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Human Monoclonal C-MYC Primary Antibody pour FACS, IHC (p) - ABIN302092
Veracini, Simon, Richard, Schraven, Horejsi, Roche, Benistant: The Csk-binding protein PAG regulates PDGF-induced Src mitogenic signaling via GM1. dans The Journal of cell biology 2008
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Human Monoclonal C-MYC Primary Antibody pour FACS, IHC (p) - ABIN302017
Wang, Campoli, Ko, Luo, Ferrone: Enhancement of scFv fragment reactivity with target antigens in binding assays following mixing with anti-tag monoclonal antibodies. dans Journal of immunological methods 2004
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All Species Monoclonal C-MYC Primary Antibody pour 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. dans Science (New York, N.Y.) 1984
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Chicken Monoclonal C-MYC Primary Antibody pour ChIP, CyTOF - ABIN152253
Locker, Dowle, Ellis, Elston, Blamey, Sikora, Evan, Robins: c-myc oncogene product expression and prognosis in operable breast cancer. dans British journal of cancer 1989
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All Species Monoclonal C-MYC Primary Antibody pour IHC, IHC (p) - ABIN4994828
Hilpert, Hansen, Wessner, Küttner, Welfle, Seifert, Höhne: Anti-c-myc antibody 9E10: epitope key positions and variability characterized using peptide spot synthesis on cellulose. dans Protein engineering 2001
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Human Monoclonal C-MYC Primary Antibody pour IHC (fro), IF - ABIN2477762
Quant, Woo: Normal values of eye position in the Chinese population of Hong Kong. dans Optometry and vision science : official publication of the American Academy of Optometry 1992
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Human Monoclonal C-MYC Primary Antibody pour FACS, IHC (p) - ABIN536092
Fujiwara, Poikonen, Aleman, Valtavaara, Saksela, Mayer: A single-chain antibody/epitope system for functional analysis of protein-protein interactions. dans Biochemistry 2002
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Human Polyclonal C-MYC Primary Antibody pour IF (cc), IF (p) - ABIN1387773
Gao, Zhao, Song, Yang: Expression pattern of embryonic stem cell markers in DFAT cells and ADSCs. dans Molecular biology reports 2012
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Human Monoclonal C-MYC Primary Antibody pour EMSA, IP - ABIN2668816
Sommer, Bousset, Kremmer, Austen, Lüscher: Identification and characterization of specific DNA-binding complexes containing members of the Myc/Max/Mad network of transcriptional regulators. dans The Journal of biological chemistry 1998
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Results provide evidence that myc expression level is regulated by BRD4 (Montrer BRD4 Anticorps) in gastric neoplasm through transcriptional and epigenetic regulation.
These results indicated that cMyc and Fas (Montrer FAS Anticorps) regulated the sensitivity of A549 cells to irradiation by regulating caspase8-mediated Bid (Montrer BID Anticorps) activation and the subsequent association with the mitochondrial pathway of apoptosis.
These results indicate that Merlin (Montrer NF2 Anticorps)/YAP (Montrer YAP1 Anticorps)/cMyc/mTOR (Montrer FRAP1 Anticorps) signaling axis promotes human cholangiocarcinoma (CCA (Montrer FBN2 Anticorps)) cell proliferation by overriding contact inhibition. We propose that overriding cMycmediated contact inhibition is implicated in the development of CCA (Montrer FBN2 Anticorps).
PLGF (Montrer PGF Anticorps) promotes Epithelial-mesenchymal transition (EMT (Montrer ITK Anticorps)) and tumorsphere formation through inducing miR (Montrer MLXIP Anticorps)-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 (Montrer CD274 Anticorps) and HLA class I (Montrer MICA Anticorps) represents a novel prognostic biomarker for neuroblastoma (Montrer ARHGEF16 Anticorps). Pharmacologic inhibition of MYCN (Montrer MYCN Anticorps) and MYC may be exploited to target PD-L1 (Montrer CD274 Anticorps) and restore an efficient antitumor immunity in high-risk neuroblastoma (Montrer ARHGEF16 Anticorps).
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 (Montrer BCR Anticorps)-PI3K (Montrer PIK3CA Anticorps) 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 (Montrer HELLS Anticorps)-associated loss of NUDT16 (Montrer NUDT16 Anticorps), which contributes to the natural history of the disease by stabilizing transforming factors, such as is the case of the leukemogenic protein C (Montrer PROC Anticorps)-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 (Montrer 0 Anticorps) 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 Anticorps) 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 (Montrer NACC1 Anticorps) overexpression promotes ESC proliferation and delays ESC differentiation in the absence of leukemia inhibitory factor (LIF (Montrer LIF Anticorps)). Furthermore, we demonstrated that Nac1 (Montrer NACC1 Anticorps) directly binds to the c-Myc promoter and regulates c-Myc transcription.
this study demonstrates that miR (Montrer MLXIP Anticorps)-451 regulates T cell proliferative responses in part via a Myc-dependent mechanism
AKAP1 (Montrer AKAP1 Anticorps) is a transcriptional target of Myc, and it supports mTOR (Montrer FRAP1 Anticorps) pathway and the growth of cancer cells.
Apoptosis was also observed with myca expression; introduction of homozygous tp53 (Montrer TP53 Anticorps)(-/-) 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 Anticorps) 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 Anticorps) 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 Anticorps) signaling-induced cell death. dMyc impedes physiologically activated JNK (Montrer MAPK8 Anticorps) pathway-mediated cell death. Loss of dMyc triggers JNK (Montrer MAPK8 Anticorps) pathway activation and JNK (Montrer MAPK8 Anticorps)-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 Anticorps)-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 Anticorps) 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 Anticorps)-Notch (Montrer NOTCH1 Anticorps)-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 Anticorps), and the essential nucleotide biosynthetic enzyme CTPsyn.
MYC and S6K (Montrer RPS6KB1 Anticorps) cooperate through coordinate activation of the essential Pol I transcription initiation factor TIF-1A (Montrer RRN3 Anticorps).
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