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Chicken Monoclonal C-MYC Primary Antibody for ChIP, CyTOF - ABIN152253
Locker, Dowle, Ellis, Elston, Blamey, Sikora, Evan, Robins: c-myc oncogene product expression and prognosis in operable breast cancer. in British journal of cancer 1989
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Human Monoclonal C-MYC Primary Antibody for FACS, IHC (p) - ABIN302064
Veracini, Simon, Richard, Schraven, Horejsi, Roche, Benistant: The Csk-binding protein PAG regulates PDGF-induced Src mitogenic signaling via GM1. in The Journal of cell biology 2008
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All Species Monoclonal C-MYC Primary Antibody for FACS, IP - ABIN2749043
Persson, Hennighausen, Taub, DeGrado, Leder: Antibodies to human c-myc oncogene product: evidence of an evolutionarily conserved protein induced during cell proliferation. in Science (New York, N.Y.) 1984
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Human Monoclonal C-MYC Primary Antibody for FACS, IHC (p) - ABIN302092
Wang, Campoli, Ko, Luo, Ferrone: Enhancement of scFv fragment reactivity with target antigens in binding assays following mixing with anti-tag monoclonal antibodies. in Journal of immunological methods 2004
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Human Monoclonal C-MYC Primary Antibody for FACS, IHC (p) - ABIN302017
Fujiwara, Poikonen, Aleman, Valtavaara, Saksela, Mayer: A single-chain antibody/epitope system for functional analysis of protein-protein interactions. in Biochemistry 2002
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Human Polyclonal C-MYC Primary Antibody for ELISA, ICC - ABIN6263457
Tang, Peng, Huang, Xie, Chen, Shen, Gao, You, Xie, Chen: Neoisoliquiritigenin Inhibits Tumor Progression by Targeting GRP78-β- catenin Signaling in Breast Cancer. in Current cancer drug targets 2018
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Human Polyclonal C-MYC Primary Antibody for DB - ABIN537691
Domínguez-Cáceres, García-Martínez, Calcabrini, González, Porque, León, Martín-Pérez: Prolactin induces c-Myc expression and cell survival through activation of Src/Akt pathway in lymphoid cells. in Oncogene 2004
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Human Monoclonal C-MYC Primary Antibody for IHC (fro), IF - ABIN2477762
Quant, Woo: Normal values of eye position in the Chinese population of Hong Kong. in Optometry and vision science : official publication of the American Academy of Optometry 1992
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Human Polyclonal C-MYC Primary Antibody for IHC (p), WB - ABIN546358
Baudino, Cleveland: The Max network gone mad. in Molecular and cellular biology 2001
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Study shows that recessive dystrophic epidermolysis bullosa- squamous cell carcinoma (SCC) tumors harbor genetic alterations similar to those in UV-related SCCs. Mutations in NOTCH1/2/4 and TP53 and copy number alterations in MYC, together with the activation of the TGFbeta receptor signaling pathway, seem to play a major role in this malignancy.
propose that under conditions of oxidative stress given by the internalization of oxLDL, macrophages employ the formation of the amphiphysin 2(Bin1)/c-Myc complex as a control mechanism to initially avoid the process of cell death
DPT regulates CDK4, CDK6 and p21, through MEK-ERK-MYC signaling to repress papillary thyroid cancer proliferation.
MYC protein interactome profiling reveals functionally distinct regions that cooperate to drive tumorigenesis.
MTOR2/C-MYC/GFAT1 axis is responsible for the modulation on the crosstalk between glycolysis and glutaminolysis in glioblastoma cells.
In cisplatin-resistant ovarian cancer cells c-Myc enhances the expression of EZH2 by directly suppressing miR-137 that targets EZH2 mRNA. Inhibition of c-Myc-miR-137-EZH2 pathway re-sensitizes resistant cells to cisplatin. Clinical studies further confirm the activated c-Myc-miR-137-EZH2 pathway in platinum drug-resistant or recurrent ovarian cancer patients.
c-Myc transactivates miR-141 expression and that BRD7, a direct target of c-Myc, serves as a cofactor of c-Myc and forms a negative feedback loop with c-Myc in miR-141 transcription in NPC.
Study demonstrates that the plasmacytoid dendritic cells (pDCs)-specific RUNX2 super-enhancer is hijacked to activate expression of MYC via t(6;8) in blastic plasmacytoid dendritic cell neoplasm (BPDCN) cells, and unveil the molecular mechanisms underlying the pathogenesis of BPDCN, which originates from a precursor of pDCs.
PHF10 expression in cells of different lines is activated by the c-MYC oncogene. Since PHF10 stimulates cell proliferation, its c-MYC-dependent activation in cancer cells should lead to an increase in their proliferation rate.
C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT.
Mitochondrial AKAP1 supports mTOR pathway and tumor growth.
MYC protein is expressed in variable degrees among pediatric small round blue cell tumors (SRBCT), and expression of this protein can be upregulated/deregulated in many ways. Findings provide a baseline for MYC expression in pediatric SRBCT and suggest that there may be multiple mechanisms of MYC upregulation in these different neoplasms.
Our study highlighted the high colorectal cancer risk of people carrying MYC rs6983267 G and KBTBD11 rs11777210 C alleles
miR-105 promotes MYC-mediated metabolic reprogramming of breast cancer stromal cells, contributing to sustained tumour growth by conditioning the shared metabolic environment.
The high expression of c-myc may promote the invasion and metastasis of cervical cancer, and the high expression of bcat1 may promote the proliferation, invasion and metastasis of cervical cancer, which may have a synergistic effect in the pathogenesis of cervical cancer.
