et al. Studies of genetic variability of the hepatocyte nuclear factor-1α gene in an Indian maturity-onset diabetes of the young family. Cell Biosci. 2016;6:29doi: 10.1186/s13578-016-0095-5.
Yang, J., Jiang, F., Guo, H., Soniya, T., Yan, C. X., Tian, Z. F., & Shi, B. Y. (2016). Studies of genetic variability of the hepatocyte nuclear factor-1α gene in an Indian maturity-onset diabetes of the young family. Cell & bioscience, 629. https://doi.org/10.1186/s13578-016-0095-5
Yang, Jing, et al. "Studies of genetic variability of the hepatocyte nuclear factor-1α gene in an Indian maturity-onset diabetes of the young family." Cell & bioscience vol. 6 (2016): 29. doi: https://doi.org/10.1186/s13578-016-0095-5
Yang J, Jiang F, Guo H, Soniya T, Yan CX, Tian ZF, Shi BY. Studies of genetic variability of the hepatocyte nuclear factor-1α gene in an Indian maturity-onset diabetes of the young family. Cell Biosci. 2016 May 04;6:29. doi: 10.1186/s13578-016-0095-5. eCollection 2016. PMID: 27148439; PMCID: PMC4855895.
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Phosphorylation of LSD1 by PLK1 promotes its chromatin release during mitosis.

Cell & bioscience

Peng B, Shi R, Jiang W, Ding YH, Dong MQ, Zhu WG, Xu X.
PMID: 28344766
Cell Biosci. 2017 Mar 23;7:15. doi: 10.1186/s13578-017-0142-x. eCollection 2017.

BACKGROUND: Lysine-specific histone demethylase 1 (LSD1) modulates chromatin status through demethylation of H3K4 and H3K9. It has been demonstrated that LSD1 is hyperphosphorylated and dissociates from chromatin during mitosis. However, the molecular mechanism of LSD1 detachment is unknown.RESULTS: In...

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Peng B, Shi R, Jiang W, et al. Phosphorylation of LSD1 by PLK1 promotes its chromatin release during mitosis. Cell Biosci. 2017;7:15doi: 10.1186/s13578-017-0142-x.
Peng, B., Shi, R., Jiang, W., Ding, Y. H., Dong, M. Q., Zhu, W. G., & Xu, X. (2017). Phosphorylation of LSD1 by PLK1 promotes its chromatin release during mitosis. Cell & bioscience, 715. https://doi.org/10.1186/s13578-017-0142-x
Peng, Bin, et al. "Phosphorylation of LSD1 by PLK1 promotes its chromatin release during mitosis." Cell & bioscience vol. 7 (2017): 15. doi: https://doi.org/10.1186/s13578-017-0142-x
Peng B, Shi R, Jiang W, Ding YH, Dong MQ, Zhu WG, Xu X. Phosphorylation of LSD1 by PLK1 promotes its chromatin release during mitosis. Cell Biosci. 2017 Mar 23;7:15. doi: 10.1186/s13578-017-0142-x. eCollection 2017. PMID: 28344766; PMCID: PMC5364692.
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Subcellular fractionation method to study endosomal trafficking of Kaposi's sarcoma-associated herpesvirus.

Cell & bioscience

Walker LR, Hussein HA, Akula SM.
PMID: 26779333
Cell Biosci. 2016 Jan 15;6:1. doi: 10.1186/s13578-015-0066-2. eCollection 2016.

BACKGROUND: Virus entry involves multiple steps and is a highly orchestrated process on which successful infection collectively depends. Entry processes are commonly analyzed by monitoring internalized virus particles via Western blotting, polymerase chain reaction, and imaging techniques that allow...

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Walker LR, Hussein HA, Akula SM. Subcellular fractionation method to study endosomal trafficking of Kaposi's sarcoma-associated herpesvirus. Cell Biosci. 2016;6:1doi: 10.1186/s13578-015-0066-2.
Walker, L. R., Hussein, H. A., & Akula, S. M. (2016). Subcellular fractionation method to study endosomal trafficking of Kaposi's sarcoma-associated herpesvirus. Cell & bioscience, 61. https://doi.org/10.1186/s13578-015-0066-2
Walker, Lia R, et al. "Subcellular fractionation method to study endosomal trafficking of Kaposi's sarcoma-associated herpesvirus." Cell & bioscience vol. 6 (2016): 1. doi: https://doi.org/10.1186/s13578-015-0066-2
Walker LR, Hussein HA, Akula SM. Subcellular fractionation method to study endosomal trafficking of Kaposi's sarcoma-associated herpesvirus. Cell Biosci. 2016 Jan 15;6:1. doi: 10.1186/s13578-015-0066-2. eCollection 2016. PMID: 26779333; PMCID: PMC4714431.
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SIRT1 inhibits adipogenesis and promotes myogenic differentiation in C3H10T1/2 pluripotent cells by regulating Wnt signaling.

Cell & bioscience

Zhou Y, Zhou Z, Zhang W, Hu X, Wei H, Peng J, Jiang S.
PMID: 26568817
Cell Biosci. 2015 Nov 12;5:61. doi: 10.1186/s13578-015-0055-5. eCollection 2015.

BACKGROUND: The directed differentiation of mesenchymal stem cells (MSCs) is tightly controlled by a complex network. Wnt signaling pathways have an important function in controlling the fate of MSCs. However, the mechanism through which Wnt/β-catenin signaling is regulated in...

