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Showing 1 to 12 of 48 entries
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Chemically induced degradation of CDK9 by a proteolysis targeting chimera (PROTAC).

Chemical communications (Cambridge, England)

Robb CM, Contreras JI, Kour S, Taylor MA, Abid M, Sonawane YA, Zahid M, Murry DJ, Natarajan A, Rana S.
PMID: 28636052
Chem Commun (Camb). 2017 Jul 04;53(54):7577-7580. doi: 10.1039/c7cc03879h.

Cyclin-dependent kinase 9 (CDK9), a member of the cyclin-dependent protein kinase (CDK) family, is involved in transcriptional elongation of several target genes. CDK9 is ubiquitously expressed and has been shown to contribute to a variety of malignancies such as...

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Robb CM, Contreras JI, Kour S, et al. Chemically induced degradation of CDK9 by a proteolysis targeting chimera (PROTAC). Chem Commun (Camb). 2017;53(54):7577-7580doi: 10.1039/c7cc03879h.
Robb, C. M., Contreras, J. I., Kour, S., Taylor, M. A., Abid, M., Sonawane, Y. A., Zahid, M., Murry, D. J., Natarajan, A., & Rana, S. (2017). Chemically induced degradation of CDK9 by a proteolysis targeting chimera (PROTAC). Chemical communications (Cambridge, England), 53(54), 7577-7580. https://doi.org/10.1039/c7cc03879h
Robb, Caroline M, et al. "Chemically induced degradation of CDK9 by a proteolysis targeting chimera (PROTAC)." Chemical communications (Cambridge, England) vol. 53,54 (2017): 7577-7580. doi: https://doi.org/10.1039/c7cc03879h
Robb CM, Contreras JI, Kour S, Taylor MA, Abid M, Sonawane YA, Zahid M, Murry DJ, Natarajan A, Rana S. Chemically induced degradation of CDK9 by a proteolysis targeting chimera (PROTAC). Chem Commun (Camb). 2017 Jul 04;53(54):7577-7580. doi: 10.1039/c7cc03879h. PMID: 28636052; PMCID: PMC5555382.
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P-TEFb goes viral.

Inside the cell

Zaborowska J, Isa NF, Murphy S.
PMID: 27398404
Inside Cell. 2016 Apr;1(2):106-116. doi: 10.1002/icl3.1037. Epub 2015 Nov 25.

Positive transcription elongation factor b (P-TEFb), which comprises cyclin-dependent kinase 9 (CDK9) kinase and cyclin T subunits, is an essential kinase complex in human cells. Phosphorylation of the negative elongation factors by P-TEFb is required for productive elongation of...

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Zaborowska J, Isa NF, Murphy S. P-TEFb goes viral. Inside Cell. 2015;1(2):106-116doi: 10.1002/icl3.1037.
Zaborowska, J., Isa, N. F., & Murphy, S. (2016). P-TEFb goes viral. Inside the cell, 1(2), 106-116. https://doi.org/10.1002/icl3.1037
Zaborowska, Justyna, et al. "P-TEFb goes viral." Inside the cell vol. 1,2 (2016): 106-116. doi: https://doi.org/10.1002/icl3.1037
Zaborowska J, Isa NF, Murphy S. P-TEFb goes viral. Inside Cell. 2016 Apr;1(2):106-116. doi: 10.1002/icl3.1037. Epub 2015 Nov 25. PMID: 27398404; PMCID: PMC4863834.
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Positive cyclin T expression as a favorable prognostic factor in treating gastric gastrointestinal stromal tumors.

Molecular and clinical oncology

Lin LF, Jin JS, Chen JC, Huang CC, Sheu JH, Chen W, Tsao TY, Hsu CW.
PMID: 27284431
Mol Clin Oncol. 2016 Jun;4(6):971-975. doi: 10.3892/mco.2016.835. Epub 2016 Mar 30.

Positive transcriptional elongation factor b (P-TEFb) contains the catalytic subunit cyclin-dependent kinase 9 (Cdk9) and the regulatory subunit cyclin T. Cyclin T1 and Cdk9 are the key factors of the PTEFb pathways and are overexpressed in the human head...

