Results 51 to 60 of about 14,797,528 (308)

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

MYC and N-MYC are overexpressed in MYC-ER and N-MYC-ER-expressing cells, and naturally overexpressed MYC controls circadian gene expression.

open access: yes, 2023
A.MYCN was determined in parental SKNAS, SKNAS N-MYC-ER, or SHEP N-MYC-ER by qPCR in n = 3 replicates by quantitative PCR (qPCR), normalized to β2M. MYCN overexpression is shown relative to parental SKNAS, since SHEP do not express MYCN. B.
Brian J. Altman (16819407)   +12 more
core   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
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

Network divergence analysis identifies adaptive gene modules and two orthogonal vulnerability axes in pancreatic cancer

open access: yesMolecular Oncology, EarlyView.
Tumors contain diverse cellular states whose behavior is shaped by context‐dependent gene coordination. By comparing gene–gene relationships across biological contexts, we identify adaptive transcriptional modules that reorganize into distinct vulnerability axes.
Brian Nelson   +9 more
wiley   +1 more source

The Expression and Localization of N-Myc Downstream-Regulated Gene 1 in Human Trophoblasts [PDF]

open access: yes, 2013
The protein N-Myc downstream-regulated gene 1 (NDRG1) is implicated in the regulation of cell proliferation, differentiation, and cellular stress response.
Shi, Xiao-Hua   +22 more
core   +1 more source

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

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau   +8 more
wiley   +1 more source

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