Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
about
Coordinated regulation of iron-controlling genes, H-ferritin and IRP2, by c-MYCNmi protein interacts with regions that differ between MycN and Myc and is localized in the cytoplasm of neuroblastoma cells in contrast to nuclear MycNMlx, a new Max-like bHLHZip family member: the center stage of a novel transcription factors regulatory pathway?A novel 16-kilodalton cellular protein physically interacts with and antagonizes the functional activity of c-myc promoter-binding protein 1Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiationMyc-Max heterodimers activate a DEAD box gene and interact with multiple E box-related sites in vivoc-MYC activates protein kinase A (PKA) by direct transcriptional activation of the PKA catalytic subunit beta (PKA-Cbeta) geneRegulation of expression of nuclear and mitochondrial forms of human uracil-DNA glycosylasep73 Interacts with c-Myc to regulate Y-box-binding protein-1 expressionDirect activation of HSP90A transcription by c-Myc contributes to c-Myc-induced transformationDNA binding specificities and pairing rules of the Ah receptor, ARNT, and SIM proteinsc-Myc directly regulates the transcription of the NBS1 gene involved in DNA double-strand break repairBiological stoichiometry in human cancer.Mechanisms of apoptosis by c-Myc.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 apoptosisMyc and Mad bHLHZ domains possess identical DNA-binding specificities but only partially overlapping functions in vivo.The Max b-HLH-LZ can transduce into cells and inhibit c-Myc transcriptional activities.Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.Functional analysis of the AUG- and CUG-initiated forms of the c-Myc proteinReverse engineering the neuroblastoma regulatory network uncovers MAX as one of the master regulators of tumor progression.Suppression of Myc, but not E1a, transformation activity by Max-associated proteins, Mad and Mxi1Involvement of simultaneous multiple transcription factor expression, including cAMP responsive element binding protein and OCT-1, for synovial cell outgrowth in patients with rheumatoid arthritisGcn5p-dependent acetylation induces degradation of the meiotic transcriptional repressor Ume6pc-Myc transactivation of LDH-A: implications for tumor metabolism and growth.An essential domain of the c-myc protein interacts with a nuclear factor that is also required for E1A-mediated transformationA link between increased transforming activity of lymphoma-derived MYC mutant alleles, their defective regulation by p107, and altered phosphorylation of the c-Myc transactivation domain.Rearranged NFKB-2 genes in lymphoid neoplasms code for constitutively active nuclear transactivators.Variant Max protein, derived by alternative splicing, associates with c-Myc in vivo and inhibits transactivationAn essential E box in the promoter of the gene encoding the mRNA cap-binding protein (eukaryotic initiation factor 4E) is a target for activation by c-myc.The Myc negative autoregulation mechanism requires Myc-Max association and involves the c-myc P2 minimal promoter.A minimal regulatory region maintains constitutive expression of the max gene.Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation.An 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.Identification of a Myc-dependent step during the formation of active G1 cyclin-cdk complexes.c-Myc represses transcription in vivo by a novel mechanism dependent on the initiator element and Myc box IIDistinct DNA binding preferences for the c-Myc/Max and Max/Max dimers.
P2860
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P2860
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年論文
@yue
1993年論文
@zh-hant
1993年論文
@zh-hk
1993年論文
@zh-mo
1993年論文
@zh-tw
1993年论文
@wuu
1993年论文
@zh
1993年论文
@zh-cn
name
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
@ast
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
@en
type
label
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
@ast
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
@en
prefLabel
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
@ast
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
@en
P2093
P2860
P356
P1476
Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.
@en
P2093
P2860
P304
P356
10.1073/PNAS.90.7.2935
P407
P577
1993-04-01T00:00:00Z