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Lin LF, Jin JS, Chen JC, et al. Positive cyclin T expression as a favorable prognostic factor in treating gastric gastrointestinal stromal tumors. Mol Clin Oncol. 2016;4(6):971-975doi: 10.3892/mco.2016.835.
Lin, L. F., Jin, J. S., Chen, J. C., Huang, C. C., Sheu, J. H., Chen, W., Tsao, T. Y., & Hsu, C. W. (2016). Positive cyclin T expression as a favorable prognostic factor in treating gastric gastrointestinal stromal tumors. Molecular and clinical oncology, 4(6), 971-975. https://doi.org/10.3892/mco.2016.835
Lin, Lien-Fu, et al. "Positive cyclin T expression as a favorable prognostic factor in treating gastric gastrointestinal stromal tumors." Molecular and clinical oncology vol. 4,6 (2016): 971-975. doi: https://doi.org/10.3892/mco.2016.835
Lin LF, Jin JS, Chen JC, Huang CC, Sheu JH, Chen W, Tsao TY, Hsu CW. Positive cyclin T expression as a favorable prognostic factor in treating gastric gastrointestinal stromal tumors. Mol Clin Oncol. 2016 Jun;4(6):971-975. doi: 10.3892/mco.2016.835. Epub 2016 Mar 30. PMID: 27284431; PMCID: PMC4887899.
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Antineoplastic effects of selective CDK9 inhibition with atuveciclib on cancer stem-like cells in triple-negative breast cancer.

Oncotarget

Brisard D, Eckerdt F, Marsh LA, Blyth GT, Jain S, Cristofanilli M, Horiuchi D, Platanias LC.
PMID: 30647871
Oncotarget. 2018 Dec 18;9(99):37305-37318. doi: 10.18632/oncotarget.26468. eCollection 2018 Dec 18.

Treatment options for triple-negative breast cancer (TNBC) are limited due to the lack of efficient targeted therapies, frequently resulting in recurrence and metastatic disease. Accumulating evidence suggests that a small population of cancer stem-like cells (CSLCs) is responsible for...

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Brisard D, Eckerdt F, Marsh LA, et al. Antineoplastic effects of selective CDK9 inhibition with atuveciclib on cancer stem-like cells in triple-negative breast cancer. Oncotarget. 2018;9(99):37305-37318doi: 10.18632/oncotarget.26468.
Brisard, D., Eckerdt, F., Marsh, L. A., Blyth, G. T., Jain, S., Cristofanilli, M., Horiuchi, D., & Platanias, L. C. (2018). Antineoplastic effects of selective CDK9 inhibition with atuveciclib on cancer stem-like cells in triple-negative breast cancer. Oncotarget, 9(99), 37305-37318. https://doi.org/10.18632/oncotarget.26468
Brisard, Daphne, et al. "Antineoplastic effects of selective CDK9 inhibition with atuveciclib on cancer stem-like cells in triple-negative breast cancer." Oncotarget vol. 9,99 (2018): 37305-37318. doi: https://doi.org/10.18632/oncotarget.26468
Brisard D, Eckerdt F, Marsh LA, Blyth GT, Jain S, Cristofanilli M, Horiuchi D, Platanias LC. Antineoplastic effects of selective CDK9 inhibition with atuveciclib on cancer stem-like cells in triple-negative breast cancer. Oncotarget. 2018 Dec 18;9(99):37305-37318. doi: 10.18632/oncotarget.26468. eCollection 2018 Dec 18. PMID: 30647871; PMCID: PMC6324664.
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CDK9 Inhibitor Induces the Apoptosis of B-Cell Acute Lymphocytic Leukemia by Inhibiting c-Myc-Mediated Glycolytic Metabolism.

Frontiers in cell and developmental biology

Huang WL, Abudureheman T, Xia J, Chu L, Zhou H, Zheng WW, Zhou N, Shi RY, Li MH, Zhu JM, Qing K, Ji C, Liang KW, Guo S, Yin G, Duan CW.
PMID: 33748130
Front Cell Dev Biol. 2021 Mar 04;9:641271. doi: 10.3389/fcell.2021.641271. eCollection 2021.

