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Human C-MYC Protein expressed in HEK-293 Cells - ABIN2715370
Garcia-Sanz, Quintanilla, Lafita, Moreno-Bueno, García-Gutierrez, Tabor, Varela, Shiio, Larsson, Portillo, Leon: Sin3b interacts with Myc and decreases Myc levels. in The Journal of biological chemistry 2014
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Results provide evidence that myc expression level is regulated by BRD4 (show BRD4 Proteins) in gastric neoplasm through transcriptional and epigenetic regulation.
These results indicated that cMyc and Fas (show FAS Proteins) regulated the sensitivity of A549 cells to irradiation by regulating caspase8-mediated Bid (show BID Proteins) activation and the subsequent association with the mitochondrial pathway of apoptosis.
These results indicate that Merlin (show NF2 Proteins)/YAP (show YAP1 Proteins)/cMyc/mTOR (show FRAP1 Proteins) signaling axis promotes human cholangiocarcinoma (CCA (show FBN2 Proteins)) cell proliferation by overriding contact inhibition. We propose that overriding cMycmediated contact inhibition is implicated in the development of CCA (show FBN2 Proteins).
PLGF (show PGF Proteins) promotes Epithelial-mesenchymal transition (EMT (show ITK Proteins)) and tumorsphere formation through inducing miR (show MLXIP Proteins)-19a expression by upregulating c-MYC.
MYC negatively regulated the expression of genes involved in mitochondrial biogenesis and maintenance but positively regulated genes involved in DNA and histone methylation. Knockdown of MYC in colorectal cancer cells reset the altered metabolism and suppressed cell growth.
The combination of PD-L1 (show CD274 Proteins) and HLA class I (show MICA Proteins) represents a novel prognostic biomarker for neuroblastoma (show ARHGEF16 Proteins). Pharmacologic inhibition of MYCN (show MYCN Proteins) and MYC may be exploited to target PD-L1 (show CD274 Proteins) and restore an efficient antitumor immunity in high-risk neuroblastoma (show ARHGEF16 Proteins).
This study identifies a novel signaling involving SYK/c-MYC/MALAT1 as a promising therapeutic target for the treatment of Ewing sarcoma.
Overexpression of MYC in diffuse large B-cell lymphoma can be driven by the BCR (show BCR Proteins)-PI3K (show PIK3CA Proteins) signalling pathway
The study suggests that nuclear overexpression of cMYC correlates with tumorigenesis / dedifferentiation in follicular cell derived thyroid carcinomas.
data suggest the existence in T-ALL of a disrupted RNA decapping pathway, mediated by the DNA methylation (show HELLS Proteins)-associated loss of NUDT16 (show NUDT16 Proteins), which contributes to the natural history of the disease by stabilizing transforming factors, such as is the case of the leukemogenic protein C (show PROC Proteins)-MYC
Ouabain-induced proliferation might be attributed, at least in part, to decrease of intracellular free calcium and increase of c-myc mRNA expression, and that may be directly or indirectly involved in regulation of blood pressure.
report the isolation of complete coding regions of rabbit SOX2, KLF4, C-MYC and NANOG, which encode transcription factors that play crucial regulatory roles during early mammalian embryonic development
c-Myc repression during development is crucial for the maturation of preacinar cells, and c-Myc overexpression can contribute to pancreatic carcinogenesis through the induction of a dedifferentiated state.
High myc expression is associated with Intestinal Tumorigenesis.
results shed light on how overexpressed MYC alters the various phases of the RNAPII cycle and the resulting transcriptional response.
c-Myc overexpression stimulated proliferation and activation of renal fibroblasts by inducing integrin alphav-mediated TGF-beta (show TGFB1 Proteins) signaling.
In the Myc-induced liver tumor model in zebrafish, a dramatic increase of liver size with neoplastic features was observed, as well as enhanced angiogenesis, and increase liver-infiltrated neutrophils and hypoxia. This model provides an excellent platform for study of tumor microenvironment.
Using inducible genetic mosaics, we overexpressed Myc in the epicardium and determined the differential expansion of Myc-overexpressing cells with respect to their wild type counterparts. Myc-overexpressing cells overcolonized all epicardial-derived lineages and showed increased ability to invade the myocardium and populate the vasculature.
