Both TEL and AML-1 Contribute Repression Domains to the t(12;21) Fusion Protein

No abstract is available for this paper.

• Publication year

  1999

• Venue

  Molecular and Cellular Biology

• Publication date

  1999-10-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1128/MCB.19.10.6566PMID 10490596PMCID PMC84626
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Three distinct domains in TEL-AML1 are required for transcriptional repression of the IL-3 promoter

  1999cited by this paper
• The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation.

  1998cited by this paper
• Transcriptional repression by AML1 and LEF-1 is mediated by the TLE/Groucho corepressors.

  1998cited by this paper
• ETO, a Target of t(8;21) in Acute Leukemia, Interacts with the N-CoR and mSin3 Corepressors

  1998cited by this paper
• The t(8;21) Fusion Product, AML-1–ETO, Associates with C/EBP-α, Inhibits C/EBP-α-Dependent Transcription, and Blocks Granulocytic Differentiation

  1998cited by this paper
• Analysis of TEL proteins in human leukemias

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• E2F-1 and E2F-3 are functionally distinct in their ability to promote myeloid cell cycle progression and block granulocyte differentiation.

  1998cited by this paper
• Distinct requirements for chromatin assembly in transcriptional repression by thyroid hormone receptor and histone deacetylase

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• Interaction and functional cooperation of the leukemia‐associated factors AML1 and p300 in myeloid cell differentiation

  1998cited by this paper
• The ets Family Member Tel Binds to the Fli-1 Oncoprotein and Inhibits Its Transcriptional Activity*

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• ETV6-NTRK3 gene fusions and trisomy 11 establish a histogenetic link between mesoblastic nephroma and congenital fibrosarcoma.

  1998cited by this paper
• The partner gene of AML1 in t(16;21) myeloid malignancies is a novel member of the MTG8(ETO) family.

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• A complex containing N-CoR, mSln3 and histone deacetylase mediates transcriptional repression

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• Cell growth inhibition by the Mad/Max complex through recruitment of histone deacetylase activity.

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• Functional characterization of ETV6 and ETV6/CBFA2 in the regulation of the MCSFR proximal promoter.

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• TEL is one of the targets for deletion on 12p in many cases of childhood B-lineage acute lymphoblastic leukemia

  1997cited by this paper
• Deletions of CDKN1B and ETV6 in acute myeloid leukemia and myelodysplastic syndromes without cytogenetic evidence of 12p abnormalities

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• ETV6 is the target of chromosome 12p deletions in t(12;21) childhood acute lymphocytic leukemia

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  1996cited by this paper
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  1996cited by this paper
• Biallelic alterations of both ETV6 and CDKN1B genes in a t(12;21) childhood acute lymphoblastic leukemia case.

  1996cited by this paper
• The TEL/platelet-derived growth factor beta receptor (PDGF beta R) fusion in chronic myelomonocytic leukemia is a transforming protein that self-associates and activates PDGF beta R kinase-dependent signaling pathways.

  1996influential reference
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  1996cited by this paper
• Deletion of the short arm of chromosome 12 is a secondary event in acute lymphoblastic leukemia with t(12;21).

  1996cited by this paper
• The TEL/platelet-derived growth factor β receptor (PDGFβR) fusion in chronic myelomonocytic leukemia is a transforming protein that self-associates and activates PDGFβR kinase-dependent signaling pathways

  1996cited by this paper
• Repression of I-Aβ Gene Expression by the Transcription Factor PU.1 (*)

  1995cited by this paper
• TEL/AML1 fusion resulting from a cryptic t(12;21) is the most common genetic lesion in pediatric ALL and defines a subgroup of patients with an excellent prognosis.

  1995influential reference
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  1995cited by this paper
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  1995cited by this paper
• Fusion of the TEL gene on 12p13 to the AML1 gene on 21q22 in acute lymphoblastic leukemia.

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• High frequency of t(12;21) in childhood B-lineage acute lymphoblastic leukemia.

  1995influential reference
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  2024cites this paper
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