B-cell acute lymphocytic leukemia (B-ALL), a common blood cancer in children, leads to high mortality. Cyclin-dependent kinase 9 inhibitor (CDK9i) effectively attenuates acute myeloid leukemia and chronic lymphoblastic leukemia by inducing apoptosis and inhibiting cell proliferation. However, the effect...

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Huang WL, Abudureheman T, Xia J, et al. CDK9 Inhibitor Induces the Apoptosis of B-Cell Acute Lymphocytic Leukemia by Inhibiting c-Myc-Mediated Glycolytic Metabolism. Front Cell Dev Biol. 2021;9:641271doi: 10.3389/fcell.2021.641271.
Huang, W. L., Abudureheman, T., Xia, J., Chu, L., Zhou, H., Zheng, W. W., Zhou, N., Shi, R. Y., Li, M. H., Zhu, J. M., Qing, K., Ji, C., Liang, K. W., Guo, S., Yin, G., & Duan, C. W. (2021). CDK9 Inhibitor Induces the Apoptosis of B-Cell Acute Lymphocytic Leukemia by Inhibiting c-Myc-Mediated Glycolytic Metabolism. Frontiers in cell and developmental biology, 9641271. https://doi.org/10.3389/fcell.2021.641271
Huang, Wen-Li, et al. "CDK9 Inhibitor Induces the Apoptosis of B-Cell Acute Lymphocytic Leukemia by Inhibiting c-Myc-Mediated Glycolytic Metabolism." Frontiers in cell and developmental biology vol. 9 (2021): 641271. doi: https://doi.org/10.3389/fcell.2021.641271
Huang WL, Abudureheman T, Xia J, Chu L, Zhou H, Zheng WW, Zhou N, Shi RY, Li MH, Zhu JM, Qing K, Ji C, Liang KW, Guo S, Yin G, Duan CW. CDK9 Inhibitor Induces the Apoptosis of B-Cell Acute Lymphocytic Leukemia by Inhibiting c-Myc-Mediated Glycolytic Metabolism. Front Cell Dev Biol. 2021 Mar 04;9:641271. doi: 10.3389/fcell.2021.641271. eCollection 2021. PMID: 33748130; PMCID: PMC7969802.
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Bromodomain-containing-protein-4 and cyclin-dependent-kinase-9 inhibitors interact synergistically in vitro and combined treatment reduces post-traumatic osteoarthritis severity in mice.

Osteoarthritis and cartilage

Fukui T, Yik JHN, Doyran B, Davis J, Haudenschild AK, Adamopoulos IE, Han L, Haudenschild DR.
PMID: 33164842
Osteoarthritis Cartilage. 2021 Jan;29(1):68-77. doi: 10.1016/j.joca.2020.07.012. Epub 2020 Oct 23.

OBJECTIVE: Joint injury rapidly induces expression of primary response genes (PRGs), which activate a cascade of secondary genes that destroy joint tissues and initiate post-traumatic osteoarthritis (PTOA). Bromodomain-containing-protein-4 (Brd4) and cyclin-dependent-kinase-9 (CDK9) cooperatively control the rate-limiting step of PRG...

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Fukui T, Yik JHN, Doyran B, et al. Bromodomain-containing-protein-4 and cyclin-dependent-kinase-9 inhibitors interact synergistically in vitro and combined treatment reduces post-traumatic osteoarthritis severity in mice. Osteoarthritis Cartilage. 2020;29(1):68-77doi: 10.1016/j.joca.2020.07.012.
Fukui, T., Yik, J. H. N., Doyran, B., Davis, J., Haudenschild, A. K., Adamopoulos, I. E., Han, L., & Haudenschild, D. R. (2021). Bromodomain-containing-protein-4 and cyclin-dependent-kinase-9 inhibitors interact synergistically in vitro and combined treatment reduces post-traumatic osteoarthritis severity in mice. Osteoarthritis and cartilage, 29(1), 68-77. https://doi.org/10.1016/j.joca.2020.07.012
Fukui, T, et al. "Bromodomain-containing-protein-4 and cyclin-dependent-kinase-9 inhibitors interact synergistically in vitro and combined treatment reduces post-traumatic osteoarthritis severity in mice." Osteoarthritis and cartilage vol. 29,1 (2021): 68-77. doi: https://doi.org/10.1016/j.joca.2020.07.012
Fukui T, Yik JHN, Doyran B, Davis J, Haudenschild AK, Adamopoulos IE, Han L, Haudenschild DR. Bromodomain-containing-protein-4 and cyclin-dependent-kinase-9 inhibitors interact synergistically in vitro and combined treatment reduces post-traumatic osteoarthritis severity in mice. Osteoarthritis Cartilage. 2021 Jan;29(1):68-77. doi: 10.1016/j.joca.2020.07.012. Epub 2020 Oct 23. PMID: 33164842; PMCID: PMC7785706.
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Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis.