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Zhou Y, Zhou Z, Zhang W, et al. SIRT1 inhibits adipogenesis and promotes myogenic differentiation in C3H10T1/2 pluripotent cells by regulating Wnt signaling. Cell Biosci. 2015;5:61doi: 10.1186/s13578-015-0055-5.
Zhou, Y., Zhou, Z., Zhang, W., Hu, X., Wei, H., Peng, J., & Jiang, S. (2015). SIRT1 inhibits adipogenesis and promotes myogenic differentiation in C3H10T1/2 pluripotent cells by regulating Wnt signaling. Cell & bioscience, 561. https://doi.org/10.1186/s13578-015-0055-5
Zhou, Yuanfei, et al. "SIRT1 inhibits adipogenesis and promotes myogenic differentiation in C3H10T1/2 pluripotent cells by regulating Wnt signaling." Cell & bioscience vol. 5 (2015): 61. doi: https://doi.org/10.1186/s13578-015-0055-5
Zhou Y, Zhou Z, Zhang W, Hu X, Wei H, Peng J, Jiang S. SIRT1 inhibits adipogenesis and promotes myogenic differentiation in C3H10T1/2 pluripotent cells by regulating Wnt signaling. Cell Biosci. 2015 Nov 12;5:61. doi: 10.1186/s13578-015-0055-5. eCollection 2015. PMID: 26568817; PMCID: PMC4643498.
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"Slow" skeletal muscles across vertebrate species.

Cell & bioscience

Luna VM, Daikoku E, Ono F.
PMID: 26568818
Cell Biosci. 2015 Nov 14;5:62. doi: 10.1186/s13578-015-0054-6. eCollection 2015.

Skeletal muscle fibers are generally classified into two groups: slow (type I) and fast (type II). Fibers in each group are uniquely designed for specific locomotory needs based on their intrinsic cellular properties and the types of motor neurons...

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Luna VM, Daikoku E, Ono F. "Slow" skeletal muscles across vertebrate species. Cell Biosci. 2015;5:62doi: 10.1186/s13578-015-0054-6.
Luna, V. M., Daikoku, E., & Ono, F. (2015). "Slow" skeletal muscles across vertebrate species. Cell & bioscience, 562. https://doi.org/10.1186/s13578-015-0054-6
Luna, Victor M, et al. ""Slow" skeletal muscles across vertebrate species." Cell & bioscience vol. 5 (2015): 62. doi: https://doi.org/10.1186/s13578-015-0054-6
Luna VM, Daikoku E, Ono F. "Slow" skeletal muscles across vertebrate species. Cell Biosci. 2015 Nov 14;5:62. doi: 10.1186/s13578-015-0054-6. eCollection 2015. PMID: 26568818; PMCID: PMC4644285.
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A review on hepatocyte nuclear factor-1beta and tumor.

Cell & bioscience

Yu DD, Guo SW, Jing YY, Dong YL, Wei LX.
PMID: 26464794
Cell Biosci. 2015 Oct 13;5:58. doi: 10.1186/s13578-015-0049-3. eCollection 2015.

Hepatocyte nuclear factor-1beta (HNF1β) was initially identified as a liver-specific transcription factor. It is a homeobox transcription factor that functions as a homodimer or heterodimer with HNF1α. HNF1β plays an important role in organogenesis during embryonic stage, especially of...

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Yu DD, Guo SW, Jing YY, et al. A review on hepatocyte nuclear factor-1beta and tumor. Cell Biosci. 2015;5:58doi: 10.1186/s13578-015-0049-3.
Yu, D. D., Guo, S. W., Jing, Y. Y., Dong, Y. L., & Wei, L. X. (2015). A review on hepatocyte nuclear factor-1beta and tumor. Cell & bioscience, 558. https://doi.org/10.1186/s13578-015-0049-3
Yu, Dan-Dan, et al. "A review on hepatocyte nuclear factor-1beta and tumor." Cell & bioscience vol. 5 (2015): 58. doi: https://doi.org/10.1186/s13578-015-0049-3
Yu DD, Guo SW, Jing YY, Dong YL, Wei LX. A review on hepatocyte nuclear factor-1beta and tumor. Cell Biosci. 2015 Oct 13;5:58. doi: 10.1186/s13578-015-0049-3. eCollection 2015. PMID: 26464794; PMCID: PMC4603907.
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Epigenetic regulation in cancer progression.

Cell & bioscience

Baxter E, Windloch K, Gannon F, Lee JS.
PMID: 25949794
Cell Biosci. 2014 Aug 19;4:45. doi: 10.1186/2045-3701-4-45. eCollection 2014.

Cancer is a disease arising from both genetic and epigenetic modifications of DNA that contribute to changes in gene expression in the cell. Genetic modifications include loss or amplification of DNA, loss of heterozygosity (LOH) as well as gene...

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Baxter E, Windloch K, Gannon F, et al. Epigenetic regulation in cancer progression. Cell Biosci. 2014;4:45doi: 10.1186/2045-3701-4-45.
Baxter, E., Windloch, K., Gannon, F., & Lee, J. S. (2014). Epigenetic regulation in cancer progression. Cell & bioscience, 445. https://doi.org/10.1186/2045-3701-4-45
Baxter, Eva, et al. "Epigenetic regulation in cancer progression." Cell & bioscience vol. 4 (2014): 45. doi: https://doi.org/10.1186/2045-3701-4-45
Baxter E, Windloch K, Gannon F, Lee JS. Epigenetic regulation in cancer progression. Cell Biosci. 2014 Aug 19;4:45. doi: 10.1186/2045-3701-4-45. eCollection 2014. PMID: 25949794; PMCID: PMC4422217.
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Showing 1 to 12 of 993 entries