Sequence-specific transcriptional activation by Myc and repression by Max.
about
Nmi protein interacts with regions that differ between MycN and Myc and is localized in the cytoplasm of neuroblastoma cells in contrast to nuclear MycNMad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiationTranscriptional activation by Myc is under negative control by the transcription factor AP-2Transcription enhancer factor 1 interacts with a basic helix-loop-helix zipper protein, Max, for positive regulation of cardiac alpha-myosin heavy-chain gene expressionN-Myc regulates a widespread euchromatic program in the human genome partially independent of its role as a classical transcription factorPou5f1/Oct4 promotes cell survival via direct activation of mych expression during zebrafish gastrulationRtg3p, a basic helix-loop-helix/leucine zipper protein that functions in mitochondrial-induced changes in gene expression, contains independent activation domains.Mcm1 is required to coordinate G2-specific transcription in Saccharomyces cerevisiae.p73 Interacts with c-Myc to regulate Y-box-binding protein-1 expressionMutation of the MXI1 gene in prostate cancerThe nerve growth factor-responsive PC12 cell line does not express the Myc dimerization partner MaxEarly nuclear exclusion of the transcription factor max is associated with retinal ganglion cell death independent of caspase activityActivation of cyclin-dependent kinases by Myc mediates induction of cyclin A, but not apoptosisPhosphatidylserine increases IKBKAP levels in familial dysautonomia cellsCo-localization of the oncogenic transcription factor MYCN and the DNA methyl binding protein MeCP2 at genomic sites in neuroblastoma.c-Myc target genes involved in cell growth, apoptosis, and metabolismMad1 function is regulated through elements within the carboxy terminusHMG-I/Y, a new c-Myc target gene and potential oncogeneInduction of cell cycle progression and acceleration of apoptosis are two separable functions of c-Myc: transrepression correlates with acceleration of apoptosisTargeted deletion of the S-phase-specific Myc antagonist Mad3 sensitizes neuronal and lymphoid cells to radiation-induced apoptosis.Myc and Mad bHLHZ domains possess identical DNA-binding specificities but only partially overlapping functions in vivo.Overexpression of the c-Myc oncoprotein blocks the growth-inhibitory response but is required for the mitogenic effects of transforming growth factor beta 1.Functional analysis of the AUG- and CUG-initiated forms of the c-Myc proteinMyc represses the p21(WAF1/CIP1) promoter and interacts with Sp1/Sp3.Assembly of b/HLH/z proteins c-Myc, Max, and Mad1 with cognate DNA: importance of protein-protein and protein-DNA interactions.An essential domain of the c-myc protein interacts with a nuclear factor that is also required for E1A-mediated transformationVariant Max protein, derived by alternative splicing, associates with c-Myc in vivo and inhibits transactivationCyclin D3 sensitizes tumor cells to tumor necrosis factor-induced, c-Myc-dependent apoptosis.A minimal regulatory region maintains constitutive expression of the max gene.Identification of downstream-initiated c-Myc proteins which are dominant-negative inhibitors of transactivation by full-length c-Myc proteins.Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation.Repression of cyclin D1: a novel function of MYCHierarchical phosphorylation at N-terminal transformation-sensitive sites in c-Myc protein is regulated by mitogens and in mitosis.Myc-mediated apoptosis is blocked by ectopic expression of Bcl-2Cell cycle regulation of the c-Myc transcriptional activation domain.A bipartite nuclear localization signal in the retinoblastoma gene product and its importance for biological activityAn E-box element localized in the first intron mediates regulation of the prothymosin alpha gene by c-mycA link between c-Myc-mediated transcriptional repression and neoplastic transformation.Sin3 corepressor function in Myc-induced transcription and transformation.Epigenetic silencing of the RASSF1A tumor suppressor gene through HOXB3-mediated induction of DNMT3B expression.
P2860
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P2860
Sequence-specific transcriptional activation by Myc and repression by Max.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年学术文章
@wuu
1993年学术文章
@zh-cn
1993年学术文章
@zh-hans
1993年学术文章
@zh-my
1993年学术文章
@zh-sg
1993年學術文章
@yue
1993年學術文章
@zh
1993年學術文章
@zh-hant
name
Sequence-specific transcriptional activation by Myc and repression by Max.
@en
type
label
Sequence-specific transcriptional activation by Myc and repression by Max.
@en
prefLabel
Sequence-specific transcriptional activation by Myc and repression by Max.
@en
P2093
P2860
P356
P1476
Sequence-specific transcriptional activation by Myc and repression by Max.
@en
P2093
P2860
P304
P356
10.1128/MCB.13.1.383
P407
P577
1993-01-01T00:00:00Z