Molecular therapy. Nucleic acids

He X, Lian Z, Yang Y, Wang Z, Fu X, Liu Y, Li M, Tian J, Yu T, Xin H.
PMID: 32916601
Mol Ther Nucleic Acids. 2020 Aug 19;22:84-98. doi: 10.1016/j.omtn.2020.08.013. Epub 2020 Aug 19.

Long non-coding RNAs (lncRNAs) play a crucial role in the growth of vascular smooth muscle cells (VSMCs), the dysfunction of which is closely associated with the initiation and progression of cardiovascular diseases (CVDs). Abnormal phenotypic switching and proliferation of...

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He X, Lian Z, Yang Y, et al. Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis. Mol Ther Nucleic Acids. 2020;22:84-98doi: 10.1016/j.omtn.2020.08.013.
He, X., Lian, Z., Yang, Y., Wang, Z., Fu, X., Liu, Y., Li, M., Tian, J., Yu, T., & Xin, H. (2020). Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis. Molecular therapy. Nucleic acids, 2284-98. https://doi.org/10.1016/j.omtn.2020.08.013
He, Xingqiang, et al. "Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis." Molecular therapy. Nucleic acids vol. 22 (2020): 84-98. doi: https://doi.org/10.1016/j.omtn.2020.08.013
He X, Lian Z, Yang Y, Wang Z, Fu X, Liu Y, Li M, Tian J, Yu T, Xin H. Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis. Mol Ther Nucleic Acids. 2020 Aug 19;22:84-98. doi: 10.1016/j.omtn.2020.08.013. Epub 2020 Aug 19. PMID: 32916601; PMCID: PMC7490454.
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Targeting cyclin-dependent kinase 9 by a novel inhibitor enhances radiosensitization and identifies Axl as a novel downstream target in esophageal adenocarcinoma.

Oncotarget

Veeranki OL, Tong Z, Dokey R, Mejia A, Zhang J, Qiao Y, Singh PK, Katkhuda R, Mino B, Tailor R, Canales JR, Bassett R, Ajani J, Wu JY, Kopetz S, Blum M, Hofstetter W, Tetzlaff M, Krishnan S, Lin SH, Maru D.
PMID: 31384397
Oncotarget. 2019 Jul 23;10(45):4703-4718. doi: 10.18632/oncotarget.27095. eCollection 2019 Jul 23.

Cyclin-dependent kinase 9 (CDK9) transcriptionally regulates several proteins and cellular pathways central to radiation induced tissue injury. We investigated a role of BAY1143572, a new highly specific CDK9 inhibitor, as a sensitizer to radiation in esophageal adenocarcinoma.

