Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation. - Wikidata - awgldk - TriplyDB

Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation.

Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation.

http://www.wikidata.org/entity/Q33888207

about

Role of MXD3 in proliferation of DAOY human medulloblastoma cells Overexpressed BCL6 (LAZ3) oncoprotein triggers apoptosis, delays S phase progression and associates with replication foci Role of Mxi1 in ageing organ systems and the regulation of normal and neoplastic growth Mad4 is regulated by a transcriptional repressor complex that contains Miz-1 and c-Myc The transcriptional repressor gene Mad3 is a novel target for regulation by E2F1 MondoA, a novel basic helix-loop-helix-leucine zipper transcriptional activator that constitutes a positive branch of a max-like network IKKalpha, a critical regulator of epidermal differentiation and a suppressor of skin cancer Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis Specific distribution of the Saccharomyces cerevisiae linker histone homolog HHO1p in the chromatin.Perinatal synthetic lethality and hematopoietic defects in compound mafG::mafK mutant mice Dynamic in vivo interactions among Myc network members Targeting of the transcription factor Max during apoptosis: phosphorylation-regulated cleavage by caspase-5 at an unusual glutamic acid residue in position P1 RNF17, a component of the mammalian germ cell nuage, is essential for spermiogenesis Expression of Mad1 in T cells leads to reduced thymic cellularity and impaired mitogen-induced proliferation tRNA synthetase counteracts c-Myc to develop functional vasculature.New Myc-interacting proteins: a second Myc network emerges.The Mad protein family links transcriptional repression to cell differentiation.TGFβ1 enhances MAD1 expression and stimulates promoter-bound Pol II phosphorylation: basic functions of C/EBP, SP and SMAD3 transcription factors A new functional classification of tumor-suppressing genes and its therapeutic implications.Origin of bistability underlying mammalian cell cycle entry The transcriptional repressor dMnt is a regulator of growth in Drosophila melanogaster c-Myc target genes involved in cell growth, apoptosis, and metabolism Mad1 function is regulated through elements within the carboxy terminus Targeted deletion of the S-phase-specific Myc antagonist Mad3 sensitizes neuronal and lymphoid cells to radiation-induced apoptosis.The Mad and Myc basic domains are functionally equivalent.A humanized Smn gene containing the SMN2 nucleotide alteration in exon 7 mimics SMN2 splicing and the SMA disease phenotype.Mad upregulation and Id2 repression accompany transforming growth factor (TGF)-beta-mediated epithelial cell growth suppression.MAD1 and p27(KIP1) cooperate to promote terminal differentiation of granulocytes and to inhibit Myc expression and cyclin E-CDK2 activity Function of RARalpha during the maturation of neutrophils.Inflammatory disease and lymphomagenesis caused by deletion of the Myc antagonist Mnt in T cells.Essential role for Max in early embryonic growth and development Loss of MXD3 induces apoptosis of Reh human precursor B acute lymphoblastic leukemia cells.Normal and leukaemic stem cells.Mnt loss triggers Myc transcription targets, proliferation, apoptosis, and transformation Specific requirement of the chromatin modifier mSin3B in cell cycle exit and cellular differentiation Keeping things quiet: roles of NuRD and Sin3 co-repressor complexes during mammalian development.An overview of MYC and its interactome.MAD1 and c-MYC regulate UBF and rDNA transcription during granulocyte differentiation Downregulation of Max dimerization protein 3 is involved in decreased visceral adipose tissue by inhibiting adipocyte differentiation in zebrafish and mice.Mxi1 is a potential cellular target of carcinogens and frequently mutated in experimental rat tumors and tumor cell lines.

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P2860

Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation.

http://www.wikidata.org/entity/Q33888207

description

1998 nî lūn-bûn

@nan

1998 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

1998 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

1998年の論文

@ja

1998年論文

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1998年論文

@zh-hant

1998年論文

@zh-hk

1998年論文

@zh-mo

1998年論文

@zh-tw

1998年论文

@wuu

name

Targeted disruption of the MYC ...... g granulocyte differentiation.

@ast

Targeted disruption of the MYC ...... g granulocyte differentiation.

@en

type

label

Targeted disruption of the MYC ...... g granulocyte differentiation.

@ast

Targeted disruption of the MYC ...... g granulocyte differentiation.

@en

prefLabel

Targeted disruption of the MYC ...... g granulocyte differentiation.

@ast

Targeted disruption of the MYC ...... g granulocyte differentiation.

@en

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The EMBO Journal

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Targeted disruption of the MYC ...... ng granulocyte differentiation

@en

P2093

C Quéva

http://www.w3.org/2001/XMLSchema#string

G A McArthur

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K P Foley

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P J Hurlin

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R N Eisenman

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P2860

Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc

Rox, a novel bHLHZip protein expressed in quiescent cells that heterodimerizes with Max, binds a non-canonical E box and acts as a transcriptional repressor.

Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation

Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity

Mxi1, a protein that specifically interacts with Max to bind Myc-Max recognition sites

Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3

An amino-terminal domain of Mxi1 mediates anti-Myc oncogenic activity and interacts with a homolog of the yeast transcriptional repressor SIN3

Histone deacetylase activity is required for full transcriptional repression by mSin3A

Histone deacetylases associated with the mSin3 corepressor mediate mad transcriptional repression

Transcriptional enhancer factor 1 disruption by a retroviral gene trap leads to heart defects and embryonic lethality in mice

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774-785

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scholarly article

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10.1093/EMBOJ/17.3.774

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3

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17

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Philippe Soriano

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1998-02-01T00:00:00Z

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13779732

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9451002

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1170426

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