Results 71 to 80 of about 19,933,051 (310)
c-Myc induced changes in higher order rDNA structure accompany growth factor stimulation of quiescent cells [PDF]
Human c-Myc is believed to be a high level coordinator of protein synthesis capacity and cell growth rate, capable of activating transcription by all three nuclear RNA Polymerases.
Rachel G. Berkson +2 more
core
The nucleolar RNA methyltransferase Misu (NSun2) is required for mitotic spindle stability [PDF]
Myc-induced SUN domain–containing protein (Misu or NSun2) is a nucleolar RNA methyltransferase important for c-Myc–induced proliferation in skin, but the mechanisms by which Misu contributes to cell cycle progression are unknown.
Michaela Frye +15 more
core +1 more source
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober +16 more
wiley +1 more source
Western blot analysis was performed according to standard procedures. The primary antibodies used were anti-c-Myc (Abcam ab32072) and anti-GAPDH (Santa Cruz sc47724), each at a dilution of 1:1000.
Morito Kurata (8164626)
core +1 more source
MITF maintains genome stability in nonmelanocyte lineages
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 +13 more
wiley +1 more source
DNA-dependent protein kinase catalytic subunit modulates the stability of c-Myc oncoprotein
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 +8 more
doaj +1 more source
AID Is Required for the Chromosomal Breaks in c-myc that Lead to c-myc/IgH Translocations [PDF]
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. +10 more
openaire +2 more sources
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 +10 more
wiley +1 more source
Nucleolar localization of hepatic c-Myc: a potential mechanism for c-Myc regulation
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. +1 more
openaire +2 more sources
SCP1 regulates c-Myc stability and functions through dephosphorylating c-Myc Ser62 [PDF]
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 +8 more
openaire +2 more sources