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Veeranki OL, Tong Z, Dokey R, et al. Targeting cyclin-dependent kinase 9 by a novel inhibitor enhances radiosensitization and identifies Axl as a novel downstream target in esophageal adenocarcinoma. Oncotarget. 2019;10(45):4703-4718doi: 10.18632/oncotarget.27095.
Veeranki, O. L., Tong, Z., Dokey, R., Mejia, A., Zhang, J., Qiao, Y., Singh, P. K., Katkhuda, R., Mino, B., Tailor, R., Canales, J. R., Bassett, R., Ajani, J., Wu, J. Y., Kopetz, S., Blum, M., Hofstetter, W., Tetzlaff, M., Krishnan, S., Lin, S. H., & Maru, D. (2019). Targeting cyclin-dependent kinase 9 by a novel inhibitor enhances radiosensitization and identifies Axl as a novel downstream target in esophageal adenocarcinoma. Oncotarget, 10(45), 4703-4718. https://doi.org/10.18632/oncotarget.27095
Veeranki, Omkara Lakshmi, et al. "Targeting cyclin-dependent kinase 9 by a novel inhibitor enhances radiosensitization and identifies Axl as a novel downstream target in esophageal adenocarcinoma." Oncotarget vol. 10,45 (2019): 4703-4718. doi: https://doi.org/10.18632/oncotarget.27095
Veeranki OL, Tong Z, Dokey R, Mejia A, Zhang J, Qiao Y, Singh PK, Katkhuda R, Mino B, Tailor R, Canales JR, Bassett R, Ajani J, Wu JY, Kopetz S, Blum M, Hofstetter W, Tetzlaff M, Krishnan S, Lin SH, Maru D. Targeting cyclin-dependent kinase 9 by a novel inhibitor enhances radiosensitization and identifies Axl as a novel downstream target in esophageal adenocarcinoma. Oncotarget. 2019 Jul 23;10(45):4703-4718. doi: 10.18632/oncotarget.27095. eCollection 2019 Jul 23. PMID: 31384397; PMCID: PMC6659793.
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Limited redundancy in genes regulated by Cyclin T2 and Cyclin T1.

BMC research notes

Ramakrishnan R, Yu W, Rice AP.
PMID: 21791050
BMC Res Notes. 2011 Jul 26;4:260. doi: 10.1186/1756-0500-4-260.

BACKGROUND: The elongation phase, like other steps of transcription by RNA Polymerase II, is subject to regulation. The positive transcription elongation factor b (P-TEFb) complex allows for the transition of mRNA synthesis to the productive elongation phase. P-TEFb contains...

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Ramakrishnan R, Yu W, Rice AP. Limited redundancy in genes regulated by Cyclin T2 and Cyclin T1. BMC Res Notes. 2011;4:260doi: 10.1186/1756-0500-4-260.
Ramakrishnan, R., Yu, W., & Rice, A. P. (2011). Limited redundancy in genes regulated by Cyclin T2 and Cyclin T1. BMC research notes, 4260. https://doi.org/10.1186/1756-0500-4-260
Ramakrishnan, Rajesh, et al. "Limited redundancy in genes regulated by Cyclin T2 and Cyclin T1." BMC research notes vol. 4 (2011): 260. doi: https://doi.org/10.1186/1756-0500-4-260
Ramakrishnan R, Yu W, Rice AP. Limited redundancy in genes regulated by Cyclin T2 and Cyclin T1. BMC Res Notes. 2011 Jul 26;4:260. doi: 10.1186/1756-0500-4-260. PMID: 21791050; PMCID: PMC3160394.
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Complex effects of flavopiridol on the expression of primary response genes.

Cell division

Keskin H, Garriga J, Georlette D, Graña X.
PMID: 22458775
Cell Div. 2012 Mar 29;7:11. doi: 10.1186/1747-1028-7-11.

BACKGROUND: The Positive Transcription Elongation Factor b (P-TEFb) is a complex of Cyclin Dependent Kinase 9 (CDK9) with either cyclins T1, T2 or K. The complex phosphorylates the C-Terminal Domain of RNA polymerase II (RNAPII) and negative elongation factors,...

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Keskin H, Garriga J, Georlette D, et al. Complex effects of flavopiridol on the expression of primary response genes. Cell Div. 2012;7:11doi: 10.1186/1747-1028-7-11.
Keskin, H., Garriga, J., Georlette, D., & Graña, X. (2012). Complex effects of flavopiridol on the expression of primary response genes. Cell division, 711. https://doi.org/10.1186/1747-1028-7-11
Keskin, Havva, et al. "Complex effects of flavopiridol on the expression of primary response genes." Cell division vol. 7 (2012): 11. doi: https://doi.org/10.1186/1747-1028-7-11
Keskin H, Garriga J, Georlette D, Graña X. Complex effects of flavopiridol on the expression of primary response genes. Cell Div. 2012 Mar 29;7:11. doi: 10.1186/1747-1028-7-11. PMID: 22458775; PMCID: PMC3339560.
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Cyclin-dependent kinase 9 may as a novel target in downregulating the atherosclerosis inflammation (Review).

