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36 results on '"Seachrist, Darcie D"'

5. S2 Legend from TLE3 Sustains Luminal Breast Cancer Lineage Fidelity to Suppress Metastasis

Author

Anstine, Lindsey J., primary, Majmudar, Parth R., primary, Aponte, Amy, primary, Singh, Salendra, primary, Zhao, Ran, primary, Weber-Bonk, Kristen L., primary, Abdul-Karim, Fadi W., primary, Valentine, Mitchell, primary, Seachrist, Darcie D., primary, Grennel-Nickelson, Katelyn E., primary, Cuellar-Vite, Leslie, primary, Sizemore, Gina M., primary, Sizemore, Steven T., primary, Webb, Bryan M., primary, Thompson, Cheryl L., primary, and Keri, Ruth A., primary

Published
2023
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6. S8 from TLE3 Sustains Luminal Breast Cancer Lineage Fidelity to Suppress Metastasis

Author

Anstine, Lindsey J., primary, Majmudar, Parth R., primary, Aponte, Amy, primary, Singh, Salendra, primary, Zhao, Ran, primary, Weber-Bonk, Kristen L., primary, Abdul-Karim, Fadi W., primary, Valentine, Mitchell, primary, Seachrist, Darcie D., primary, Grennel-Nickelson, Katelyn E., primary, Cuellar-Vite, Leslie, primary, Sizemore, Gina M., primary, Sizemore, Steven T., primary, Webb, Bryan M., primary, Thompson, Cheryl L., primary, and Keri, Ruth A., primary

Published
2023
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7. Table S1 from TLE3 Sustains Luminal Breast Cancer Lineage Fidelity to Suppress Metastasis

Author

Anstine, Lindsey J., primary, Majmudar, Parth R., primary, Aponte, Amy, primary, Singh, Salendra, primary, Zhao, Ran, primary, Weber-Bonk, Kristen L., primary, Abdul-Karim, Fadi W., primary, Valentine, Mitchell, primary, Seachrist, Darcie D., primary, Grennel-Nickelson, Katelyn E., primary, Cuellar-Vite, Leslie, primary, Sizemore, Gina M., primary, Sizemore, Steven T., primary, Webb, Bryan M., primary, Thompson, Cheryl L., primary, and Keri, Ruth A., primary

Published
2023
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8. Data from TLE3 Sustains Luminal Breast Cancer Lineage Fidelity to Suppress Metastasis

Author

Anstine, Lindsey J., primary, Majmudar, Parth R., primary, Aponte, Amy, primary, Singh, Salendra, primary, Zhao, Ran, primary, Weber-Bonk, Kristen L., primary, Abdul-Karim, Fadi W., primary, Valentine, Mitchell, primary, Seachrist, Darcie D., primary, Grennel-Nickelson, Katelyn E., primary, Cuellar-Vite, Leslie, primary, Sizemore, Gina M., primary, Sizemore, Steven T., primary, Webb, Bryan M., primary, Thompson, Cheryl L., primary, and Keri, Ruth A., primary

Published
2023
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9. Data from LIN9 and NEK2 Are Core Regulators of Mitotic Fidelity That Can Be Therapeutically Targeted to Overcome Taxane Resistance

Author

Roberts, Melyssa S., primary, Sahni, Jennifer M., primary, Schrock, Morgan S., primary, Piemonte, Katrina M., primary, Weber-Bonk, Kristen L., primary, Seachrist, Darcie D., primary, Avril, Stefanie, primary, Anstine, Lindsey J., primary, Singh, Salendra, primary, Sizemore, Steven T., primary, Varadan, Vinay, primary, Summers, Matthew K., primary, and Keri, Ruth A., primary

Published
2023
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10. Figure S5 from LIN9 and NEK2 Are Core Regulators of Mitotic Fidelity That Can Be Therapeutically Targeted to Overcome Taxane Resistance

Author

Roberts, Melyssa S., primary, Sahni, Jennifer M., primary, Schrock, Morgan S., primary, Piemonte, Katrina M., primary, Weber-Bonk, Kristen L., primary, Seachrist, Darcie D., primary, Avril, Stefanie, primary, Anstine, Lindsey J., primary, Singh, Salendra, primary, Sizemore, Steven T., primary, Varadan, Vinay, primary, Summers, Matthew K., primary, and Keri, Ruth A., primary

