Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Daniel J. Kelpsch"'
Autor:
Danielle E. Talbot, Bailey J. Vormezeele, Garrett C. Kimble, Dylane M. Wineland, Daniel J. Kelpsch, Michelle S. Giedt, Tina L. Tootle
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 11 (2023)
Prostaglandins (PGs), locally acting lipid signals, regulate female reproduction, including oocyte development. However, the cellular mechanisms of PG action remain largely unknown. One cellular target of PG signaling is the nucleolus. Indeed, across
Externí odkaz:
https://doaj.org/article/2ea295a7aaa44f3c87517c5a8850bede
DNMT3B7 expression promotes tumor progression to a more aggressive phenotype in breast cancer cells.
Autor:
Patrick R Brambert, Daniel J Kelpsch, Rabia Hameed, Charmi V Desai, Gianfranco Calafiore, Lucy A Godley, Stacey L Raimondi
Publikováno v:
PLoS ONE, Vol 10, Iss 1, p e0117310 (2015)
Epigenetic changes, such as DNA methylation, have been shown to promote breast cancer progression. However, the mechanism by which cancer cells acquire and maintain abnormal DNA methylation is not well understood. We have previously identified an abe
Externí odkaz:
https://doaj.org/article/6907d7fd857c4f47ba4e32f80fed7911
Autor:
Viravuth P. Yin, Daniel J. Kelpsch, Megan Beauchemin, Erika G. Stroh, Tina L. Tootle, Ashley M. Smith, MaryLynn FitzSimons, Maureen C. Lamb
Publikováno v:
Scientific Reports, Vol 10, Iss 1, Pp 1-10 (2020)
The inability to effectively stimulate cardiomyocyte proliferation remains a principle barrier to regeneration in the adult human heart. A tightly regulated, acute inflammatory response mediated by a range of cell types is required to initiate regene
Publikováno v:
The Anatomical Record. 301:2014-2036
While nuclear actin was reported ~50 years ago, it's in vivo prevalence and structure remain largely unknown. Here, we use Drosophila oogenesis, that is, follicle development, to characterize nuclear actin. We find that three different reagents-DNase
Autor:
Daniel J. Kelpsch, Tina L. Tootle
Publikováno v:
The Anatomical Record. 301:1999-2013
While actin was discovered in the nucleus over 50 years ago, research lagged for decades due to strong skepticism. The revitalization of research into nuclear actin occurred after it was found that cellular stresses induce the nuclear localization an
Autor:
MaryLynn, FitzSimons, Megan, Beauchemin, Ashley M, Smith, Erika G, Stroh, Daniel J, Kelpsch, Maureen C, Lamb, Tina L, Tootle, Viravuth P, Yin
Publikováno v:
Scientific Reports
The inability to effectively stimulate cardiomyocyte proliferation remains a principle barrier to regeneration in the adult human heart. A tightly regulated, acute inflammatory response mediated by a range of cell types is required to initiate regene
Publikováno v:
Molecular Biology of the Cell
Study of Drosophila oogenesis reveals that the nuclear localization of actin is controlled by both development and Fascin. Fascin regulates both endogenous nuclear actin and ectopic nuclear actin rod formation by controlling Cofilin.
Drosophila
Drosophila
Publikováno v:
Molecular Biology of the Cell
Tight regulation of actin remodeling is essential for development, and misregulation results in disease. Cytoskeletal dynamics are regulated by prostaglandins (PGs)—lipid signals. PGs temporally regulate actin remodeling during Drosophila oogenesis
Autor:
Meera K. Advani, Stacey L. Raimondi, Michael F. Lahey, Daniel J. Kelpsch, Christopher L. Hulstein, Amy Du, Lauren E. Williams
Publikováno v:
BIOS. 83:17-25
Breast cancer is the second leading cause of cancer death in women, with 1 in 8 developing an invasive breast cancer in her lifetime. Changes in gene expression are common as tumors progress and epigenetics studies alterations in gene expression wher
Autor:
Patrick R. Brambert, Gianfranco Calafiore, Charmi V. Desai, Stacey L. Raimondi, Lucy A. Godley, Rabia Hameed, Daniel J. Kelpsch
Publikováno v:
PLoS ONE
PLoS ONE, Vol 10, Iss 1, p e0117310 (2015)
PLoS ONE, Vol 10, Iss 1, p e0117310 (2015)
Epigenetic changes, such as DNA methylation, have been shown to promote breast cancer progression. However, the mechanism by which cancer cells acquire and maintain abnormal DNA methylation is not well understood. We have previously identified an abe