Biomedical reports

Han Y, Zhan Y, Hou G, Li L.
PMID: 25279144
Biomed Rep. 2014 Nov;2(6):775-779. doi: 10.3892/br.2014.322. Epub 2014 Jul 31.

Inflammation is a key component of atherosclerosis. Genes coding for inflammatory or anti-inflammatory molecules are considered good candidates for estimating the risk of developing atherosclerosis. Cyclin-dependent kinase 9 (CDK9), the kinase of positive transcription elongation factor b (P-TEFb), is...

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Han Y, Zhan Y, Hou G, et al. Cyclin-dependent kinase 9 may as a novel target in downregulating the atherosclerosis inflammation (Review). Biomed Rep. 2014;2(6):775-779doi: 10.3892/br.2014.322.
Han, Y., Zhan, Y., Hou, G., & Li, L. (2014). Cyclin-dependent kinase 9 may as a novel target in downregulating the atherosclerosis inflammation (Review). Biomedical reports, 2(6), 775-779. https://doi.org/10.3892/br.2014.322
Han, Yeming, et al. "Cyclin-dependent kinase 9 may as a novel target in downregulating the atherosclerosis inflammation (Review)." Biomedical reports vol. 2,6 (2014): 775-779. doi: https://doi.org/10.3892/br.2014.322
Han Y, Zhan Y, Hou G, Li L. Cyclin-dependent kinase 9 may as a novel target in downregulating the atherosclerosis inflammation (Review). Biomed Rep. 2014 Nov;2(6):775-779. doi: 10.3892/br.2014.322. Epub 2014 Jul 31. PMID: 25279144; PMCID: PMC4179722.
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Increased cyclin T1 expression as a favorable prognostic factor in treating gastric adenocarcinoma.

Oncology letters

Jin JS, Lin LF, Chen JC, Huang CC, Sheu JH, Chen W, Tsao TY, Hsu CW.
PMID: 26788195
Oncol Lett. 2015 Dec;10(6):3712-3718. doi: 10.3892/ol.2015.3749. Epub 2015 Sep 25.

The expression of cyclin A, B1, D1 and E in gastric adenocarcinoma is known to be associated with clinical outcome. However, few studies have investigated the role of cyclin T1 and cyclin-dependent kinase 9 (CDK9) in gastric adenocarcinoma. Therefore,...

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Jin JS, Lin LF, Chen JC, et al. Increased cyclin T1 expression as a favorable prognostic factor in treating gastric adenocarcinoma. Oncol Lett. 2015;10(6):3712-3718doi: 10.3892/ol.2015.3749.
Jin, J. S., Lin, L. F., Chen, J. C., Huang, C. C., Sheu, J. H., Chen, W., Tsao, T. Y., & Hsu, C. W. (2015). Increased cyclin T1 expression as a favorable prognostic factor in treating gastric adenocarcinoma. Oncology letters, 10(6), 3712-3718. https://doi.org/10.3892/ol.2015.3749
Jin, Jong-Shiaw, et al. "Increased cyclin T1 expression as a favorable prognostic factor in treating gastric adenocarcinoma." Oncology letters vol. 10,6 (2015): 3712-3718. doi: https://doi.org/10.3892/ol.2015.3749
Jin JS, Lin LF, Chen JC, Huang CC, Sheu JH, Chen W, Tsao TY, Hsu CW. Increased cyclin T1 expression as a favorable prognostic factor in treating gastric adenocarcinoma. Oncol Lett. 2015 Dec;10(6):3712-3718. doi: 10.3892/ol.2015.3749. Epub 2015 Sep 25. PMID: 26788195; PMCID: PMC4665173.
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Showing 1 to 12 of 48 entries