Published
2023
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12. Supplementary Materials from LIN9 and NEK2 Are Core Regulators of Mitotic Fidelity That Can Be Therapeutically Targeted to Overcome Taxane Resistance

Author

Roberts, Melyssa S., primary, Sahni, Jennifer M., primary, Schrock, Morgan S., primary, Piemonte, Katrina M., primary, Weber-Bonk, Kristen L., primary, Seachrist, Darcie D., primary, Avril, Stefanie, primary, Anstine, Lindsey J., primary, Singh, Salendra, primary, Sizemore, Steven T., primary, Varadan, Vinay, primary, Summers, Matthew K., primary, and Keri, Ruth A., primary

Published
2023
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17. TLE3 Sustains Luminal Breast Cancer Lineage Fidelity to Suppress Metastasis

Author

Anstine, Lindsey J., primary, Majmudar, Parth R., additional, Aponte, Amy, additional, Singh, Salendra, additional, Zhao, Ran, additional, Weber Bonk, Kristen L., additional, Abdul-Karim, Fadi W., additional, Valentine, Mitchell, additional, Seachrist, Darcie D., additional, Grenell-Nickelson, Katelyn E., additional, Cuellar-Vite, Leslie, additional, Sizemore, Gina M., additional, Sizemore, Steven T., additional, Webb, Bryan M., additional, Thompson, Cheryl L., additional, and Keri, Ruth A., additional

Published
2023
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18. UbcH7 regulates 53BP1 stability and DSB repair

Author

Han, Xiangzi, Zhang, Lei, Chung, Jinsil, Pozo, Franklin Mayca, Tran, Amanda, Seachrist, Darcie D., Jacobberger, James W., Keri, Ruth A., Gilmore, Hannah, and Zhang, Youwei

Published
2014

22. Additional file 2 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 2: Figure S2. Identification of a KLF4-regulated protein signature reveals EGFR as a downstream target. The top a 63 downregulated proteins and b 14 upregulated proteins after KLF4 overexpression. c Protein-Protein interaction network including proteins with greater than 2-fold expression decrease after AdKLF4 infection and RPPA analysis. Colored nodes indicate query proteins and the first shell of interactors. Teal and purple lines indicate known interactions. Green, red, yellow and blue lines indicate predicted interactions. d REVERT staining of total protein in MDA-MB-231 cells after transduction with AdGFP (AdG) or AdKLF4 (AdK).

Published
2020
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23. Additional file 3 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 3: Figure S3. KLF4 negatively regulates the EGFR signaling pathway. a REVERT staining of total protein in Fig. 3a. b REVERT staining of total protein in Fig. 3c. c REVERT staining of total protein in Fig. 3e.

Published
2020
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24. Additional file 1 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Subjects
skin and connective tissue diseases
Abstract

Additional file 1: Figure S1. KLF4 represses migration, invasion, and cell growth in breast epithelial cells. a REVERT staining of total protein across eight different breast cell lines: MCF10A (10A), MCF7, T47D, SKBR3, SUM159, HCC70, MDA-MB-468 (468), and MDA-MB-231 (231). b REVERT staining of total protein in MCF10A cells as well as MDA-MB-231 and MDA-MB-468 after transduction with AdGFP (G) or AdKLF4 (K). c REVERT staining of total protein in MCF10A cells after transfection with siNS or siKLF4 (siK).

Published
2020
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25. Additional file 5 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 5: Table S1. ChIP-PCR primer sequences. Primer sequences targeting six regions within the EGFR promoter are listed.

Published
2020
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26. Additional file 4 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 4: Figure S4. Repression of EGFR is an obligatory intermediate step for KLF4 to inhibit aggressive breast cancer phenotypes. a REVERT staining of total protein in Fig. 5a. b REVERT staining of total protein in Fig. 5b.

Published
2020
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27. The transcriptional repressor BCL11A promotes breast cancer metastasis

Author

Seachrist, Darcie D., primary, Hannigan, Molly M., additional, Ingles, Natasha N., additional, Webb, Bryan M., additional, Weber-Bonk, Kristen L., additional, Yu, Peng, additional, Bebek, Gurkan, additional, Singh, Salendra, additional, Sizemore, Steven T., additional, Varadan, Vinay, additional, Licatalosi, Donny D., additional, and Keri, Ruth A., additional

Published
2020
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28. Correction: Bromodomain and extraterminal protein inhibition blocks growth of triple-negative breast cancers through the suppression of aurora kinases.