Nac1 (show NACC1 Proteins) overexpression promotes ESC proliferation and delays ESC differentiation in the absence of leukemia inhibitory factor (LIF (show LIF Proteins)). Furthermore, we demonstrated that Nac1 (show NACC1 Proteins) directly binds to the c-Myc promoter and regulates c-Myc transcription.
this study demonstrates that miR (show MLXIP Proteins)-451 regulates T cell proliferative responses in part via a Myc-dependent mechanism
AKAP1 (show AKAP1 Proteins) is a transcriptional target of Myc, and it supports mTOR (show FRAP1 Proteins) pathway and the growth of cancer cells.
Apoptosis was also observed with myca expression; introduction of homozygous tp53 (show TP53 Proteins)(-/-) mutation into the myca transgenic fish reduced apoptosis and accelerated tumor progression.
MYC down-regulation induces mitochondrial apoptosis in T lymphoblasts.
These findings not only reveal a novel role of Mad1 (show MXD1 Proteins) in regulating developmental cell death but also suggest that a balance of Mad and Myc controls cell fate determination during adult organ development.
Thyroid hormone (show PTH Proteins) activates protein arginine methyltransferase 1 expression by directly inducing c-Myc transcription during Xenopus intestinal stem cell development.(
c-Myc has a direct role in the control of DNA replication
Findings support a model in which Myc, Twist and Slug/Snail2 function in a regulatory circuit within lateral plate mesoderm that directs normal vessel formation in both the vascular and lymphatic systems.
Expression of Drosophila Myc (dMyc) suppresses, whereas loss of dMyc enhances, ectopically activated JNK (show MAPK8 Proteins) signaling-induced cell death. dMyc impedes physiologically activated JNK (show MAPK8 Proteins) pathway-mediated cell death. Loss of dMyc triggers JNK (show MAPK8 Proteins) pathway activation and JNK (show MAPK8 Proteins)-dependent cell death.
tissue-specific downregulation of the Drosophila homolog of human c-myc proto-oncogene (dMyc) suppresses tau-mediated morphological and functional deficits by reducing abnormal tau hyperphosphorylation and restoring the heterochromatin loss.
dMyc has an essential role in preventing JNK (show MAPK8 Proteins)-mediated retinal glial activation
the key target of the Psi/MED network in controlling developmentally regulated tissue growth is the transcription factor MYC.
Myc dosage plays crucial role in determining sex-specific size in Drosophila larvae and adult tissue. Double dose of Myc in females serves at least twice in development to promote sexual size dimorphism.
BicC (show BICC1 Proteins) down regulates Myc in the Malpighian tubule.
activation of the TOR-Myc axis in midgut stem and progenitor cells influences a variety of traits in Drosophila
Drosophila adult muscle precursors display homing behavior to muscle niche and the niche-driven Insulin (show INS Proteins)-Notch (show NOTCH1 Proteins)-dMyc cascade plays a key role in setting the activated state of adult muscle precursors.
a functional link between Myc, a renowned oncogene (show RAB1A Proteins), and the essential nucleotide biosynthetic enzyme CTPsyn.
MYC and S6K (show RPS6KB1 Proteins) cooperate through coordinate activation of the essential Pol I transcription initiation factor TIF-1A (show RRN3 Proteins).
The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene.
avian myelocytomatosis viral oncogene homolog
, class E basic helix-loop-helix protein 39
, myc proto-oncogene protein
, myc-related translation/localization regulatory factor
, proto-oncogene c-Myc
, transcription factor p64
, v-myc myelocytomatosis viral oncogene homolog
, c-myc proto-oncogene
, avian myelocytomatosis viral (v-myc) oncogene homolog
, Avian myelocytomatosis viral (v-myc) oncogene homolog
, myelocytomatosis viral oncogene homolog
, v-myc avian myelocytomatosis viral oncogene homolog
, cellular myelocytomatosis oncogene
, Proto-oncogene c-Myc
, Transcription factor p64
, transcriptional regulator Myc-A
, MYC II
, transcriptional regulator Myc-B
, Myc proto-oncogene protein
, CG10798 gene product from transcript CG10798-RB
, Diminutive protein
, lethal (1) G0354
, lethal (1) G0359