MYC activity underlies intrinsic resistance to ibrutinib in MCL. As a client protein of HSP90, MYC can be inhibited via PU-H71 to overcome primary ibrutinib resistance.
RMRP functions as a miR-34a-5p sponge to promote cell proliferation and repress cell apoptosis through upregulation of c-Myc in MM
Authors show that loss of the tumor suppressor p53 increased MYC mRNA levels even in the absence of estrogen stimulation. However, in cells with wild-type p53, SRC acted to overcome p53-mediated inhibition of estrogen-stimulated cell cycle entry and progression.
Study reports a high-resolution crystal structure (2.35 A) of the major quadruplex formed in the NHE III1 region of the c-MYC promoter. The crystal structure is in general agreement with the solution NMR structure, however, key differences are observed in the position of nucleotides outside the G-quartet core.
Findings suggested that KPNA2, a potential tumor oncogene, performs its function in part via regulating cellular metabolism through c-myc signaling axis. It would provide a possible explanation for Warburg effect and thus offer a new perspective to the roles of KPNA2 in gliomagenesis.
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
Reprogramming factors (Oct4, Sox2, Klf4, c-myc) induce proliferation and inhibit apoptosis of melanoma cells by changing the expression of particular genes.
These findings suggest Myc-nick as a novel proresolving mediator that has a fundamental function in maintaining homeostasis under inflammatory conditions
We propose Myc as a candidate susceptibility gene, regulated by the gene desert locus, and a potential role for Fam84b in modifying breast cancer development.
observed that Myc and ChREBP cooperatively up-regulated virtually all ribosomal protein genes
Across cell types Dppa4 shows a preference for binding to regions with active chromatin signatures, and can influence chromatin modifications at target genes. Data provide novel insights into Dppa4 function in both pluripotent and oncogenic contexts.
Sustained exposure of cells to TGF-beta resulted in recovery from proliferative arrest in association with amplification of the Myc proto-oncogene, with MYC inhibiting TRIM26 induction by TGF-beta.
High myc is associated with tumourigenic transformation.
Our results show that reprogramming is enhanced in MEFs deficient in BAK and BAX, but only when MYC is part of the reprogramming cocktail. Thus, the propensity for Myc overexpression to elicit apoptosis creates a significant roadblock to reprogramming under OKSM conditions.
These findings established a link between GCN5 and the FGF signaling pathway and highlighted specific GCN5-MYC partnerships in gene regulation during early differentiation.
amino acid-controlled cMyc has an essential role in NK cell metabolism and function
GATAD2B interacts with C-MYC to enhance KRAS driven tumor growth.
Kidney specific MYC activation results in papillary clear cell renal cell carcinoma.
c-Myc is essential for tumor initiation, maintenance, and metastasis.
Genomic characterization of Emu-Myc mouse lymphomas identifies Bcor as a Myc cooperative tumor-suppressor gene.
The data supports an indispensable role for Mule in cardiac homeostasis through the regulation of mitochondrial function via maintenance of Pgc-1alpha and Pink1 expression and persistent negative regulation of c-Myc.
MYC binding is enriched at neuroendocrine genes in tumor cells and loss of MYC reduces ductal-neuroendocrine lineage heterogeneity, while deregulated MYC expression in KRAS mutants increases this phenotype.
Although either BCR or CD40 ligation induced c-Myc in naive B cells, both signals were required to highly induce c-Myc, a critical mediator of GC B cell survival and cell cycle reentry.
Myc is a component that links neuromesodermal progenitors maintenance and pre-somitic mesoderm maturation during the body axis elongation stages of mouse embryogenesis.
Myc potentiates the Wnt/beta-catenin signalling pathway, which cooperates with the transcriptional regulatory network in sustaining embryonic stem cell self-renewal.
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.
Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair during kidney injury and development
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(-/-) 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 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 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.
findings reveal an evolutionarily conserved functional link between Myc, the Tip60 complex, and the molecular network controlling cell polarity and asymmetric cell division.
An ankyrin-binding motif regulates nuclear levels of L1-type neuroglian and expression of the oncogene Myc in Drosophila neurons.
tissue specific downregulation of dMyc (Drosophila homolog of human c-myc proto-oncogene) alleviates h-tau mediated cellular and functional deficits by restricting the formation of NFTs in neuronal tissues.
Expression of Drosophila Myc (dMyc) suppresses, whereas loss of dMyc enhances, ectopically activated JNK signaling-induced cell death. dMyc impedes physiologically activated JNK pathway-mediated cell death. Loss of dMyc triggers JNK pathway activation and JNK-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-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 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-Notch-dMyc cascade plays a key role in setting the activated state of adult muscle precursors.
a functional link between Myc, a renowned oncogene, and the essential nucleotide biosynthetic enzyme CTPsyn.
MYC and S6K cooperate through coordinate activation of the essential Pol I transcription initiation factor TIF-1A.
The data demonstrate that dMYC repression and dMYC-dependent overgrowth in the Hfp hypomorph is further impaired in the C-terminal Hay/XPB mutant background.
Myc acts as a master regulator of small nucleolar ribonucleoprotein biogenesis.
In this review, we focus on studies of MYC in the fruitfly with particular emphasis on metabolism and cell competition, highlighting the contributions of this model system in the last decade to our understanding of MYC's complex biological nature
Review discussing competitive interactions that are regulated by cell-to-cell differences in MYC activity and their role in tumor formation.
Myc may act as a pro-aging factor, possibly through its ability to greatly increase genome instability
a basal level of dMyc expression is required for Intestinal stem cell maintenance, proliferation and lineage differentiation during normal tissue homeostasis.
These novel results give additional support for finding future approaches to specifically inhibit the growth of cancer cells addicted to oncogenic Myc.
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