Results 31 to 40 of about 239,540 (278)

N-myc Down-Regulates Activin A

open access: yesBiochemical and Biophysical Research Communications, 2000
N-myc oncogene amplification is frequent in human neuroblastoma and predicts poor prognosis, but the molecular consequences have remained obscure. We report here that enhanced N-myc expression correlates with low or undetectable expression of activin A, but not other closely related members of the transforming growth factor-beta superfamily.
Breit, Stephen   +3 more
openaire   +4 more sources

N-myc and Noncoding RNAs in Neuroblastoma [PDF]

open access: yesMolecular Cancer Research, 2012
Abstract Neuroblastoma is a pediatric tumor of the sympathetic nervous system. Amplification and overexpression of the MYCN proto-oncogene occurs in approximately 20% of neuroblastomas and is associated with advanced stage disease, rapid tumor progression, and poor prognosis. MYCN encodes the transcriptional regulator N-myc, which has
Jochen, Buechner, Christer, Einvik
openaire   +2 more sources

N-Myc expression enhances the oncolytic effects of vesicular stomatitis virus in human neuroblastoma cells

open access: yesMolecular Therapy: Oncolytics, 2016
N-myc oncogene amplification is associated but not present in all cases of high-risk neuroblastoma (NB). Since oncogene expression could often modulate sensitivity to oncolytic viruses, we wanted to examine if N-myc expression status would determine ...
Juan C Corredor   +6 more
doaj   +1 more source

N-Myc knockdown and apigenin treatment controlled growth of malignant neuroblastoma cells having N-Myc amplification [PDF]

open access: yesGene, 2013
Malignant neuroblastomas mostly occur in children and are frequently associated with N-Myc amplification. Oncogene amplification, which is selective increase in copy number of the oncogene, provides survival advantages in solid tumors including malignant neuroblastoma.
Md Motarab, Hossain   +2 more
openaire   +2 more sources

HAUSP deubiquitinates and stabilizes N-Myc in neuroblastoma [PDF]

open access: yesNature Medicine, 2016
The MYCN proto-oncogene is amplified in a number of advanced-stage human tumors, such as neuroblastomas. Similar to other members of the MYC family of oncoproteins, MYCN (also known as N-Myc) is a transcription factor, and its stability and activity are tightly controlled by ubiquitination-dependent proteasome degradation.
Tavana, Omid   +10 more
openaire   +2 more sources

C/EBPa controls acquisition and maintenance of adult hematopoietic stem cell quiescence [PDF]

open access: yes, 2014
Summary In blood, transcription factor C/EBPa is essential for myeloid differentiation and has been implicated in regulating self-renewal of fetal liver (FL) hematopoietic stem cells (HSCs). However, its function in adult HSCs has remained unknown. Here,
Alberich-Jordà, Meritxell   +10 more
core   +1 more source

Expression of n-MYC, NAMPT and SIRT1 in Basal Cell Carcinomas and their Cells of Origin

open access: yesActa Dermato-Venereologica, 2018
Deregulated Hedgehog signalling is a driver of basal cell carcinomas. One effector of the Hedgehog pathway is n-MYC. c/n-MYC proteins, NAMPT and DBC1 are linked to SIRT1 in a positive feedback loop that may contribute to tumorigenesis of basal cell ...
Lydia Brandl   +3 more
doaj   +1 more source

Structural basis of N-Myc binding by Aurora-A and its destabilization by kinase inhibitors [PDF]

open access: yes, 2016
Myc family proteins promote cancer by inducing widespread changes in gene expression. Their rapid turn-over by the ubiquitin-proteasome pathway is regulated through phosphorylation of Myc Box I and ubiquitination by SCFFbxw7.
Bayliss, R   +6 more
core   +2 more sources

Mitoribosomal synthetic lethality overcomes multidrug resistance in MYC-driven neuroblastoma

open access: yesCell Death and Disease, 2023
Mitochondria are central for cancer responses to therapy-induced stress signals. Refractory tumors often show attenuated sensitivity to apoptotic signaling, yet clinically relevant molecular actors to target mitochondria-mediated resistance remain ...
Karolina Borankova   +7 more
doaj   +1 more source

Bcl-2 and N-Myc Coexpression Increases IGF-IR and Features of Malignant Growth in Neuroblastoma Cell Lines

open access: yesNeoplasia: An International Journal for Oncology Research, 2001
The bcl-2 and c-myc oncogenes cooperate to transform multiple cell types. In the pediatric malignancy NB2, Bcl2 is highly expressed. In tumors with a poor prognosis, N-Myc, a protein homologous to c-Myc, is overexpressed as a result of gene amplification.
Rama Jasty   +8 more
doaj   +1 more source

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