Author

Sahni, Jennifer M., primary, Gayle, Sylvia S., additional, Bonk, Kristen L. Weber, additional, Vite, Leslie Cuellar, additional, Yori, Jennifer L., additional, Webb, Bryan, additional, Ramos, Erika K., additional, Seachrist, Darcie D., additional, Landis, Melissa D., additional, Chang, Jenny C., additional, Bradner, James E., additional, and Keri, Ruth A., additional

Published
2020
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29. LIN9 and NEK2 Are Core Regulators of Mitotic Fidelity That Can Be Therapeutically Targeted to Overcome Taxane Resistance

Author

Roberts, Melyssa S., primary, Sahni, Jennifer M., additional, Schrock, Morgan S., additional, Piemonte, Katrina M., additional, Weber-Bonk, Kristen L., additional, Seachrist, Darcie D., additional, Avril, Stefanie, additional, Anstine, Lindsey J., additional, Singh, Salendra, additional, Sizemore, Steven T., additional, Varadan, Vinay, additional, Summers, Matthew K., additional, and Keri, Ruth A., additional

Published
2020
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33. Mitotic Vulnerability in Triple-Negative Breast Cancer Associated with LIN9 Is Targetable with BET Inhibitors

Author

Sahni, Jennifer M., primary, Gayle, Sylvia S., additional, Webb, Bryan M., additional, Weber-Bonk, Kristen L., additional, Seachrist, Darcie D., additional, Singh, Salendra, additional, Sizemore, Steven T., additional, Restrepo, Nicole A., additional, Bebek, Gurkan, additional, Scacheri, Peter C., additional, Varadan, Vinay, additional, Summers, Matthew K., additional, and Keri, Ruth A., additional

Published
2017
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35. Bromodomain and Extraterminal Protein Inhibition Blocks Growth of Triple-negative Breast Cancers through the Suppression of Aurora Kinases

Author

Sahni, Jennifer M., primary, Gayle, Sylvia S., additional, Bonk, Kristen L. Weber, additional, Vite, Leslie Cuellar, additional, Yori, Jennifer L., additional, Webb, Bryan, additional, Ramos, Erika K., additional, Seachrist, Darcie D., additional, Landis, Melissa D., additional, Chang, Jenny C., additional, Bradner, James E., additional, and Keri, Ruth A., additional

Published
2016
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36. UbcH7 regulates 53BP1 stability and DSB repair.

Author

Xiangzi Han, Lei Zhang, Jinsil Chung, Pozo, Franklin Mayca, Tran, Amanda, Seachrist, Darcie D., Jacobberger, James W., Keri, Ruth A., Gilmore, Hannah, and Youwei Zhang

Subjects
UBIQUITIN-conjugating enzymes, DNA repair, TUMOR suppressor proteins, UBIQUITINATION, PROTEASOMES
Abstract

DNA double-strand break (DSB) repair is not only key to genome stability but is also an important anticancer target. Through an shRNA library-based screening, we identified ubiquitin-conjugating enzyme H7 (UbcH7, also known as Ube2L3), a ubiquitin E2 enzyme, as a critical player in DSB repair. UbcH7 regulates both the steady-state and replicative stress-induced ubiquitination and proteasome-dependent degradation of the tumor suppressor p53-binding protein 1 (53BP1). Phosphorylation of 53BP1 at the N terminus is involved in the replicative stress-induced 53BP1 degradation. Depletion of UbcH7 stabilizes 53BP1, leading to inhibition of DSB end resection. Therefore, UbcH7-depleted cells display increased nonhomologous end-joining and reduced homologous recombination for DSB repair. Accordingly, UbcH7-depleted cells are sensitive to DNA damage likely because they mainly used the error-prone nonhomologous end-joining pathway to repair DSBs. Our studies reveal a novel layer of regulation of the DSB repair choice and propose an innovative approach to enhance the effect of radiotherapy or chemotherapy through stabilizing 53BP1. [ABSTRACT FROM AUTHOR]

Published
2014
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