Results 81 to 90 of about 20,867,404 (313)

Cell penetrating thiazole peptides inhibit c-MYC expression via site-specific targeting of c-MYC G-quadruplex

Nucleic Acids Research, 2018
The structural differences among different G-quadruplexes provide an opportunity for site-specific targeting of a particular G-quadruplex structure. However, majority of G-quadruplex ligands described thus far show little selectivity among different G ...
Debasish Dutta, M. Debnath, D. Müller, Rakesh Paul, T. Das, Irene Bessi, H. Schwalbe, Jyotirmayee Dash   +7 more
semanticscholar   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

Molecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir, Adrián López García de Lomana, Thejus B. Venkatesh, Kritika Kirty, Snaevar Sigurdsson, Linda Vidarsdottir, Ramile Dilshat, Erla Sveinbjornsdottir, Snaedis Ragnarsdottir, Daniel H Magnusson, Maria R. Bustos, Eirikur Steingrimsson, Thorkell Gudjonsson, Stefan Sigurdsson   +13 more
wiley   +1 more source

AID Is Required for the Chromosomal Breaks in c-myc that Lead to c-myc/IgH Translocations [PDF]

Cell, 2008
Chromosomal translocation requires formation of paired double-strand DNA breaks (DSBs) on heterologous chromosomes. One of the most well characterized oncogenic translocations juxtaposes c-myc and the immunoglobulin heavy-chain locus (IgH) and is found in Burkitt's lymphomas in humans and plasmacytomas in mice.
Robbiani, Davide F., Bothmer, Anne, Callen, Elsa, Reina-San-Martin, Bernardo, Dorsett, Yair, Difilippantonio, Simone, Bolland, Daniel J., Chen, Hua Tang, Corcoran, Anne E., Nussenzweig, André, Nussenzweig, Michel C.   +10 more
openaire   +2 more sources

PAK1 activation drives divergent resistance mechanisms to aromatase inhibition and tamoxifen in a luminal: A breast cancer model

Molecular Oncology, EarlyView.
Breast cancer remains a major cause of cancer death in women, frequently developing endocrine therapy resistance. This study demonstrates that upregulated p21‐activated kinase 1 (PAK1) activity drives resistance to tamoxifen and long‐term estrogen deprivation in ER+ breast cancer models.
Luisa Schwarzmüller, Janina Müller, Efstathios‐Iason Vlachavas, Lukas Beumers, Lena Fleischhacker, Sara Burmester, Angelika Wörner, Sabine Karolus, Dominic Helm, Cindy Körner, Stefan Wiemann   +10 more
wiley   +1 more source

Nucleolar localization of hepatic c-Myc: a potential mechanism for c-Myc regulation

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2005
The c-myc proto-oncogene encodes a transcription factor that is involved in cell proliferation, growth, differentiation, and apoptosis. Previous studies on the regulation of hepatic c-myc have focused on control of its mRNA expression, which generally correlates with hepatocyte proliferation during both liver development and liver regeneration. However,
Sanders, Jennifer A., Gruppuso, Philip A.   +1 more
openaire   +2 more sources

SCP1 regulates c-Myc stability and functions through dephosphorylating c-Myc Ser62 [PDF]

Oncogene, 2015
Serine 62 (Ser62) phosphorylation affects the c-Myc protein stability in cancer cells. However, the mechanism for dephosphorylating c-Myc is not well understood. In this study, we identified carboxyl-terminal domain RNA polymerase II polypeptide A small phosphatase 1 (SCP1) as a novel phosphatase specifically dephosphorylating c-Myc Ser62.
W, Wang, P, Liao, M, Shen, T, Chen, Y, Chen, Y, Li, X, Lin, X, Ge, P, Wang   +8 more
openaire   +2 more sources

SUMO protease SENP1 deSUMOylates and stabilizes c-Myc

Proceedings of the National Academy of Sciences of the United States of America, 2018
Significance c-Myc is dynamically regulated by posttranslational modifications, including SUMOylation. However, how SUMOylation regulates c-Myc activity and stability remains elusive.
Xiao-Xin Sun, Ying-Xiao Chen, Yulong Su, Xiaoyan Wang, Krishna M. Chauhan, Juan Liang, Colin J. Daniel, R. Sears, Mu-Shui Dai   +8 more
semanticscholar   +1 more source

Inhibition of cyclin‐dependent kinases 12/13 using CT7439 as a treatment for colorectal cancer with CDK12 upregulation

Molecular Oncology, EarlyView.
The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington, Divya L. Dayanidhi, Mohammad Zokaasadi, John B. Mantyh, Pelumi D. Olawuni, Gabrielle Rupprecht, Jeremy M. Force, Shannon McCall, Ashwani K. Bahl, David S. Hsu, Jason A. Somarelli   +10 more
wiley   +1 more source

Direct Activation of HSP90A Transcription by c-Myc Contributes to c-Myc-induced Transformation [PDF]

Journal of Biological Chemistry, 2004
The c-myc proto-oncogene encodes a ubiquitous transcription factor involved in the control of cell growth and differentiation and implicated in inducing tumorigenesis. Understanding the function of c-Myc and its role in cancer depends upon the identification of c-Myc target genes.
Teng, Shu-Chun, Chen, Yung-Yi, Su, Yi-Ning, Chou, Po-Chien, Chiang, Yu-Chi, Tseng, Shun-Fu, Wu, Kou-Juey   +6 more
openaire   +2 more sources

DNA-dependent protein kinase catalytic subunit modulates the stability of c-Myc oncoprotein

Molecular Cancer, 2008
Background C-Myc is a short-lived oncoprotein that is destroyed by ubiquitin-mediated proteolysis. Dysregulated accumulation of c-Myc commonly occurs in human cancers. Some of those cases with the dysregulated c-Myc protein accumulation are attributed to
Wang Yu, Shang Zeng-Fu, Huo Yan-Ying, Zhang Shi-Meng, Xu Qin-Zhi, Yang Dong-Yan, An Jing, Wu De-Chang, Zhou Ping-Kun   +8 more
doaj   +1 more source