Results 61 to 70 of about 18,976,803 (305)

Mechanisms of c-myc degradation by nickel compounds and hypoxia.

open access: yesPLoS ONE, 2009
Nickel (Ni) compounds have been found to cause cancer in humans and animal models and to transform cells in culture. At least part of this effect is mediated by stabilization of hypoxia inducible factor (HIF1a) and activating its downstream signaling ...
Qin Li, Thomas Kluz, Hong Sun, Max Costa
doaj   +1 more source

siRNA directed against c-Myc inhibits proliferation and downregulates human telomerase reverse transcriptase in human colon cancer Colo 320 cells

open access: yesJournal of Experimental & Clinical Cancer Research, 2008
The c-Myc and human telomerase reverse transcriptase gene (hTERT) gene are frequently deregulated and overexpressed in malignancy. hTERT activity is induced by c-Myc and strategies designed to inhibit c-Myc expression in cancer cells may have ...
Guofu Huang   +9 more
doaj   +1 more source

Western Blot for c-MYC

open access: yes, 2020
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

Epigenetic reprogramming of lineage switching in cancer

open access: yesFEBS Letters, EarlyView.
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı   +4 more
wiley   +1 more source

PDCD11 Stabilizes C‐MYC Oncoprotein by Hindering C‐MYC‐SKP2 Negative Feedback Loop to Facilitate Progression of p53‐Mutant Breast and Colon Malignancies

open access: yesAdvanced Science
C‐MYC is a proto‐oncoprotein whose dysregulation triggers tumorigenesis and tumor progression in ≈70% of cancer cases. It is presently demonstrated that aberrantly upregulated MYC is caused by the overexpressed and “extra‐nucleolar” PDCD11 in p53‐mutant ...
Li Ding   +12 more
doaj   +1 more source

Inhibition of c-Myc overcomes cytotoxic drug resistance in acute myeloid leukemia cells by promoting differentiation. [PDF]

open access: yesPLoS ONE, 2014
Nowadays, drug resistance still represents a major obstacle to successful acute myeloid leukemia (AML) treatment and the underlying mechanism is not fully elucidated. Here, we found that high expression of c-Myc was one of the cytogenetic characteristics
Xiao-Na Pan   +8 more
doaj   +1 more source

c-Myc induced changes in higher order rDNA structure accompany growth factor stimulation of quiescent cells [PDF]

open access: yes, 2007
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  

Golgi enzymes are retrieved from the plasma membrane to the trans‐Golgi network

open access: yesFEBS Letters, EarlyView.
Golgi enzymes are traditionally considered resident proteins retained within the Golgi apparatus. Here, we demonstrate that a subset transiently reaches the cell surface and is subsequently retrieved to the trans‐Golgi network via retrograde transport. Using a nanobody‐based toolkit, we uncover a dynamic trafficking cycle of several Golgi enzymes.
Dominik P. Buser, Tina Junne
wiley   +1 more source

C-myc and immunoglobulin kappa light chain constant genes are on the 8q+ chromosome of three Burkitt lymphoma lines with t(2;8) translocations [PDF]

open access: yes, 1984
We have determined the localization of c-myc and the immunoglobulin kappa light chain genes on the 8q+/2p- chromosomes of the three Burkitt lymphoma lines BL21, LY66 and LY91 with t(2;8) translocation by in situ hybridization.
Cremer, Thomas   +7 more
core   +1 more source

Palmitic acid activates c-Myc via dual palmitoylation-dependent pathways to promote colon cancer

open access: yesCell Discovery
c-Myc is broadly hyperactivated in colon cancer, yet the mechanisms sustaining its transcriptional activation remain elusive. Here we identify palmitic acid (PA) as a metabolite cue that activates c-Myc via dual palmitoylation-dependent pathways ...
Wenxin Du   +8 more
doaj   +1 more source

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