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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. dans The Journal of biological chemistry 2014
Show all 3 Pubmed References
The present findings show that expression of c-MYC has prognostic value in squamous cell carcinoma of the tongue, and could be useful in choice of therapy.
Multivariable analysis indicated that IPI (P = 0.002), chemotherapy regimens (P = 0.017), and MYC gene rearrangements (P = 0.004) were independent adverse prognostic factors for all diffuse large B cell Lymphoma(DLBCL) patients in this study. Results demonstrated that the poor survival of DLBCL patients with HBV infection was closely involved in chemotherapy regimens, IPI, and MYC gene rearrangements
MYC extra copy in diffuse large B-cell lymphoma is an independent poor prognostic factor
The c-Myc/miR (Montrer MLXIP Protéines)-200b/PRDX2 (Montrer PRDX2 Protéines) loop regulates colorectal cancer (CRC (Montrer CALR Protéines)) progression and its disruption enhances tumor metastasis and chemotherapeutic resistance in CRC (Montrer CALR Protéines).
We found that the combination of alpha-mangostin with TRAIL induced apoptosis of SAS (Montrer TSPAN31 Protéines) cells through the mitochondrial pathway via activation of caspase-9 (Montrer CASP9 Protéines) and -3/7, following release of cytochrome c (Montrer CYCS Protéines). This apoptosis was induced by S/G2 (Montrer STRN3 Protéines)/M-phase arrest. Immunopositivity for c-Myc was observed in the cytoplasm of tumor cells in 16 (40%) of the 40 cases of human oral squamous cell carcinoma (HOSCC).
current data demonstrate that both INSR (Montrer INSR Protéines) and IGF1R (Montrer IGF1R Protéines) are directly targeted by C-myc and exert similar effects to promote the tumorigenesis and metastasis of TSCC through the NF-kappaB (Montrer NFKB1 Protéines) pathway.
clusters of enhancers, such as BENC in the MYC gene, form highly combinatorial systems that allow precise control of gene expression across normal cellular hierarchies and which also can be hijacked in malignancies
This study elucidates the molecular basis of the c-Myc/EGLN1 (Montrer EGLN1 Protéines)-mediated induction of LSH (Montrer HELLS Protéines) expression that inhibits ferroptosis
the findings outlined in the current study suggest that PCAT-1 regulates the invasiveness and drug resistance in CRC (Montrer CALR Protéines) cells and that PCAT-1 may promote CRC (Montrer CALR Protéines) cell invasion by modulating the expression of c-Myc.
data show that Hdac1 (Montrer HDAC1 Protéines) and Hdac2 (Montrer HDAC2 Protéines) impact on Emu-myc B cell proliferation and apoptosis and suggest that a critical level of Hdac (Montrer HDAC3 Protéines) activity may be required for Emu-myc tumorigenesis and proper B cell development
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
Although mnt heterozygosity clearly slowed lymphomagenesis in vavP-MYC10 and Emu-myc mice, the change(s) in cellular properties responsible for this effect remain to be identified.
clusters of enhancers, such as BENC in the myc gene, form highly combinatorial systems that allow precise control of gene expression across normal cellular hierarchies and which also can be hijacked in malignancies
Conditional deletion of Myc in hyaloid vascular endothelial cells suppressed both proliferation and cell death.
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.
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.
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 (Montrer TGFB1 Protéines) 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.
Methylparabens exposure increased malformations, LPO, apoptosis, ccnd1 and myca expressions, and decreased GST activities and NO levels compared with the control group.
Apoptosis was also observed with myca expression; introduction of homozygous tp53 (Montrer TP53 Protéines)(-/-) 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 (Montrer MXD1 Protéines) 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 (Montrer PTH Protéines) 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 (Montrer MAPK8 Protéines) signaling-induced cell death. dMyc impedes physiologically activated JNK (Montrer MAPK8 Protéines) pathway-mediated cell death. Loss of dMyc triggers JNK (Montrer MAPK8 Protéines) pathway activation and JNK (Montrer MAPK8 Protéines)-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 (Montrer MAPK8 Protéines)-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 (Montrer BICC1 Protéines) 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 (Montrer INS Protéines)-Notch (Montrer NOTCH1 Protéines)-dMyc cascade plays a key role in setting the activated state of adult muscle precursors.
a functional link between Myc, a renowned oncogene (Montrer RAB1A Protéines), and the essential nucleotide biosynthetic enzyme CTPsyn.
MYC and S6K (Montrer RPS6KB1 Protéines) cooperate through coordinate activation of the essential Pol I transcription initiation factor TIF-1A (Montrer RRN3 Protéines).
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