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miR-17-92-dependent tuning of LKB1 (show STK11 ELISA Kits) levels regulates both the metabolic potential of Myc+ lymphomas and tumor growth in vivo.
Under diabetic oxidative stress or H2O2 stimulation, nuclear beta-catenin (show CTNNB1 ELISA Kits) accumulation upregulated downstream c-Myc and further facilitated DNA damage and p53 (show TP53 ELISA Kits)-mediated apoptosis as well as cell viability reduction, followed by phenotypic changes of cardiac dysfunction, interstitial fibrosis deposition and myocardial atrophy.
deficiency alters the expression of a crucial subset of TAL1 (show TAL1 ELISA Kits)- and NOTCH1 (show NOTCH1 ELISA Kits)-regulated genes, including the MYB (show MYB ELISA Kits) and MYC oncogenes, respectively.
B-cell receptor controls fitness of MYC-driven lymphoma cells via GSK3beta (show GSK3b ELISA Kits) inhibition
High Myc expression is associated with hepatocarcinogenesis.
Myc-high embryonic stem cells (ESCs (show NR2E3 ELISA Kits)) approach the naive pluripotency state, whereas Myc-low ESCs (show NR2E3 ELISA Kits) are closer to the differentiation-primed state.
Authors here report the first MBG3 model from embryonic cerebellar cells by Myc activation and loss of Trp53 (show TP53 ELISA Kits) function using in utero electroporation (EP)-based in vivo gene transfer combined to a Cre/LoxP-mediated technology.
by controlling both nanodomain decompaction and PolII promoter escape Myc stands as a master regulator of transcriptome amplification during B cell activation (show BLNK ELISA Kits).
these results indicate that PIAS1 (show PIAS1 ELISA Kits) is a positive regulator of MYC.
this study shows that that deletion of Sox2 (show SOX2 ELISA Kits) increases the frequency of IgH:c-Myc translocations
Apoptosis was also observed with myca expression; introduction of homozygous tp53 (show TP53 ELISA Kits)(-/-) mutation into the myca transgenic fish reduced apoptosis and accelerated tumor progression.
MYC down-regulation induces mitochondrial apoptosis in T lymphoblasts.
Data show that MYC, BCL2 (show BCL2 ELISA Kits) and BCL6 (show BCL6 ELISA Kits) translocation had no prognostic impact with respect to progression free survival (PFS) or overall survival (OS).
Study demonstrated that local recurrent gastric cancer patients showed higher c-Myc and hTERT expression at the protein and mRNA levels, and that acidified bile acids enhance tumor progression and telomerase activity in gastric cancer via Myc activity.
EBNA2 recruits the BRG1 (show SMARCA4 ELISA Kits) ATPase (show DNAH8 ELISA Kits) of the SWI (show SMARCA1 ELISA Kits)/SNF (show SNRPA ELISA Kits) remodeller to MYC enhancers and BRG1 (show SMARCA4 ELISA Kits) is required for enhancer-promoter interactions in Epstein-Barr virus-infected cells.
No significant difference in survival was found between patients with DLBCL with MYC ICN and patients with no MYC aberrations
High myc expression is associated with brain cancer.
MYC positively regulates RUNX3 (show RUNX3 ELISA Kits) transcription in NKTL cell lines. MYC interacts with RUNX3 (show RUNX3 ELISA Kits). Potential binding sites for MYC were identified in the RUNX3 (show RUNX3 ELISA Kits) enhancer region. MYC-inhibitor JQ1 caused significant downregulation of MYC and RUNX3 (show RUNX3 ELISA Kits), leading to apoptosis in NKTL cells. MYC may be an important upstream driver of RUNX3 (show RUNX3 ELISA Kits) upregulation.
High myc expression is associated with lung cancer.
MYC/BCL2 (show BCL2 ELISA Kits) co-expression is associated with a poorer prognosis and is independent of cell-of-origin classification in diffuse large B-cell lymphoma of the CNS.
Functional validation of the oncogenic cooperativity and targeting potential of tuberous sclerosis mutation in medulloblastoma using a MYC-amplified model cell line
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
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.
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.
v-myc myelocytomatosis viral oncogene homolog
, Avian myelocytomatosis viral (v-myc) oncogene homolog
, myc proto-oncogene protein
, myelocytomatosis viral oncogene homolog
, proto-oncogene c-Myc
, transcription factor p64
, v-myc avian myelocytomatosis viral oncogene homolog
, c-myc proto-oncogene
, cellular myelocytomatosis oncogene
, transcriptional regulator Myc-A
, avian myelocytomatosis viral oncogene homolog
, class E basic helix-loop-helix protein 39
, myc-related translation/localization regulatory factor
, avian myelocytomatosis viral (v-myc) oncogene homolog
, Proto-oncogene c-Myc
, Transcription factor p64
, Myc proto-oncogene protein